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Article Contents

Answer to part 1, answer to part 2, answer to part 3, answer to part 4, answer to part 5.

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Educational Case: A 57-year-old man with chest pain

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Nikhil Aggarwal, Subothini Selvendran, Vassilios Vassiliou, Educational Case: A 57-year-old man with chest pain, Oxford Medical Case Reports , Volume 2016, Issue 4, April 2016, Pages 62–65, https://doi.org/10.1093/omcr/omw008

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This is an educational case report including multiple choice questions and their answers. For the best educational experience we recommend the interactive web version of the exercise which is available via the following link: http://www.oxfordjournals.org/our_journals/omcr/ec01p1.html

A 57 year-old male lorry driver, presented to his local emergency department with a 20-minute episode of diaphoresis and chest pain. The chest pain was central, radiating to the left arm and crushing in nature. The pain settled promptly following 300 mg aspirin orally and 800 mcg glyceryl trinitrate (GTN) spray sublingually administered by paramedics in the community. He smoked 20 cigarettes daily (38 pack years) but was not aware of any other cardiovascular risk factors. On examination he appeared comfortable and was able to complete sentences fully. There were no heart murmurs present on cardiac auscultation. Blood pressure was 180/105 mmHg, heart rate was 83 bpm and regular, oxygen saturation was 97%.

What is the most likely diagnosis?

An ECG was requested and is shown in figure 1.

How would you manage the patient? (The patient has already received 300 mg aspirin).

30 minutes later the patient's chest pain returned with greater intensity whilst waiting in the emergency department. Now, he described the pain as though “an elephant is sitting on his chest”. The nurse has already done an ECG by the time you were called to see him. This is shown in figure 2.

ECG on admission.

ECG 30 minutes after admission.

What would be the optimal management for this patient?

He was taken to the catheterization lab where the left anterior descending coronary artery (LAD) was shown to be completely occluded. Following successful percutaneous intervention and one drug eluding stent implantation in the LAD normal flow is restored (Thrombosis in myocardial infarction, TIMI = 3). 72 hours later, he is ready to be discharged home. The patient is keen to return to work and asks when he could do so.

When would you advise him that he could return to work?

One week later, he receives a letter informing him that he is required to attend cardiac rehabilitation. The patient is confused as to what cardiac rehabilitation entails, although he does remember a nurse discussing this with him briefly before he was discharged. He phones the hospital in order to get some more information.

Which of the following can be addressed during cardiac rehabilitation?

A - Acute coronary syndrome

Although the presentation could be attributable to any of the above differential diagnoses, the most likely etiology given the clinical picture and risk factors is one of cardiac ischemia. Risk factors include gender, smoking status and age making the diagnosis of acute coronary syndrome the most likely one. The broad differential diagnosis in patients presenting with chest pain has been discussed extensively in the medical literature. An old but relevant review can be found freely available 1 as well as more recent reviews. 2 , 3

C - Atorvastatin 80 mg, Clopidogrel 300 mcg, GTN 500 mcg, Ramipril 2.5 mg,

In patients with ACS, medications can be tailored to the individual patient. Some medications have symptomatic benefit but some also have prognostic benefit. Aspirin 4 , Clopidogrel 5 , Atenolol 6 and Atorvastatin 7 have been found to improve prognosis significantly. ACE inhibitors have also been found to improve left ventricular modeling and function after an MI. 8 , 9 Furthermore, GTN 10 and morphine 11 have been found to be of only significant symptomatic benefit.

Oxygen should only to be used when saturations <95% and at the lowest concentration required to keep saturations >95%. 12

There is no evidence that diltiazem, a calcium channel blocker, is of benefit. 13

His ECG in figure 1 does not fulfil ST elevation myocardial infarction (STEMI) criteria and he should therefore be managed as a Non-STEMI. He would benefit prognostically from beta-blockade however his heart rate is only 42 bpm and therefore this is contraindicated. He should receive a loading dose of clopidogrel (300 mg) followed by daily maintenance dose (75 mg). 14 , 15 He might not require GTN if he is pain-free but out of the available answers 3 is the most correct.

D - Proceed to coronary angiography

The ECG shows ST elevation in leads V2-V6 and confirms an anterolateral STEMI, which suggests a completely occluded LAD. This ECG fulfils the criteria to initiate reperfusion therapy which traditionally require one of the three to be present: According to guidance, if the patient can undergo coronary angiography within 120 minutes from the onset of chest pain, then this represents the optimal management. If it is not possible to undergo coronary angiography and potentially percutaneous intervention within 2 hours, then thrombolysis is considered an acceptable alternative. 12 , 16

≥ 1 mm of ST change in at least two contiguous limb leads (II, III, AVF, I, AVL).

≥ 2 mm of ST change in at least two contiguous chest leads (V1-V6).

New left bundle branch block.

GTN and morphine administration can be considered in parallel but they do not have a prognostic benefit.

E - Not before an exercise test

This patient is a lorry driver and therefore has a professional heavy vehicle driving license. The regulation for driving initiation in a lorry driver following a NSTEMI/ STEMI may be different in various countries and therefore the local regulations should be followed.

In the UK, a lorry driver holds a category 2 driving license. He should therefore refrain from driving a lorry for at least 6 weeks and can only return to driving if he completes successfully an exercise evaluation. An exercise evaluation is performed on a bicycle or treadmill. Drivers should be able to complete 3 stages of the standard Bruce protocol 17 or equivalent (e.g. Myocardial perfusion scan) safely, having refrained from taking anti-anginal medication for 48 hours and should remain free from signs of cardiovascular dysfunction during the test, notably: angina pectoris, syncope, hypotension, sustained ventricular tachycardia, and/or electrocardiographic ST segment shift which is considered as being indicative of myocardial ischemia (usually >2 mm horizontal or down-sloping) during exercise or the recovery period. 18

For a standard car driving license (category 1), driving can resume one week after successful intervention providing that no other revascularization is planned within 4 weeks; left ventricular ejection fraction (LVEF) is at least 40% prior to hospital discharge and there is no other disqualifying condition.

Therefore if this patent was in the UK, he could restart driving a normal car one week later assuming an echocardiogram confirmed an EF > 40%. However, he could only continue lorry driving once he has passed the required tests. 18

E - All of the above

Cardiac rehabilitation bridges the gap between hospitals and patients' homes. The cardiac rehabilitation team consists of various healthcare professions and the programme is started during hospital admission or after diagnosis. Its aim is to educate patients about their cardiac condition in order to help them adopt a healthier lifestyle. This includes educating patients' about their diet, exercise, risk factors associated with their condition such as smoking and alcohol intake and finally, about the medication recommended. There is good evidence that adherence to cardiac rehabilitation programmes improves survival and leads to a reduction in future cardiovascular events.​ 19 , 20

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Baigent C , Collins R , Appleby P , Parish S , Sleight P , Peto R . ISIS-2: 10 year survival among patients with suspected acute myocardial infarction in randomised comparison of intravenous streptokinase, oral aspirin, both, or neither. the ISIS-2 (second international study of infarct survival) collaborative group . BMJ . 1998 ; 316 (7141) : 1337 – 1343 . http://www.ncbi.nlm.nih.gov/pmc/articles/PMC28530/ .

Yusuf S , Zhao F , Mehta S , Chrolavicius S , Tognoni G , Fox K . Clopidogrel in unstable angina to prevent recurrent events trail investigators . effects of clopidogrel in addition to aspirin in patients with acute coronary syndromes without ST-segment elevation . N Engl J Med . 2001 ; 345 (7) : 494 – 502 . http://www.nejm.org/doi/full/10.1056/NEJMoa010746#t=articleTop .

Yusuf S , Peto R , Lewis J , Collins R , Sleight P . Beta blockade during and after myocardial infarction: An overview of the randomized trials . Prog Cardiovasc Dis . 1985 ; 27 (5) : 335 – 371 . http://www.sciencedirect.com/science/article/pii/S0033062085800037 .

Schwartz GG , Olsson AG , Ezekowitz MD et al.  . Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: The MIRACL study: A randomized controlled trial . JAMA . 2001 ; 285 (13) : 1711 – 1718 . http://jama.jamanetwork.com/article.aspx?articleid=193709 .

Pfeffer MA , Lamas GA , Vaughan DE , Parisi AF , Braunwald E . Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction . N Engl J Med . 1988 ; 319 (2) : 80 – 86 . http://content.onlinejacc.org/article.aspx?articleid=1118054 .

Sharpe N , Smith H , Murphy J , Hannan S . Treatment of patients with symptomless left ventricular dysfunction after myocardial infarction . The Lancet . 1988 ; 331 (8580) : 255 – 259 . http://www.sciencedirect.com/science/article/pii/S0140673688903479 .

Ferreira JC , Mochly-Rosen D . Nitroglycerin use in myocardial infarction patients . Circ J . 2012 ; 76 (1) : 15 – 21 . http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527093/ .

Herlitz J , Hjalmarson A , Waagstein F . Treatment of pain in acute myocardial infarction . Br Heart J . 1989 ; 61 (1) : 9 – 13 . http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1216614/ .

Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC), Steg PG, James SK, et al . ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation . Eur Heart J . 2012 ; 33 (20) : 2569 – 2619 . http://eurheartj.oxfordjournals.org/content/33/20/2569 .

The effect of diltiazem on mortality and reinfarction after myocardial infarction . the multicenter diltiazem postinfarction trial research group . N Engl J Med . 1988 ; 319 (7) : 385 – 392 . http://www.nejm.org/doi/full/10.1056/NEJM198808183190701 .

Jneid H , Anderson JL , Wright RS et al.  . 2012 ACCF/AHA focused update of the guideline for the management of patients with unstable angina/Non–ST-elevation myocardial infarction (updating the 2007 guideline and replacing the 2011 focused update) A report of the american college of cardiology foundation/american heart association task force on practice guidelines . J Am Coll Cardiol . 2012 ; 60 (7) : 645 – 681 . http://circ.ahajournals.org/content/123/18/2022.full .

Hamm CW , Bassand JP , Agewall S et al.  . ESC guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The task force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the european society of cardiology (ESC) . Eur Heart J . 2011 ; 32 (23) : 2999 – 3054 . http://eurheartj.oxfordjournals.org/content/32/23/2999.long .

O'Gara PT , Kushner FG , Ascheim DD et al.  . 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: Executive summary: A report of the american college of cardiology foundation/american heart association task force on practice guidelines . J Am Coll Cardiol . 2013 ; 61 (4) : 485 – 510 . http://content.onlinejacc.org/article.aspx?articleid=1486115 .

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A Case Report: Acute Myocardial Infarction in a 29-year-old Male

The heart score is a go-to tool in assessing the risk of an acute coronary syndrome. but in this case, a score of 3 did not mean the 29-year-old patient was safe..

Cardiovascular disease (CVD) is currently the leading cause of death in both men and women across the United States. The term describes a group of diseases that includes coronary artery disease, myocardial infarction (MI), stroke, and heart failure. There are both modifiable and non-modifiable risk factors that can increase the risk of a person’s susceptibility to CVD. Non-modifiable risk factors include ethnicity, family history of CVD, sex, and age. Historically, studies regarding CVD use 40-45 years old as the lower limit defining a “young” patient with CVD. These studies have found that 5-10% of patients experiencing an MI are younger than 40. 1

When a patient presents to the ED with chest pain, the HEART score is often used to assess the risk of an acute coronary syndrome (ACS). The parameters of the HEART score include a suspicious h istory, ischemic E CG findings, a ge, number of cardiac r isk factors, and initial t roponin levels. Each category will receive a value of 0, 1, or 2 for a maximum score of 10; a patient under 45 years old receives 0 points for the age category. A patient’s total HEART score can classify their 6-week risk of a major cardiac event as low, moderate, or high. In the case below, the patient received a HEART score of 3, a low score representing 0.9-1.7% 2 risk of having a major cardiac event.

CASE REPORT A 29-year-old Caucasian male with history of acute lymphoblastic leukemia (ALL) treated with full body radiation, marrow transplant and chemotherapy 12 years ago, presents to the ER with acute chest pain and SOB that began 3.5 hours prior to arrival, while delivering food. He then walked into the local CVS to check his blood pressure, which was “150s/90s.” Although unable to describe the quality of the pain, he is writhing in pain on the stretcher and rates it a 10/10. Nothing seems to be giving him any relief. He denies any similar past episodes. The patient does is not currently on any medications, denies a history of smoking or illicit drug use. The patient’s father has a history of CAD in his 50s, and his mother’s health is unremarkable. The patient has been in complete remission from ALL for 12 years; he has no other medical conditions. 

Figure 1. Initial EKG Reading

The patient’s initial workup in the ED included an ECG, chest X-ray, complete blood count, comprehensive metabolic panel, cardiac enzymes, lipase, and coagulation studies. His initial vitals were unremarkable. His initial EKG (Figure 1) performed in triage, showed normal sinus rhythm with hyperacute T wave changes in V2-V6; his potassium was 4.3. His other labs were unremarkable except for a troponin-I of 0.41.

A repeat ECG (Figure 2) was obtained 1.5 hours after the first, which showed normal sinus rhythm with significant ST segment elevation in leads I, II, and V1 through V6, suggesting an anterolateral MI.

The patient was immediately given aspirin, morphine, nitroglycerin, and heparin and was taken for emergent cardiac catheterization. Upon catheterization, he was found to have a 100-percent occlusion along the middle portion of the left anterior descending (LAD) artery; no occlusions were found in the right coronary artery or the the circumflex artery.

Stents were placed along the first and second diagonal branches of the LAD. During the procedure, the patient had several episodes of ventricular tachycardia, which resolved with deep coughing, and also had an episode of ventricular fibrillation requiring cardioversion to sinus rhythm. The catheterization lab report also noted that patient had an anterolateral apical hypokinesia and a left ventricular function of 40%.

Following percutaneous coronary intervention, the patient was admitted to the intensive care unit for further monitoring.

Discussion As a patient with low CVD risk factors, is important to consider the history of pediatric cancer. When the patient presented to the ED, he had been in complete remission from ALL for 12 years. As a child, he had undergone numerous combinations of chemotherapy, radiation, and eventually a bone marrow transplant. Studies have examined the development of atherosclerosis in patients who have received radiation. 3 In pediatric cancer patients, individuals who live more than 5 years following their radiation have shown an eightfold increase in their risk of developing atherosclerosis compared to the general population later in their life. 3

Another factor to consider in an ECG of a patient complaining of chest pain is the T wave. The T wave in an ECG is a reflection of the repolarization of the ventricles of the heart. The majority of T waves have a positive direction and should be asymmetric with a slow upstroke and a rapid downstroke. 4 The T waves in the limb leads should be less than 5 mm, and those in the chest leads should be less than 10 mm. 4 Upon the initial ECG of this patient, it was important to rule out any abnormalities in T wave presentation that could reflect underlying pathology of the heart. No evidence of hyperkalemia in the form of peaked T waves that could lead to fatal arrhythmias were seen at the time. However, hyperacute T waves were seen in leads II and V2 through V6. Hyperacute T waves are often, but not always, known to precede ST segment elevation. They are the earliest available electrical event that can be detected on an ECG during an acute ischemic event and can rapidly progress into ST segment elevation. 4 While a hyperacute T wave is not always associated with ST elevation, if detected on an ECG, the emergency physician should consider ordering serial ECGs along with the cardiac biomarkers to look out for any acute cardiac event.

References 1. Azar RR. Coronary heart disease and myocardial infarction in young men and women . UptoDate. Accessed November 6, 2018. 2. Wilson PWF. Cardiovascular disease risk assessment for primary prevention: Risk calculators . UpToDate. Accessed November 6, 2018. 3. Haddy N, Diallo S, El-Fayech C, et al. Cardiac Diseases Following Childhood Cancer Treatment .  Circulation . 2016;133(1):31-38. 4. Prutkin JM. ECG Tutorial: ST and T wave changes . UpToDate. Accessed November 6, 2018.

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• Introduction
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• Article Information

The start of the early coronavirus disease 2019 (COVID-19) period (February 23, 2020) and later COVID-19 period (March 29, 2020), as defined by segmented regression analysis, are indicated by vertical lines. Dotted lines indicate the best-fit regression lines for the 3 periods (including the before COVID-19 period). Projected volumes with 95% CIs are displayed in gray. STEMI indicates ST-segment elevation myocardial infarction.

eTable 1. ICD-10 Codes

eTable 2. MS-DRG Codes Used in Treatment Approaches Analysis

eTable 3. Weekly Case Volumes in 2020

eFigure 1. Weekly Volumes by State

eFigure 2. Treatment Approaches

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Gluckman TJ , Wilson MA , Chiu S, et al. Case Rates, Treatment Approaches, and Outcomes in Acute Myocardial Infarction During the Coronavirus Disease 2019 Pandemic. JAMA Cardiol. 2020;5(12):1419–1424. doi:10.1001/jamacardio.2020.3629

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Case Rates, Treatment Approaches, and Outcomes in Acute Myocardial Infarction During the Coronavirus Disease 2019 Pandemic

• 1 Center for Cardiovascular Analytics, Research and Data Science (CARDS), Providence Heart Institute, Providence St Joseph Health, Portland, Oregon
• 2 Clinical Analytics, Providence St Joseph Health, Renton, Washington
• 3 Heart and Vascular Institute, Providence Regional Medical Center Everett, Everett, Washington
• 4 Providence Heart Institute, Providence St Peter Hospital, Olympia, Washington

Question   How have case rates, treatment approaches, and in-hospital outcomes changed for patients with acute myocardial infarction (AMI) during the coronavirus disease 2019 (COVID-19) pandemic?

Findings   In this cross-sectional study of 15 244 hospitalizations involving 14 724 patients with AMI, case rates began to decrease on February 23, 2020, followed by a modest recovery after 5 weeks. Although no statistically significant difference in treatment approaches was found, the risk-adjusted mortality rate among patients with ST-segment elevation myocardial infarction increased substantially.

Meaning   The findings of this study show that changes in AMI hospitalizations and in-hospital outcomes occurred during the COVID-19 pandemic periods analyzed; additional research is warranted to explain the higher mortality rate among patients with ST-segment elevation myocardial infarction.

Importance   The coronavirus disease 2019 (COVID-19) pandemic has changed health care delivery worldwide. Although decreases in hospitalization for acute myocardial infarction (AMI) have been reported during the pandemic, the implication for in-hospital outcomes is not well understood.

Objective   To define changes in AMI case rates, patient demographics, cardiovascular comorbidities, treatment approaches, and in-hospital outcomes during the pandemic.

Design, Setting, and Participants   This cross-sectional study retrospectively analyzed AMI hospitalizations that occurred between December 30, 2018, and May 16, 2020, in 1 of the 49 hospitals in the Providence St Joseph Health system located in 6 states (Alaska, Washington, Montana, Oregon, California, and Texas). The cohort included patients aged 18 years or older who had a principal discharge diagnosis of AMI (ST-segment elevation myocardial infarction [STEMI] or non–ST-segment elevation myocardial infarction [NSTEMI]). Segmented regression analysis was performed to assess changes in weekly case volumes. Cases were grouped into 1 of 3 periods: before COVID-19 (December 30, 2018, to February 22, 2020), early COVID-19 (February 23, 2020, to March 28, 2020), and later COVID-19 (March 29, 2020, to May 16, 2020). In-hospital mortality was risk-adjusted using an observed to expected (O/E) ratio and covariate-adjusted multivariable model.

Exposure   Date of hospitalization.

Main Outcomes and Measures   The primary outcome was the weekly rate of AMI (STEMI or NSTEMI) hospitalizations. The secondary outcomes were patient characteristics, treatment approaches, and in-hospital outcomes of this patient population.

Results   The cohort included 15 244 AMI hospitalizations (of which 4955 were for STEMI [33%] and 10 289 for NSTEMI [67%]) involving 14 724 patients (mean [SD] age of 68 [13] years and 10 019 men [66%]). Beginning February 23, 2020, AMI-associated hospitalizations decreased at a rate of –19.0 (95% CI, –29.0 to –9.0) cases per week for 5 weeks (early COVID-19 period). Thereafter, AMI-associated hospitalizations increased at a rate of +10.5 (95% CI, +4.6 to +16.5) cases per week (later COVID-19 period). No appreciable differences in patient demographics, cardiovascular comorbidities, and treatment approaches were observed across periods. The O/E mortality ratio for AMI increased during the early period (1.27; 95% CI, 1.07-1.48), which was disproportionately associated with patients with STEMI (1.96; 95% CI, 1.22-2.70). Although the O/E mortality ratio for AMI was not statistically different during the later period (1.23; 95% CI, 0.98-1.47), increases in the O/E mortality ratio were noted for patients with STEMI (2.40; 95% CI, 1.65-3.16) and after risk adjustment (odds ratio, 1.52; 95% CI, 1.02-2.26).

Conclusions and Relevance   This cross-sectional study found important changes in AMI hospitalization rates and worse outcomes during the early and later COVID-19 periods. Future studies are needed to identify contributors to the increased mortality rate among patients with STEMI.

The coronavirus disease 2019 (COVID-19) pandemic has profoundly changed health care delivery worldwide. Although early attention to COVID-19 was disproportionately focused on efforts to flatten the (pandemic) curve, recent studies have revealed a substantial decrease in hospitalization rates for acute myocardial infarction (AMI). Reports from Austria, 1 Italy, 2 and the US (California) 3 have noted lower admission rates for both ST-segment elevation myocardial infarction (STEMI) and non–ST-segment elevation myocardial infarction (NSTEMI). This decreased hospitalization rate likely reflects multiple factors. Most worrisome among these factors has been the reluctance of patients with AMI to seek medical attention out of fear that they may become infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). 4

We performed a retrospective, cross-sectional study of all AMI hospitalizations in a large multistate health care system. We sought to define changes in AMI case rates, patient demographics, cardiovascular comorbidities, treatment approaches, and in-hospital outcomes during the pandemic.

This study included patients aged 18 years or older with a principal discharge diagnosis of AMI who were admitted between December 30, 2018, and May 16, 2020, into 1 of 49 hospitals in the Providence St Joseph Health (PSJH) system located in 6 states (Alaska, Washington, Montana, Oregon, California, and Texas). We used International Statistical Classification of Diseases and Related Health Problems, Tenth Revision , codes to define the population (eTable 1 in the Supplement ). Individuals who were admitted as an outpatient were excluded. This study was approved by the PSJH Institutional Review Board, which waived the informed consent requirement because of the retrospective nature of the study.

The primary outcome was the weekly rate of AMI (STEMI or NSTEMI) hospitalizations before and after the pandemic onset. The secondary outcomes were patient characteristics, treatment approaches, and in-hospital outcomes (mortality, length of stay, and discharge disposition) of patients with STEMI or NSTEMI. Treatment approaches were defined by Medicare Severity-Diagnosis Related Groups (MS-DRGs) for percutaneous coronary intervention, coronary artery bypass graft surgery, and medical management of AMI (eTable 2 in the Supplement ).

Weekly volumes of AMI hospitalizations (categorized as STEMI or NSTEMI) are presented in the Figure as line graphs. Segmented regression analysis was used to ascertain volume changes over time. Using 2 identified break points (February 23, 2020 and March 29, 2020), we grouped cases into 1 of 3 periods for analysis: before COVID-19 (December 30, 2018, to February 22, 2020), early COVID-19 (February 23, 2020, to March 28, 2020), and later COVID-19 (March 29, 2020, to May 16, 2020). Segmented regression analysis was also used to identify the slope change in weekly hospitalizations during the 3 periods, with consideration of time dependence in the model.

Risk-adjusted in-hospital mortality was examined with 2 models. The first was the PSJH mortality risk model, which was a lookup table consisting of more than 5430 expected mortality rates. Such data were derived from the 3M All Patient Refined DRG, risk of mortality, and severity-of-illness grouper algorithm applied to a large inpatient database in the western US (eMethods in the Supplement ). The second was a multivariable logistic model, which considered all demographic variables listed in Table 1 . Results of the multivariable model were presented as adjusted odds ratio (OR) with 95% CI.

Patient demographics, cardiovascular comorbidities, treatment approaches, and in-hospital outcomes were summarized as descriptive statistics. Categorical data were presented as frequency (percentage). Numeric data were tested for normality and presented as mean (SD) or median (interquartile range [IQR]), as appropriate. Trends among the 3 COVID-19 periods were compared using univariate χ 2 , Fisher exact, or Kruskal-Wallis tests, as appropriate, for each variable. The level of statistical significance varied from P  < .05 to P  < .008, depending on Bonferroni adjustment for multiple comparisons (eMethods in the Supplement ).

The study cohort comprised 15 244 hospitalizations for AMI (4955 for STEMI [33%] and 10 289 for NSTEMI [67%]) involving 14 724 patients. Of those hospitalized, 5225 were women (34%) and 10 019 were men (66%), with a mean (SD) age of 68 (13) years ( Table 1 ). Before the COVID-19 period, the mean (SD) weekly case rate was 222 (17) patients for AMI, 72 (9) patients for STEMI, and 150 (13) patients for NSTEMI ( Figure and eTable 3 in the Supplement ). Beginning February 23, 2020, AMI hospitalizations decreased at a rate of –19.0 (95% CI, –29.0 to –9.0) cases per week for 5 weeks, marking the early COVID-19 period ( Figure ). Thereafter, AMI hospitalizations increased at a rate of +10.5 (95% CI, +4.6 to +16.5) cases per week, marking the later COVID-19 period. Weekly AMI hospitalization rates had not returned to baseline, however, by the last week evaluated (May 10, 2020; eTable 3 in the Supplement ). Similar trends in hospitalization for AMI, STEMI, and NSTEMI were observed in the PSJH system in all 6 states (eFigure 1 in the Supplement ).

Patients hospitalized for AMI in the early and later COVID-19 periods vs the before period were slightly younger (mean [SD] age, 67 [13] years vs 68 [13] years; P  < .001) and more likely to be Asian (50 [6%] and 62 [6%] vs 667 [5%]; P  = .01) or Native American individuals (20 [2%] and 21 [2%] vs 151 [1%]; P  = .01) ( Table 1 ). Treatment approaches for patients with STEMI or NSTEMI were not statistically different across periods (eFigure 2 in the Supplement ). Median (IQR) length of stay for patients with AMI was shorter in the early COVID-19 period by 7 hours and in the later COVID-19 period by 6 hours compared with the before period (56 [41-115] hours and 57 [41-116] hours vs 63 [43-122] hours, respectively; P  < .001) ( Table 2 ). Similar trends were observed for both types of AMI. A greater number of patients with AMI were discharged to home in the early and later COVID-19 periods vs the before COVID-19 period, with consistent findings among those with STEMI (235 [83%] and 284 [81%] vs 3402 [79%]; P  = .02) and NSTEMI (465 [81%] and 587 [83%] vs 6976 [77%]; P  = .006).

The observed (crude) in-hospital mortality rate was similar between periods for all groups ( Table 2 ). Compared with the before COVID-19 period, however, patients with STEMI had a statistically greater risk of mortality during the later COVID-19 period after adjusting for patient demographic characteristics and comorbidities (OR, 1.52; 95% CI, 1.02-2.26). Using the PSJH model, the observed to expected (O/E) hospital mortality ratio for patients with AMI was statistically increased in the early COVID-19 period (O/E ratio, 1.27; 95% CI, 1.07-1.48), with consistent findings in the later period as well (O/E ratio, 1.23; 95% CI, 0.98-1.47). These findings, however, were different for patients with STEMI vs those with NSTEMI. For patients with STEMI, the O/E mortality ratio was substantially higher in all 3 COVID-19 periods. These patients had a stepwise increase in the O/E mortality ratio from the before period (O/E ratio, 1.48; 95% CI, 1.34-1.62) to the early (O/E ratio, 1.96; 95% CI, 1.22-2.70) and later (O/E ratio, 2.40; 95% CI, 1.65-3.16) periods. The O/E mortality ratio for STEMI in the later period was statistically greater than the before period. In contrast, patients with NSTEMI had a consistently lower O/E mortality ratio for all 3 periods (before: O/E ratio, 0.80 [95% CI, 0.71-0.88]; early: O/E ratio, 0.91 [95% CI, 0.46-1.36]; later: O/E ratio, 0.71 [95% CI, 0.49-0.93]).

Consistent with previous reports, this study found a substantial decrease in AMI hospitalization rates in the early COVID-19 period. Beginning March 29, 2020, however, hospitalizations for AMI began to increase, albeit at a slower rate. Among the many factors likely associated with this rebound in cases was encouragement of patients with symptoms or signs of AMI to seek immediate medical attention, even amid the pandemic. 5 , 6

Although patient demographics and treatment approaches were fairly consistent across periods, patients with AMI hospitalized during the COVID-19 period were 1 to 3 years younger, had a shorter length of stay, and were more likely to be discharged to home. Possible explanations for these findings were greater reluctance by older patients to seek medical attention, hospital efforts to maintain bed availability, patient preference for early discharge, and concern about risk of contracting SARS-CoV-2 in post–acute care facilities.

Notable differences in risk-adjusted mortality were observed over the periods analyzed. Patients hospitalized for AMI during the early COVID-19 period had an increased O/E mortality ratio, associated disproportionately with patients with STEMI. In this population, the O/E ratio and risk-adjusted mortality rates were even greater during the later COVID-19 period. Given the time-sensitive nature of STEMI, any delay by patients, emergency medical services, the emergency department, or cardiac catheterization laboratory may have played a role. 7 , 8 Additional complications from delayed reperfusion (eg, conduction disturbances, heart failure, cardiogenic shock, and mechanical complications) 9 may have occurred in some patients. Further research is needed to identify factors associated with the higher mortality rate in patients with STEMI.

In the weeks and months to come, clinicians may see greater numbers of patients with more severe manifestations of AMI. With the uncertainty on timing of a COVID-19 vaccine, this study reinforces the need to address important care processes for patients with AMI to help mitigate further risk.

This study has several limitations. First, because the cohort was defined by coding data, it is possible that the primary reason for hospitalization was misclassified as an AMI. Second, the treatment analysis excluded outpatients and those with other MS-DRG codes. Although this group represented a small percentage of the total patient cohort (8% [1165]), treatment shifts may have been underappreciated. Third, the data set did not allow us to evaluate potential timing-related factors that may have contributed to higher in-hospital mortality (eg, time of symptom onset, first medical contact, and hospital arrival). Fourth, although the PSJH mortality risk model is not AMI-specific, we found consistent results with a multivariable model adjusted for patient demographic characteristics and comorbidities. Fifth, the COVID-19 status of patients included in the analysis was not available. As such, the higher observed rate of AMI mortality during the COVID-19 period could have been associated with concurrent SARS-CoV-2 infection.

Results of this cross-sectional study appear to validate previous concerns that large numbers of patients with AMI initially avoided hospitalization during the COVID-19 pandemic, likely out of fear of contracting SARS-CoV-2. Hospitalization rates for AMI have begun to increase but so has the risk of in-hospital mortality. Further research into factors associated with an increase in the STEMI mortality rate is warranted.

Accepted for Publication: July 10, 2020.

Corresponding Author: Ty J. Gluckman, MD, Center for Cardiovascular Analytics, Research and Data Science (CARDS), Providence Heart Institute, Providence St Joseph Health, 9427 SW Barnes Rd, Ste 594, Portland, OR 97225 ( [email protected] ).

Published Online: August 7, 2020. doi:10.1001/jamacardio.2020.3629

Author Contributions: Drs Gluckman and Chiu had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Gluckman, Chiu, Penny, Spinelli.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Gluckman, Chiu, Spinelli.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Chiu.

Administrative, technical, or material support: Gluckman, Wilson, Penny, Chepuri, Waggoner, Spinelli.

Supervision: Gluckman, Spinelli.

Conflict of Interest Disclosures: None reported.

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Myocardial Infarction (MI) Case Study (45 min)

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Definition of Myocardial Infarction (MI)

Myocardial infarction, commonly known as a heart attack, is a critical medical event that occurs when the blood supply to the heart muscle is severely reduced or completely blocked. It is a leading cause of death worldwide and a significant public health concern.

Introduction to Myocardial Infarction (MI)

This nursing case study aims to provide a comprehensive understanding of myocardial infarction by delving into its various aspects, including its pathophysiology, risk factors, clinical presentation, diagnostic methods, and management strategies. Through the exploration of a fictional patient’s journey, we will shed light on the intricate nature of this life-threatening condition and highlight the importance of early recognition and intervention.

Background and Significance of Myocardial Infarction

Myocardial infarction is a sudden and often catastrophic event that can have profound consequences on an individual’s health and well-being. Understanding its underlying mechanisms and risk factors is essential for healthcare professionals, as timely intervention can be life-saving. This case study not only serves as a learning tool but also emphasizes the critical role of medical practitioners in identifying and managing myocardial infarctions promptly.

Pathophysiology of Myocardial Infarction

A crucial aspect of comprehending myocardial infarction is exploring its pathophysiology. We will delve into the intricate details of how atherosclerosis, the buildup of plaque in coronary arteries, leads to the formation of blood clots and the subsequent interruption of blood flow to the heart muscle. This disruption in blood supply triggers a cascade of events, ultimately resulting in the death of cardiac cells.

Risk Factors of Myocardial Infarction

Understanding the risk factors associated with myocardial infarction is vital for prevention and early detection. This case study will examine both modifiable and non-modifiable risk factors, including age, gender, family history, smoking, high blood pressure, diabetes, and high cholesterol levels. Recognizing these risk factors is instrumental in developing effective strategies for prevention and risk reduction.

Clinical Presentation Myocardial Infarction

Recognizing the signs and symptoms of myocardial infarction is crucial for timely intervention. We will present a fictional patient’s experience, illustrating the typical clinical presentation, which often includes chest pain or discomfort, shortness of breath, nausea, lightheadedness, and diaphoresis. Through this patient’s journey, we will highlight the importance of accurate symptom assessment and prompt medical attention.

Diagnostic Methods for Myocardial Infarction

Modern medicine offers various diagnostic tools to confirm a myocardial infarction swiftly and accurately. This case study will explore these diagnostic methods, such as electrocardiography (ECG), cardiac biomarkers, and imaging techniques like coronary angiography. By understanding these diagnostic modalities, healthcare professionals can make informed decisions and initiate appropriate treatments promptly.

Management Strategies for Myocardial Infarction

The management of myocardial infarction involves a multidisciplinary approach, including medication, revascularization procedures, and lifestyle modifications. We will discuss the fictional patient’s treatment plan, emphasizing the importance of reestablishing blood flow to the affected heart muscle and preventing further complications.

Nursing Case Study for Myocardial Infarction (MI)

Having established a foundational understanding of myocardial infarction, we will now delve deeper into Mr. Salazar’s case, tracing his journey through diagnosis, treatment, and recovery. This in-depth examination will shed light on the real-world application of the principles discussed in the introduction, providing valuable insights into the clinical management of myocardial infarction and its impact on patient outcomes.

Mr. Salazar, a 57-year-old male, arrives at the Emergency Department (ED) with complaints of chest pain that began approximately one hour after dinner while he was working. He characterizes the discomfort as an intense “crushing pressure” located centrally in his chest, extending down his left arm and towards his back. He rates the pain’s severity as 4/10. Upon examination, Mr. Salazar exhibits diaphoresis and pallor, accompanied by shortness of breath (SOB).

What further nursing assessments need to be performed for Mr. Salazar?

• Heart Rate (HR): The number of heartbeats per minute.
• Blood Pressure (BP): The force of blood against the walls of the arteries, typically measured as systolic (during heartbeats) and diastolic (between heartbeats) pressure.
• Respiratory Rate (RR): The number of breaths a patient takes per minute.
• Body Temperature (Temp): The measurement of a patient’s internal body heat.
• Oxygen Saturation (SpO2): The percentage of oxygen in the blood.
• S1: The first heart sound, often described as “lub,” is caused by the closure of the mitral and tricuspid valves.
• S2: The second heart sound, known as “dub,” results from the closure of the aortic and pulmonic valves.
• These sounds provide important diagnostic information about the condition of the heart.
• Clear: Normal, healthy lung sounds with no added sounds.
• Crackles (Rales): Discontinuous, often high-pitched sounds are heard with conditions like pneumonia or heart failure.
• Wheezes: Whistling, musical sounds often associated with conditions like asthma or chronic obstructive pulmonary disease (COPD).
• Pulses refer to the rhythmic expansion and contraction of arteries with each heartbeat. Common pulse points for assessment include the radial artery (wrist), carotid artery (neck), and femoral artery (groin). Evaluating pulses helps assess the strength, regularity, and rate of blood flow.
• Edema is the abnormal accumulation of fluid in body tissues, leading to swelling. It can occur in various body parts and may indicate underlying conditions such as heart failure, kidney disease, or localized injury. Edema assessment involves evaluating the degree of swelling and its location.
• Skin condition (temperature, color, etc.)

What interventions do you anticipate being ordered by the provider?

• Oxygen therapy involves administering oxygen to a patient to increase the level of oxygen in their blood. It is used to treat conditions such as respiratory distress, and hypoxia (low oxygen levels), and to support patients with breathing difficulties.
• Nitroglycerin is a medication used to treat angina (chest pain) and to relieve symptoms of heart-related conditions. It works by relaxing and widening blood vessels, which improves blood flow to the heart, reducing chest pain.
• Aspirin is a common over-the-counter medication and antiplatelet drug. In the context of myocardial infarction (heart attack), it is often administered to reduce blood clot formation, potentially preventing further blockage in coronary arteries.
• A 12-lead EKG is a diagnostic test that records the electrical activity of the heart from 12 different angles. It provides information about the heart’s rhythm, rate, and any abnormalities, helping diagnose conditions like arrhythmias, heart attacks, and ischemia.
• Cardiac enzymes are proteins released into the bloodstream when heart muscle cells are damaged or die, typically during a heart attack. Measuring these enzymes, such as troponin and creatine kinase-MB (CK-MB), helps confirm a heart attack diagnosis and assess its severity.
• A chest X-ray is a diagnostic imaging procedure that creates images of the chest and its internal structures, including the heart and lungs. It is used to identify issues like lung infections, heart enlargement, fluid accumulation, or fractures in the chest area.
• Possibly an Echocardiogram

Upon conducting a comprehensive assessment, it was observed that the patient exhibited no signs of jugular vein distention (JVD) or edema. Auscultation revealed normal heart sounds with both S1 and S2 present, while the lungs remained clear, albeit with scattered wheezes. The patient’s vital signs were recorded as follows:

• BP 140/90 mmHg SpO 2 90% on Room Air
• HR 92 bpm and regular Ht 173 cm
• RR 32 bpm Wt 104 kg
• Temp 36.9°C

The 12-lead EKG repor t indicated the presence of “Normal sinus rhythm (NSR) with frequent premature ventricular contractions (PVCs) and three- to four-beat runs of ventricular tachycardia (VT).” Additionally, there was ST-segment elevation in leads I, aVL, and V2 through V6 (3-4mm), accompanied by ST-segment depression in leads III and aVF.

Cardiac enzyme levels were collected but were awaiting results at the time of assessment. A chest x-ray was also ordered to provide further diagnostic insights.

In response to the patient’s condition, the healthcare provider prescribed the following interventions:

• Aspirin: 324 mg administered orally once.
• Nitroglycerin: 0.4 mg administered sublingually (SL), with the option of repeating the dose every five minutes for a maximum of three doses.
• Morphine: 4 mg to be administered intravenously (IVP) as needed for unrelieved chest pain.
• Oxygen: To maintain oxygen saturation (SpO2) levels above 92%.

These interventions were implemented to address the patient’s myocardial infarction (heart attack) and alleviate associated symptoms, with a focus on relieving chest pain, improving oxygenation, and closely monitoring vital signs pending further diagnostic results.

What intervention should you, as the nurse, perform right away? Why?

• Apply oxygen – this can be done quickly and easily and can help to prevent further complications from low oxygenation.
• Oxygen helps to improve oxygenation as well as to decrease myocardial oxygen demands.
• Often it takes a few minutes or more for medications to be available from the pharmacy, so it makes sense to take care of this intervention first.
• ABC’s – breathing/O 2 .

What medication should be the first one administered to this patient? Why? How often?

• Nitroglycerin 0.4mg SL – it is a vasodilator and works on the coronary arteries. The goal is to increase blood flow to the myocardium. If this is effective, the patient merely has angina. However, if it is not effective, the patient may have a myocardial infarction.
• Aspirin should also be given, but it is to decrease platelet aggregation and reduce mortality. While it can somewhat help prevent the worsening of the blockage, it does little for the current pain experienced by the patient.
• Morphine should only be given if the nitroglycerin and aspirin do not relieve the patient’s chest pain.

What is the significance of the ST-segment changes on Mr. Salazar's 12-lead EKG?

• ST-segment changes on a 12-lead EKG indicate ischemia (lack of oxygen/blood flow) or infarction (death of the muscle tissue) of the myocardium (heart muscle). 
• This indicates an emergent situation. The patient’s coronary arteries are blocked and need to be reopened by pharmacological (thrombolytic) or surgical (PCI) intervention.
• Time is tissue – the longer the coronary arteries stay blocked, the more of the patient’s myocardium that will die. Dead heart tissue doesn’t beat.

Mr. Salazar’s chest pain was unrelieved after three (3) doses of sublingual nitroglycerin (NTG). Morphine 5 mg intravenous push (IVP) was administered, as well as 324 mg chewable baby aspirin. His pain was still unrelieved at this point

Mr. Salazar’s cardiac enzyme results were as follows:

Troponin I 3.5 ng/mL

Based on the results of Mr. Salazar's labs and his response to medications, what is the next intervention you anticipate? Why?

• Mr. Salazar needs intervention. He will either receive thrombolytics or a heart catheterization (PCI).
• Based on the EKG changes, elevated Troponin level, and the fact that his symptoms are not subsiding, it’s possible the patient has a significant blockage in one or more of his coronary arteries. 
• It seems as though it may be an Anterior-Lateral MI because ST elevation is occurring in I, aVL, and V 2 -V 6 .

Mr. Salazar was taken immediately to the cath lab for a Percutaneous Coronary Intervention (PCI). The cardiologist found a 90% blockage in his left anterior descending (LAD) artery. A stent was inserted to keep the vessel open.

What is the purpose of Percutaneous Coronary Intervention (PCI), also known as a heart catheterization?

• A PCI serves to open up any coronary arteries that are blocked. First, they use contrast dye to determine where the blockage is, then they use a special balloon catheter to open the blocked vessels. 
• If that doesn’t work, they will place a cardiac stent in the vessel to keep it open.[ /faq]

[faq lesson="true" blooms="Application" question="What is the expected outcome of a PCI? What do you expect to see in your patient after they receive a heart catheterization?"]

• Blood flow will be restored to the myocardium with minimal residual damage.
• The patient should have baseline vital signs, relief of chest pain, normal oxygenation status, and absence of heart failure symptoms (above baseline).
• The patient should be able to ambulate without significant chest pain or SOB.
• The patient should be free from bleeding or hematoma at the site of catheterization (often femoral, but can also be radial or (rarely) carotid.

Mr. Salazar tolerated the PCI well and was admitted to the cardiac telemetry unit for observation overnight. Four (4) hours after the procedure, Mr. Salazar reports no chest pain. His vital signs are now as follows:

• BP 128/82 mmHg SpO 2 96% on 2L NC
• HR 76 bpm and regular RR 18 bpm
• Temp 37.1°C

Mr. Salazar will be discharged home 24 hours after his arrival to the ED and will follow up with his cardiologist next week. 

What patient education topics would need to be covered with Mr. Salazar?

• He should be taught any dietary and lifestyle changes that should be made.
• Diet – low sodium, low cholesterol, avoid sugar/soda, avoid fried/processed foods.
• Exercise – 30-45 minutes of moderate activity 5-7 days a week, u nless instructed otherwise by a cardiologist. This will be determined by the patient’s activity tolerance – how much can they do and still be able to breathe and be pain-free?
• Stop smoking and avoid caffeine and alcohol.
• Medication Instructions
• Nitroglycerin – take one SL tab at the onset of chest pain. If the pain does not subside after 5 minutes, call 911 and take a second dose. You can take a 3rd dose 5 minutes after the second if the pain does not subside. Do NOT take if you have taken Viagra in the last 24 hours.
• Aspirin – take 81 mg of baby aspirin daily
• Anticoagulant – the patient may be prescribed an anticoagulant if they had a stent placed.  They should be taught about bleeding risks.
• When to call the provider – CP unrelieved by nitroglycerin after 5 minutes. Syncope. Evidence of bleeding in stool or urine (if on anticoagulant). Palpitations, shortness of breath, or difficulty tolerating activities of daily living.

Linchpins for Myocardial Infarction Nursing Case Study

In summary, Mr. Salazar’s case highlights the urgency of recognizing and responding to myocardial infarction promptly. The application of vital signs, EKG, cardiac enzymes, and medications like aspirin, nitroglycerin, and morphine played a pivotal role in his care. Diagnostic tools like echocardiography and chest X-rays contributed to a comprehensive evaluation.

Nurses must remain vigilant and compassionate in such emergencies. This case study emphasizes the importance of adhering to best practices in the assessment, diagnosis, and management of myocardial infarction, with the ultimate goal of achieving favorable patient outcomes.

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This nursing case study course is designed to help nursing students build critical thinking.  Each case study was written by experienced nurses with first hand knowledge of the “real-world” disease process.  To help you increase your nursing clinical judgement (critical thinking), each unfolding nursing case study includes answers laid out by Blooms Taxonomy  to help you see that you are progressing to clinical analysis.We encourage you to read the case study and really through the “critical thinking checks” as this is where the real learning occurs.  If you get tripped up by a specific question, no worries, just dig into an associated lesson on the topic and reinforce your understanding.  In the end, that is what nursing case studies are all about – growing in your clinical judgement.

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Acute Myocardial Infarction - Page 1

48 year old Jason Dixon had not been feeling well all day and around 10:00 p.m he went to bed. At around 4:00 a.m. his wife awakened to see him slump to the floor, breathing with difficulty and drenched in perspiration. Alarmed when he told her of the pain in his chest, neck and arm, she called 911. Within 12 minutes, emergency response team personnel (EMTs) were on the scene. During this critical period, EMT personnel performed the standard emergency treatment protocol for a patient with symptoms of a myocardial infarction, commonly referred to as a heart attack.

• 1. What symptoms did Jason exhibit?
• 2. If you were an emergency medical technician treating a suspected myocardial infarction (heart attack), what would you do for initial assessment of the patient?
• 3. What initial treatment would you give the patient?

The patient carried several risk factors related to both lifestyle and family history. He was 80 lbs. over his ideal weight and worked long hours in a high stress environment as an advertising agency manager. He was also a moderate cigarette smoker. According to his wife, he exercised very little and paid virtually no attention to diet, often eating fast food, as well as eating late at night. His father died at age 56 from heart disease.

• 4. Summarize the lifestyle risks of the patient.

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• 10 February 2022

Heart-disease risk soars after COVID — even with a mild case

• Saima May Sidik

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Even a mild case of COVID-19 can increase a person’s risk of cardiovascular problems for at least a year after diagnosis, a new study 1 shows. Researchers found that rates of many conditions, such as heart failure and stroke, were substantially higher in people who had recovered from COVID-19 than in similar people who hadn’t had the disease.

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Nature 602 , 560 (2022)

doi: https://doi.org/10.1038/d41586-022-00403-0

Xie, Y., Xu, E., Bowe, B. & Al-Aly, Z. Nature Med . https://www.nature.com/articles/s41591-022-01689-3 (2022).

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Recognizing Myocardial Infarction in Women: A Case Study

Affiliation.

• 1 Debra L. Campo is chairperson of Level I in the St. Joseph School of Nursing, North Providence, RI. Contact author: [email protected]. The author has disclosed no potential conflicts of interest, financial or otherwise.
• PMID: 27560338
• DOI: 10.1097/01.NAJ.0000494694.48122.46

: The author presents the case of a 52-year-old woman who experienced symptoms of myocardial infarction (MI) over many months; neither her clinicians nor the patient-herself a nurse-recognized them. The author discusses the signs and symptoms of MI in women and highlights how failure to recognize them may lead to misdiagnosis and even death. This case illustrates how important it is that health care providers consider the possibility of heart disease in any woman whose symptoms could be cardiac in origin, even when the cause appears to be something else.

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• Gender differences in signs and symptoms presentation and treatment of Jordanian myocardial infarction patients. Omran S, Al-Hassan M. Omran S, et al. Int J Nurs Pract. 2006 Aug;12(4):198-204. doi: 10.1111/j.1440-172X.2006.00572.x. Int J Nurs Pract. 2006. PMID: 16834580
• 'It was not chest pain really, I can't explain it!' An exploratory study on the nature of symptoms experienced by women during their myocardial infarction. Albarran JW, Clarke BA, Crawford J. Albarran JW, et al. J Clin Nurs. 2007 Jul;16(7):1292-301. doi: 10.1111/j.1365-2702.2007.01777.x. J Clin Nurs. 2007. PMID: 17584348
• Mismatch of presenting symptoms at first and recurrent acute myocardial infarction. From the MONICA/KORA Myocardial Infarction Registry. Kirchberger I, Heier M, Golüke H, Kuch B, von Scheidt W, Peters A, Meisinger C. Kirchberger I, et al. Eur J Prev Cardiol. 2016 Mar;23(4):377-84. doi: 10.1177/2047487315588071. Epub 2015 May 20. Eur J Prev Cardiol. 2016. PMID: 25994407
• Myocardial infarction in women: promoting symptom recognition, early diagnosis, and risk assessment. Zbierajewski-Eischeid SJ, Loeb SJ. Zbierajewski-Eischeid SJ, et al. Dimens Crit Care Nurs. 2009 Jan-Feb;28(1):1-6; quiz 7-8. doi: 10.1097/01.DCC.0000325090.93411.ce. Dimens Crit Care Nurs. 2009. PMID: 19104242 Review.
• Treatment-seeking behavior among those with signs and symptoms of acute myocardial infarction. Dracup K, Moser DK. Dracup K, et al. Heart Lung. 1991 Sep;20(5 Pt 2):570-5. Heart Lung. 1991. PMID: 1894541 Review.

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Young people are more likely to die of heart attacks post-COVID, study finds. But why?

When Demi Washington, a basketball player at Vanderbilt University came down with COVID-19 in late 2020, her symptoms were mild, just a runny nose. But to ensure her safe return to the court, the school required her to undergo an MRI.

The results brought Washington to tears.

Following the infection, the now college graduate had developed myocarditis — when the heart muscle becomes inflamed, which can decrease the heart's ability to pump blood. The condition can lead to stroke or heart attack, according to Mayo Clinic . Washington was not vaccinated against COVID-19 at the time.

"I was scared because any internal organ, you’re like, 'Oh, my gosh, I need that to live,'" she recalled to TODAY. "I didn’t really know what was going to come of it, how long was it going to take for it to resolve."

Washington had to skip the rest of the 2020 to 2021 season, but ultimately she was grateful. "I think about the fact that Vanderbilt does do the MRI and a lot of other schools didn’t," she told TODAY in a segment aired Feb. 9. "The fact that I could have played if we didn’t is hard and scary to think about."

Washington's doctor never told her that she was at risk of dying, but he did stress the importance of rest and keeping her heart rate under a certain pace. She had to wear a watch to track her activity. Even though COVID was especially new at the time, Washington said her doctor felt confident her condition was due to the coronavirus, as he'd seen something similar other college athletes.

Washington said she felt no symptoms or signs that her heart had become inflamed, nor did she have a genetic predisposition. "It (just) happened to be me," she said. "I still don't really know why."

Washington has since recovered and is back to playing ball. But her experience sheds light on the thousands of young adults infected with COVID-19 whose health hasn't rebounded as successfully.

COVID-19, heart attacks and young people

Since the COVID-19 pandemic began, heart attack deaths across all age groups have become more common in the U.S., according to a September 2022 study by Cedars Sinai hospital in Los Angeles.

The age group hit the hardest? People between 25 and 44, who saw a 29.9% relative increase in heart attack deaths over the first two years of the pandemic (which means the actual number of heart attack deaths were almost 30% higher than the predicted number).

“Young people are obviously not really supposed to die of heart attack. They’re not really supposed to have heart attacks at all,” Dr. Susan Cheng, a cardiologist at Cedars Sinai and co-author of the study, told TODAY in a segment aired Feb. 9.

Adults between 45 and 64 saw a 19.6% relative increase in heart attack deaths, and those 65 and older saw a 13.7% relative increase, according to a press release from Cedars Sinai . The increase in U.S. heart attack deaths continued through the omicron surge , even though the variant is thought to cause milder illness, and spikes of heart attack deaths have aligned with the timing of COVID-19 surges in the U.S.

Los Angeles County paramedic Romeo Robles told TODAY in the Feb. 9 segment that upticks in COVID-19 would often lead to more 911 calls related to heart issues in his community.

"Surprisingly, people my age ... we would find them in cardiac arrest, and it was all predicted by these waves," he said.

Cheng called the connection "more than coincidental, that is for sure." Explaining why, she pointed out that COVID-19 can greatly impact the cardiovascular system .

"It appears to be able to increase the stickiness of the blood and increase ... the likelihood of blood clot formation," Cheng said. "It seems to stir up inflammation in the blood vessels. It seems to also cause in some people an overwhelming stress — whether it’s related directly to the infection or situations around the infection — that can also cause a spike in blood pressure."

The reason for the relative rise in young people in particular is unclear, but one theory, Cheng said, is that the virus's impact on the cardiovascular system in some people may be due to an excessive immune system response and that young people are more likely to have stronger immune systems.

COVID-19 and heart disease

For COVID-19 survivors, the risk of developing a heart condition even a year after infection, regardless of how severe symptoms were, is "substantial," according to a February 2022 study of more than 150,000 individuals with COVID-19. The risk increases even for people who don't have any other risk factors for heart disease.

Dr. Ziyad Al-Aly, a physician-scientist at Washington University School of Medicine in St. Louis and co-author of the study, estimated that about 4% of people who have COVID-19 will develop a heart problem, such as irregular heartbeat, heart failure, inflammation or heart attacks.

"It’s a small number, but really, it’s not (if) you multiply that number by the huge number of people in the United States and throughout the world who had COVID-19," he told TODAY.

One theory why this happens ties into how the body is supposed to respond to viruses — by creating inflammation, according to the National Heart, Lung and Blood Institute . "In some people with COVID-19, however, the inflammation seems to go into overdrive," the institute noted. "Too much inflammation may further damage the heart or disrupt the electrical signals that help it to beat properly, which can reduce its pumping ability or lead to abnormal heart rhythms ... or make an existing arrhythmia worse."

Some research is beginning to chip away at how COVID-19 impacts the heart. A February 2023 study found the inflammatory immune response to a COVID-19 infection can cause calcium to leak from the heart, potentially leading to a fatal, irregular heartbeat. The subjects in this study weren't vaccinated, and research shows a COVID-19 infection is more likely to cause heart problems than vaccination, according to the Centers for Disease Control and Prevention .

The National Heart, Lung and Blood Institute also points out that COVID-19 may affect the heart's cells. A January 2023 study , which began before the vaccine was available, looked at the relationship between a COVID infection and the protein troponin in the blood, which is associated with heart muscle injury or heart attack. It found that 61% of people hospitalized with COVID-19 who had high troponin levels had heart abnormalities, such a scarring from a heart attack.

Some people develop blood clots after a COVID-19 infection , sometimes in the heart, the National Heart, Lung and Blood Institute explains. The virus can attack blood vessels, causing a surge inflammatory cells, which can trigger the release of molecules that contribute to blood clotting, TODAY.com previously reported.

What's more, the risk of developing long COVID, including heart problems , increases with each COVID-19 infection an individual has, Al-Aly pointed out. As a result, Latino and Black communities, which have higher rates of reinfection, are especially high risk for heart problems post-COVID, Cheng said.

As doctors and other researchers continue to wade through the data on COVID-19 and heart disease, the best course of action is to avoid infection as best you can, Cheng and Al-Aly said. To do so:

• Wear a mask in crowded settings, and consider socializing outdoors with people outside your household.
• Stay up to date on your vaccinations . Research shows that you're 11 times more likely to develop myocarditis from COVID itself versus the vaccine, NBC News senior medical correspondent Dr. John Torres said during a TODAY segment on Feb. 9.
• Take a COVID-19 test as soon as you start to develop any symptoms and stay home when you're sick.

If you've been infected with COVID-19, especially multiple times, Cheng also encouraged staying on top of your risk factors for heart disease, such as your blood pressure, cholesterol and blood sugar. Typical signs of heart attack, per the U.S. Centers for Disease Control and Prevention , include:

• Chest pain or discomfort, such as pressure, squeezing or fullness.
• Weakness, light-headedness or fainting.
• A cold sweat.
• Pain or discomfort in the jaw, neck or back.
• Shortness of breath, either at the same time as or before chest discomfort.

Prior to the COVID-19 pandemic, heart attack deaths were trending downward in the United States, but the pandemic appears to have reversed the progress, according to the Cedars Sinai research.

"I'd love to say we're ... coming out on the other side and we can think of COVID more so like the common cold. Unfortunately, that is not the case. ... That is eminently clear from all of the data," Cheng said. "This is not even just like the flu. ... This virus is still very different from any other virus we have seen in our lifetime."

Maura Hohman is the senior health editor for TODAY.com and has been covering health and wellness since 2015.

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• Volume 101, Issue 21
• Acute myocardial infarction and influenza: a meta-analysis of case–control studies
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• Michelle Barnes ,
• Anita E Heywood ,
• Abela Mahimbo ,
• Bayzid Rahman ,
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• School of Public Health and Community Medicine, UNSW Australia , Sydney, New South Wales , Australia
• Correspondence to Dr Anita E Heywood, Faculty of Medicine, School of Public Health and Community Medicine, UNSW Australia, Sydney, NSW 2052 Australia; a.heywood{at}unsw.edu.au

Objective Acute myocardial infarction (AMI) is the leading cause of death and disability globally. There is increasing evidence from observational studies that influenza infection is associated with AMI. In patients with known coronary disease, influenza vaccination is associated with a lower risk of cardiovascular events. However, the effect of influenza vaccination on incident AMI across the entire population is less well established.

Method The purpose of our systematic review of case–control studies is twofold: (1) to estimate the association between influenza infection and AMI and (2) to estimate the association between influenza vaccination and AMI. Cases included those conducted with first-time AMI or any AMI cases. Studies were appraised for quality and meta-analyses using random effects models for the influenza exposures of infection, and vaccination were conducted.

Results 16 studies (8 on influenza vaccination, 10 on influenza infection and AMI) met the eligibility criteria, and were included in the review and meta-analysis. Recent influenza infection, influenza-like illness or respiratory tract infection was significantly more likely in AMI cases, with a pooled OR 2.01 (95% CI 1.47 to 2.76). Influenza vaccination was significantly associated with AMI, with a pooled OR of 0.71 (95% CI 0.56 to 0.91), equating to an estimated vaccine effectiveness of 29% (95% CI 9% to 44%) against AMI.

Conclusions Our meta-analysis of case–control studies found a significant association between recent respiratory infection and AMI. The estimated vaccine effectiveness against AMI was comparable with the efficacy of currently accepted therapies for secondary prevention of AMI from clinical trial data. A large-scale randomised controlled trial is needed to provide robust evidence of the protective effect of influenza vaccination on AMI, including as primary prevention.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/heartjnl-2015-307691

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Introduction

Globally, coronary heart disease (CHD), particularly acute myocardial infarction (AMI), is the leading cause of death and disability. 1 While there has been a consistent decline in the number of deaths from CHD in high-income countries, 2 deaths in low-income and middle-income countries continue to increase. 2

The epidemiological relationship between AMI and influenza was first observed in the 1930s 3 with increased cardiovascular deaths during the influenza seasons. 4 It is hypothesised that influenza infection can lead to AMI via acute coronary occlusion through thrombosis of a pre-existing, subcritical atherosclerotic plaque; 5 additionally, infection promotes atherogenesis in mouse models. 6 Infection causes tachycardia, hypoxia, release of inflammatory cytokines and a thrombophilic state, potentially contributing to AMI through multiple mechanisms. This relationship between influenza infection and AMI in humans has been largely studied using observational studies, particularly case–control studies. 7

There is a growing interest in using seasonal influenza vaccines in AMI prevention, with studies (including three randomised controlled trials (RCTs)) 8–10 focusing on secondary prevention in patients with previous AMIs or known CHD. A meta-analysis of six RCTs found an association between influenza vaccination and lower risk of composite cardiovascular events (Relative risk (RR) 0.64, 95% confidence interval (CI) 0.48 to 0.86). 11 However, only observational studies are available to measure the association between influenza infection and AMI. In mouse models, influenza vaccination is protective against AMI outside of the influenza season, with reductions in atherosclerotic plaque size, increased plaque stability with decreased proinflammatory markers. 6

Many countries recommend influenza vaccination for patients at increased risk of severe complications from influenza, including individuals with cardiovascular disease (CVD). 12–14 However, vaccine coverage remains suboptimal in this vulnerable population. 15–17 We conducted a systematic review and meta-analysis of case–control studies to examine the evidence for the relationship between AMI, influenza infection and influenza vaccination in any population. The purpose of our systematic review of case–control studies is twofold: (1) to estimate the association between influenza infection and AMI and (2) to estimate the association between influenza vaccination and AMI.

Search strategy

We performed a literature search combining Medical Subject Headings (MeSH) terms and keyword searches using Medline, EmBase, Cochrane and Index to Theses databases up to 24 June 2014, limited to English-language publications. MeSH terms for Medline and EmBase included ‘influenza, human’, ‘influenza vaccines’, ‘acute myocardial infarction’ and ‘respiratory tract infection’. Keyword searches included combinations of ‘influenz$/flu’, ‘vaccin$’, ‘immun?e$’, ‘immun?a$’, ‘ischem$/ischaem$’, ‘myocardial’, ‘cardiovascular’, ‘acute’, ‘coronary’, ‘cardi$’, ‘event’, ‘syndrome’, ‘respiratory’, ‘symptom’, ‘disease’ and ‘illness’. Search terms for the Index to Theses and Cochrane databases were ‘myocardial’, ‘infarction’, ‘acute coronary’ ‘event’ or ‘syndrome’, ‘cardiovascular’, ‘respiratory tract infection’, ‘flu’, ‘influenza’, ‘vaccine’ and ‘vaccination’. Reference lists were reviewed for additional relevant studies.

Inclusion and exclusion criteria

We included case–control studies in which the primary outcome was fatal or non-fatal AMI, including first or subsequent episode(s) of AMI. AMI was defined as a constellation of clinical features, including ischaemic symptoms, biochemical and/or electrical evidence of myocardial ischaemia, evidence of critical artery stenosis on coronary angiography or autopsy evidence of myocardial infarction. We included prospective and retrospective case–control studies in which the exposure was either influenza infection or influenza vaccination. Influenza infection broadly included laboratory-confirmed influenza, influenza-like illness (ILI) or respiratory tract infection (RTI) of any definition used by the authors. Influenza vaccination included both self-reported and database records of vaccination status. We excluded self-controlled case–control studies, case cross-over studies, case–control studies in which the cases were not exclusively AMI or case–control studies in which AMI were considered the control group.

Data extraction and quality appraisal

We developed a standardised data extraction tool and study quality grading instrument. Assessment tools of case–control study quality and bias susceptibility have been developed, but have limited generalisability. 18 We developed our own tool, modifying the Grading of Recommendations Assessment, Development and Evaluation (GRADE) risk of bias assessment for observational studies, 19 to assess individual study quality. A simple checklist with a small number of key domains was designed to critically appraise the study biases, including methodological domains of participant selection, outcome measurement, exposure measurement, control for confounding and appropriate analysis. 20 Each study was assessed as low, moderate or high risk of bias based on these domains. Papers were selected from databases by one author (MB). Two researchers (MB and AM) independently graded the included studies with differences resolved by consensus between other investigators (AEH, BR, ATN, CRM).

Statistical analysis

The number of cases and controls by exposure, and the reported adjusted odds ratios (OR) and corresponding 95% CIs for each study were extracted for use in the formal meta-analysis. The ORs from individual studies were pooled using the inverse-variance weighted random effects method. 21 Calculation of vaccine effectiveness (VE) can be done using observational epidemiological data. 22 The OR of the association between influenza vaccination and AMI was used to estimate the pooled VE of influenza vaccine against AMI using the formula: (1−OR)×100. 22 Between-study heterogeneity was quantified with the I 2 statistic, which describes the proportion of total variation in study estimates due to heterogeneity. 23 Analyses were separated by exposure type (infection and vaccination) and stratified by study type (prospective and retrospective). We conducted a meta-regression of the log of the ORs, weighted by the inverse of their variances, on the categorical variable of risk of bias separately to assess the possible impact of study quality on the effect measures. For these analyses, we fitted a random effects model with two additive variance components (within and between studies). The influence of each study on the combined risk estimate was examined by consecutively omitting each study from the meta-analysis. Finally, we tested for possible publication bias using Begg and Egger's tests and by visual inspection for asymmetry of funnel plots of the natural logarithms of the effect estimates against their SEs. 24 , 25

Statistical analysis was performed using Stata SE V.10.1 2007(Stata, College Station, Texas, USA) and RevMan V.5 2008 (The Cochrane Collaboration, Copenhagen, Denmark).

Included studies

Of the 2976 publications identified, 14 were relevant with two further articles identified through reference lists of published studies (see figure 1 ). Ten studies evaluated the association between influenza infection and the risk of AMI, defined as laboratory-diagnosed influenza in four studies, 26–29 clinical ILI in three studies 26 , 28 , 30 and RTI in seven studies. 27 , 28 , 31–35 Three studies measured multiple exposures. Seven studies examined the association between influenza vaccination and prevention of first AMI, while one 36 assessed prevention of recurrent AMI. Two studies examined the relationship between AMI and both influenza vaccination and infection. 27 , 28

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Flow chart of study selection and included studies.

Risk estimates

Influenza infection.

Two of the four studies reporting serologically diagnosed influenza infection showed a significant association, with only one remaining significant after adjustment for confounders ( table 1 ). Of studies using clinical case definitions, one ILI study 30 ( table 2 ) and two 27 , 32–35 RTI studies ( table 3 ) were significantly predictive of AMI after adjustment. Figure 2 shows the pooled meta-analysis results by diagnostic technique. Studies of ILI (OR 2.29, 95% CI 1.11 to 4.73) and RTI (OR 1.89, 95% CI 1.35 to 2.65) were significantly associated with AMI, while laboratory-diagnosed influenza studies were non-significant (OR 2.44, 95% CI 0.83 to 7.20). The overall pooled results were significant, with the odds of a recent influenza infection, ILI or RTI in AMI subjects being double (OR 2.01, 95% CI 1.47 to 2.76) than that of controls.

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Summary table of case–control studies of the association between laboratory-diagnosed influenza infection and AMI

Summary table of case–control studies of the association between ILI and AMI

Summary table of case–control studies of the association between RTI and AMI

Pooled results for analysis of infection studies by the type of measure and AMI diagnosis. AMI, acute myocardial infarction; ILI, influenza-like illness; RTI, respiratory tract infection.

There was moderate, but significant, between-study heterogeneity (I 2 67.1%, p<0.001). Influence meta-analysis did not detect any studies exerting undue influence on the pooled estimate (see online supplementary data). None of the study qualities were significantly associated with the effect measure (OR) in the meta-regression (p=0.086), and the pooled estimate from those with a moderate risk of study bias was much higher than that of studies with high or low risk of bias. This was not significant due to the small number of studies with moderate risk of bias (see online supplementary data). Cumulative meta-analysis results by year of publication showed that additional studies would not meaningfully change the pooled estimates (see online supplementary data). Funnel plots showed no evidence of publication bias (p=0.898, Egger's test, see online supplementary data).

Influenza vaccination

Table 4 summarises the seven studies examining the association between influenza vaccination and AMI prevention with four studies showing significant negative association 27 , 36–38 after adjustment. Pooled meta-analysis results are shown in figure 3 . Overall, odds of influenza vaccination was significantly lower in those with AMI (OR 0.71, 95% CI 0.56 to 0.91) compared with controls, translating to an estimated influenza VE against AMI of 29% (95% CI 9% to 44%).

Summary table of case–control studies of the association between influenza vaccination and AMI

Pooled results for the analysis of vaccination studies by study type and acute myocardial infarction diagnosis.

Between-study heterogeneity was moderate (I 2 63.0%, p=0.013). There was no undue influence of a single study on the pooled estimate. A cumulative meta-analysis by year of publication showed the pooled estimates were not stable, and additional studies may influence results (see online supplementary data). The sub-group analysis showed that studies with low risk of bias had stronger effects of vaccination (see online supplementary data), although this difference was not significant in the meta-regression of effect measure (OR) on study quality (p=0.239). No vaccination studies had a high risk of study bias. A funnel plot found no evidence of publication bias (p=0.17, Egger's test, see online supplementary data).

Quality assessment and study description

We assessed the quality of the included studies with individual study quality assessments available in the online supplementary data.

Of the 10 studies investigating the association between influenza infection and AMI, 2 27 , 28 were categorised as low risk of methodological bias, 2 29 , 32 at moderate risk and 6 26 , 30 , 31 , 33–35 at high risk ( tables 1 ⇑ – 3 ). Of the three retrospective studies using GP or hospital databases to identify subjects, three used medical coding (Read codes, 32 Oxford Medical Indexing System (OXMIS) 33 and International Classification of Diseases 9 (ICD-9) 34 ) with study quality reliant on database accuracy. Of the seven prospective studies recruiting cases from hospital admissions, two recruited community controls from GP practices 32 , 33 and five recruited controls from inpatients with non-cardiac diagnoses 26 , 28 , 35 or non-cardiac outpatient clinics. 27 , 29 Representativeness of these control groups is unclear, with few reporting baseline characteristics, only three reporting response rates (ranging from 65% to 67% 27 , 28 , 30 ) and three studies of unmatched design, with significant 27 , 29 or unknown 30 differences in baseline demographic characteristics.

Four studies reported laboratory-diagnosed influenza-based exposure on influenza antibody titres, two relying on single-point estimates 28 , 29 either correlated with self-reported symptoms and adjusted for vaccination, 28 or conducted in China (vaccination unlikely). 29 The remaining two studies 26 , 27 defined exposed as a fourfold rise in paired acute-convalescent antibody titres, including a single high antibody titre in unvaccinated subjects or a positive PCR from nasopharyngeal swabs in one study, 27 and are likely indicative of recent infection. Exposure was measured by ILI in three 26 , 28 , 30 and RTI in seven 27 , 28 , 31–35 studies with RTI differentiated from ILI by inclusion of fever as a necessary criterion in ILI studies. All prospective studies included self-reported ILI/RTI with variable timing of exposure 30 , 32 , 33 prior to AMI with only one 28 including medical record validation.

Appropriate adjustment for potential confounders was determined in three of nine studies 27 , 29 , 32 by either matching or logistic regression analysis. Only two studies adjusted for prior influenza vaccination 27 , 28 while a third assumed low vaccination coverage. 29 Four studies 26–29 restricted their study period to the influenza season, covering one, 26 , 28 two 29 or three 27 seasons.

Of the seven studies assessing the association between influenza vaccination and prevention of AMI, two were categorised as low 27 , 28 and five as moderate 36–40 risk of methodological bias ( table 4 ). Four were prospective studies defining cases as consecutively admitted patients with AMI 27 , 28 , 37 , 39 and controls as non-cardiac outpatients 27 , 39 or inpatients 28 , 37 with participant rates between 66% and 91%. Prespecified AMI diagnostic criteria and chart review 27 , 28 , 39 or ICD-9 coding 37 identified cases with controls through self-reported absence of previous AMI, 28 , 39 or absence of AMI on medical records 27 , 37 with low risk of misclassification. Retrospective studies identified cases and controls as presence or absence of AMI on hospital 36 or health maintenance 40 billing records or hospital discharge letters on general practice 38 databases. Two studies 36 , 40 validated this with medical chart review of identified cases. One study 36 assessed recurrent AMI events in a single population of cardiology outpatients.

Influenza vaccination included self-report in all four prospective studies, two validated against GP records 27 or a population-based immunisation register. 37 Of the retrospective studies, two 38 , 40 included vaccination status from database records with a chart review of vaccination-negative participants in one. 40 All studies adequately adjusted for potential confounders through either matching or multivariable analysis. Two studies did not restrict timing of AMI events to the influenza season. 38 , 40

This is the first meta-analysis of influenza infection and AMI, and shows that influenza infection is significantly associated with AMI, with cases having double the risk of influenza infection or RTI compared with controls. Our study also provides estimates of VE against AMI. Data show that vaccination is associated with a significantly lower rate of AMI. We calculated a pooled VE of 29% (95% CI 9% to 44%) in preventing AMI, on a par with or better than accepted AMI preventive measures, with the estimates of the efficacy of statins for secondary prevention of 36%, 41 antihypertensives of 15%–18% 42 and smoking cessation interventions of 26%. 43 Given the high global burden of AMI, and ischaemic heart disease being the leading cause of death and disability in the world, influenza vaccination could be added to other preventive strategies and confer additional population health benefits on AMI prevention. Vaccination is inexpensive, safe and effective. Patients with ischaemic heart disease are identified as a risk group for serious influenza infection, with many countries recommending vaccination for people with CVD. However, vaccination is underused in this population, 15 , 16 particularly in those under 65. 17 With increasing incidence of AMI after 50 years, 1 our findings add to the evidence base supporting influenza vaccination for middle-aged adults. Influenza vaccination has already been estimated to be cost-effective when used for influenza prevention in older adults, without direct consideration for cardiac protection. 44 However, it should be noted that interpretation of VE is complex, as influenza vaccination may not be equally protective against AMI during the entire year, with four of the six included vaccination studies performed during the influenza season.

Observational studies are subject to methodological biases, with case–control studies being prone to biases from participant selection and measurement of exposure. However, we found no differences in overall results when stratified by study quality and no undue influence by individual studies included in the analysis. Further, observational studies are the only ethical study type to measure the association between influenza infection and AMI, with the majority of published studies being of case–control design. The specificity of the case definition of influenza appeared important when comparing ILI with RTI. 34 Laboratory-confirmed diagnoses were not significantly associated with AMI, probably because of reduced statistical power due to small numbers and technical limitations of the current diagnostic tools. Our pooled VE concurs with a meta-analysis of published RCTs assessing the efficacy of influenza vaccination on recurrent ischaemic events. This meta-analysis found that influenza vaccine given to high-risk patients reduced their risk of AMI by 0.64, equating to a vaccine efficacy of 36% (95% CI 14% to 52.8%). 11 To expand the body of evidence supporting an association between influenza vaccination and AMI, we did not include previously pooled RCTs on influenza vaccine and AMI. Currently published RCTs are limited to recurrent events in high-risk patients, have heterogeneous outcome measures and are performed in low-income and middle-income countries without established influenza vaccination recommendations. 8–10 The generalisability of these RCTs to high-income countries with well-resourced health systems and better AMI outcomes 2 is unclear. While we provide pooled estimates of published observational case–control studies, a large-scale RCT is needed to provide the necessary evidence of the protective efficacy of influenza vaccination on AMI, including as primary prevention.

The effectiveness of annual influenza vaccines varies depending on the vaccine match to circulating strains. 45 The timing of vaccination is also important, with vaccination status being a valid predictor of AMI risk only if the vaccine was administered prior to the AMI event. The majority of included vaccination studies examined vaccination prior to AMI, but no study analysed matching between circulating and vaccine strains. We found a variable quality in studies, with lower-quality studies tending to be older. However, no single study had a large influence on the results. While it appears that study quality was not a factor, variations in study-participant characteristics and differences in the measurement of exposures may explain this heterogeneity.

Key messages

What is already known on this subject.

Acute myocardial infarction (AMI) continues to cause significant morbidity and mortality on a global scale despite coronary prevention programmes and rapid revascularisation technology. Influenza infection is associated with an increased risk of AMI, and vaccination lowers that risk in patients with previous AMI or known cardiovascular disease. However, the potential benefit of influenza vaccination in preventing AMI across the entire population is less well established.

What might this study add?

This systematic review of published case–control study data found that influenza infection was significantly associated with AMI, with a pooled OR 2.01 (95% CI 1.47 to 2.76). Influenza vaccination was negatively associated with AMI, with a pooled OR of 0.71 (95% CI 0.56 to 0.91), equating to a vaccine effectiveness of 29% (95% CI 9% to 44%) against AMI.

How might this impact on clinical practice?

Influenza vaccination is a readily available, inexpensive, straightforward and safe intervention, which may reduce the risk of AMI in people even in patients without predetermined heart disease.

• ↵ World Health Organisation . Global Health Estimates. 2014 Summary tables: Deaths by cause, age and sex, by WHO region, 2000–2012 , 2014 . Available at: http://www.who.int/healthinfo/global_burden_disease/estimates/en/index1.html (accessed 16 Feb 2015).
• ↵ World Health Organisation . Global Atlas on cardiovascular disease prevention and control . Geneva : World Health Organisation , 2011 . Available at: http://whqlibdoc.who.int/publications/2011/9789241564373_eng.pdf?ua=1 (accessed 16 Feb 2015).
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Supplementary materials

Supplementary data.

This web only file has been produced by the BMJ Publishing Group from an electronic file supplied by the author(s) and has not been edited for content.

• Data supplement 1 - Online supplement

Correction notice Since this article was first published online figure 1 has been updated. The middle box on the right hand side of the chart now includes the number 117 and not 15 as previously stated.

Contributors CRM conceived the study. CRM, MB, AEH, BR and ATN designed the study. MB, AEH and AM conducted the literature search and data extraction. BR performed the meta-analysis. CRM, MB, AEH, BR and ATN interpreted the data. MB and AEH wrote the first draft of the manuscript, and all mentioned coauthors critically revised the manuscript and provided final approval of the manuscript.

Competing interests AEH has received grant funding for investigator-driven research from GSK and Sanofi Pasteur. CRM has received funding or in-kind support from GSK, Pfizer, BioCSL and Merck for investigator-driven research on vaccines.

Provenance and peer review Not commissioned; externally peer reviewed.

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Myocardial infarction and alcohol consumption: A case-control study

Milena ilic.

1 Department of Epidemiology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia

Sandra Grujicic Sipetic

2 Institute of Epidemiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia

Branko Ristic

3 Clinic for Orthopedic Surgery and Traumatology, Clinical Center Kragujevac, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia

4 Faculty of Medicine, University of Belgrade, Belgrade, Serbia

Associated Data

All relevant data are available within the paper, its Supporting Information files and from the Harvard Dataverse ( https://doi.org/10.7910/DVN/MAI1X0 ).

Although epidemiological evidence for the beneficial effect of low alcohol consumption on myocardial infarction is strong, the impact of heavy drinking episodes is less clear.

The aim of this study was to investigate a possible association between the risk for acute myocardial infarction occurrence and alcohol consumption.

Our hospital-based case-control study comprised 374 participants (187 newly diagnosed patients with myocardial infarction and 187 controls, individually matched by gender, age, and place of residence). This study was performed in Kragujevac (a city in Serbia) during 2010. Logistic regression analysis was used to determine odds ratio (OR) with 95% confidence intervals (95% CI).

The history of alcohol consumption in patients with acute myocardial infarction and their controls did not differ significantly: the percentage of those that were consuming alcohol was slightly higher in cases (54.5%) than in controls (50.3%). The habit of binge drinking during the previous 12 months was significantly more common in cases (25.1%) than in controls (12.8%): adjusted OR = 2.2 (95%CI = 1.2–4.2, p = 0.017), p for trend = 0.015. Analysis of binge drinking by age, gender and place of residence revealed that the increase in risk for acute myocardial infarction was associated with older age (adjusted OR = 5.1, 95%CI = 1.7–15.1, p for trend = 0.010), male gender (adjusted OR = 2.3, 95%CI = 1.1–5.2, p for trend = 0.028) and rural place of residence (adjusted OR = 4.8, 95%CI = 1.3–18.5, p for trend = 0.033).

Our results suggest that binge drinking is associated with twice the risk for myocardial infarction compared to not drinking. Since consumption of alcohol is very common in the Serbian population, the effect of binge drinking on myocardial infarction should be considered an important public health issue.

Introduction

Myocardial infarction represents death of myocard cells due to irreversible ischemia progressing to necrosis [ 1 , 2 ]. According to the World Health Organization’s estimates, every year approximately 6 million people around the world experience a myocardial infarction, and the lethal outcome occurs in over 25% of cases [ 1 ]. Mortality rates for myocardial infarction are dropping in North America and many North and West European countries, while in Central and East Europe these rates are increasing [ 3 ]. In 2014, over 16560 people (10270 men and 6290 women) in Serbia suffered a heart attack, and over 5000 people died (around 3000 men and 2000 women) [ 4 , 5 ]. It is estimated that around two thirds of the myocardial infarction mortality rates decline in developed countries are due to reduced exposure to risk factors, while the last third is the result of adequate treatment and improved survival [ 6 ].

Etiology of myocardial infarction is complex and still not completely elucidated [ 7 , 8 ]. Age, smoking, hypertension, high cholesterol levels, diabetes mellitus and male sex are recognized as major risk factors for myocardial infarction [ 8 ]. Other risk factors include obesity, physical inactivity, dietary factors, positive family history and psychosocial factors. However, in some developing countries, the contribution of established myocardial infarction risk factors is not entirely known. The results available to date suggest a significant presence of conventional risk factors for acute myocardial infarction not only in patients, but also among controls (especially those under 60 years of age) [ 9 – 11 ]. The “INTERHEART” study, which involved participants from 52 countries, pointed out that in different parts of the world different risk factors were responsible for the development of myocardial infarction: factors which showed the strongest link with the development of myocardial infarction in Africa were diabetes and hypertension, in South America it was obesity and smoking, while the most important risk factors in Croatia were current smoking, diabetes, higher ApoB/Apo A-1 ratio, obesity and hypertension, while alcohol consumption was found to be protective [ 12 ].

Numerous epidemiological studies showed that moderate alcohol consumption might decrease cardiovascular mortality [ 13 , 14 ] and was associated with reduced cardiovascular risk [ 15 – 17 ]. Tavani et al [ 18 ] found that alcohol consumption inversely correlated with non-fatal myocardial infarction, independent of the type of alcohol beverage, but related to the duration of alcohol consumption. A population-based case control study in Spain showed that moderate alcohol consumption (up to 30 mg/day: including wine, beer and spirits) was related with a reduction in risk for non-fatal myocardial infarction, while heavy alcohol intake did not significantly reduce the risk [ 15 ]. A large study in China that included 64597 persons showed that alcohol consumption led to a lower risk for heart attack [ 19 ]. However, the protective effect of moderate alcohol consumption on myocardial infarction occurrence is lost when it is characterized by consumption patterns that include episodes of intake of large quantities of alcohol [ 10 , 20 – 22 ].

Although epidemiological evidence for the beneficial effects of low alcohol consumption on myocardial infarction is strong, the impact of heavy drinking episodes is less clear [ 12 , 23 ]. Some studies have shown that heavy drinking, as well as binge drinking, can lead to acute myocardial infarction [ 23 – 25 ]. The “INTERHEART” study showed that episodes of binge drinking can lead to the onset of myocardial infarction and that especially in older people [ 26 ]. In one center in Northern Ireland (Belfast) and three centers in France (Lille, Strasbourg, and Toulouse), the hazard ratio for „hard coronary events”(incident myocardial infarction and coronary death) for binge drinkers compared with regular drinkers was 1.97 (95%CI = 1.21 to 3.22) in middle aged men [ 21 ]. Risk of a major coronary event for men who consumed ≥ 9 drinks in 24 hours before the onset of symptoms was 2.26 (95% CI = 1.06 to 4.81) compared with regular drinkers who consumed no alcohol in that period [ 27 ]. Population-based case–control study in New York [ 28 ] showed that frequency of episodic alcoholic intoxication of at least once/month or more was associated with a strongly increased risk of non-fatal myocardial infarction in women aged 35–69 years compared to abstention (OR = 2.90; 95%CI = 1.01–8.29), while compared to current drinkers who never drink to this extent the risk was 6.22 (95%CI = 2.07–18.69). A nested case–control study in Sweden recorded that taking large amounts of alcohol on a single occasion was associated with an increased risk for myocardial infarction in women but not in men [ 29 ]. The beer binge drinking is associated with increased risk of fatal acute myocardial infarction in men (Kuopio, Finland) whose usual intake of beer was 6 or more bottles per session compared with men who usually consumed less than 3 bottles (relative risk was 6.50, 95%CI = 2.05–20.61) [ 30 ]. Any heavy drinking occasion was associated with a two times higher mortality from ischaemic heart disease in former drinkers compared with former drinkers without such heavy drinking occasions, and in current drinkers compared with current drinkers with average daily intake of one to two drinks [ 31 ].

A very small number of analytical epidemiological studies on the etiology of acute myocardial infarction have been conducted in Serbia. The aim of this paper was to assess the link between alcohol consumption and risk for acute myocardial infarction in our population.

Study design

This hospital-based case-control study was performed in Kragujevac (a city in Serbia with about 200,000 inhabitants) during 2010. The Clinical Center in Kragujevac, one of the four clinical centers in the country, provides tertiary health care.

The healthcare system in Serbia is free to access, universal, and covers all citizens and permanent residents. This system is free of direct charge, because all employees must pay contributions to it. The network of health care institutions throughout Serbia is organized on three levels—the primary, secondary and tertiary healthcare providing level. With political and social changes since 2000, there have been some improvements of the health system and general living circumstances in Serbia [ 32 ]. The Human Development Index values had a rising trend since 2000 (0.726), reaching 0.767 in 2010. Diagnosis and treatment of ischemic heart disease, especially myocardial infarction, have significantly improved in the last 5–10 years, and Serbia now has an epidemiological pattern similar to that in most of the neighboring countries.

Study population

The study population consisted of newly diagnosed patients with their first myocardial infarction according to the diagnostic criteria based on the European Society of Cardiology/American College of Cardiology consensus guidelines: specific symptoms of acute myocardial infarction, changes in the blood levels of specific enzymes and/or acute myocardial infarction-specific electrocardiogram changes [ 2 ]. All cases were hospitalized at the Clinical Center in Kragujevac. No one refused to participate in the study.

Controls were selected among patients who were hospitalized at the same time in the Clinical Center in Kragujevac, without either a diagnosis or a history of myocardial infarction, or any other cardiovascular disease. Controls consisted of patients who were, due to other diseases or conditions (such as closed or open fracture of the arms, legs or ribs, gonarthrosis, coxarthrosis, etc), hospitalized at the Clinic for Orthopedic Surgery and Traumatology, Clinical Center in Kragujevac. All selected controls were interviewed; no one refused to participate.

Cases and controls were individually matched by gender, age (± 2 years) and place of residence (rural / urban). All cases and controls fulfilled the same criteria for inclusion of participants in the study (they gave voluntary consent and had no criteria for exclusion). Exclusion criteria for the study were age of 18 years or less, positive history of a psychiatric illness, pregnancy and lactation, refusal to participate in research or any other objective reason that did not allow or hindered participation in the study.

Ethics considerations

This study was conducted according to the guidelines laid down in the Declaration of Helsinki and all procedures involving human subjects were approved by Ethics Committee of the Faculty of Medical Sciences, University of Kragujevac (Ref. No.: 01–529), and by the Ethics Committee of the Clinical Center Kragujevac (Ref. No.: 01–13815). Informed verbal consent was obtained from both cases and controls prior to the interview. Prior to obtaining a verbal consent, the medical doctors who conducted the interview thoroughly informed the participants of the details and purpose of the study, after which the medical doctors conducting the interview signed the questionnaire. At the time when our study was started, the Ethics Committee of the Clinical Center in Kragujevac did not require a written and signed informed consent for studies without any clinical examination that involve only interviews, such as our case-control study. The interviews were always conducted in the hospital. The interview took approximately 2 hours. A questionnaire was completed through face-to-face interviews conducted by trained interviewers (medical doctors). The mean time interval between diagnosis and interview of cases and controls was 2 weeks.

Sample size calculation

The overall sample calculation was based on the results of previously published studies of similar design. According to the data from the "INTERHEART study", the probability of exposure to the investigated risk factor (alcohol) in the control group was 47.14% [ 12 ]. With a two sided probability of the type I error alpha of 5%, based on the power of 80%, the assumed coefficient of correlation for exposure to the examined factor between the matched cases and the controls of r = 0.2, based on the applied matching and cases:controls ratio of 1:1, it is estimated that the minimum sample size required to detect the true odds ratio greater than 2.0 or less than 0.55 is 167 participants in each group. The StatsDirect statistical software (Version 3.0.184, Stats Direct Ltd, 9 Bonville Chase, Altrincham, Cheshire WA14 4QA, United Kingdom) was used to calculate the sample size.

Data collection

The epidemiological questionnaire and medical records were used as data sources in this study. The data on each participant were collected by a face-to-face interview, which lasted approximately 1.5–2 hours and was conducted by trained interviewers (medical doctors). Besides the questions about socio-demographic characteristics, the questionnaire contained questions on the exposure to potential risk factors and protective factors for acute myocardial infarction, as well as the habit of alcohol consumption (alcohol consumption anytime during lifetime, those who consumed were then asked about frequency, time of the beginning and duration of alcohol consumption, types of alcoholic beverages, average amount of beverages per day, binge drinking, cessation of consumption, duration of abstinence; additionally, we asked about frequency and amount of alcohol intake for 11 types of alcoholic beverages during the last 10 years in the special part of the questionnaire which contained questions of food intake).

Demographic variables included occupation, education level, marital status. Occupation was categorized as manual worker, farmer, clerk, professional and housewife (for retired the occupation before retirement was shown). Education level was categorized as low (≤8 years), and high (>8 years). Marital status was dichotomized as with partner versus without partner. Anthropometric measurements (weight and height) of the participants were taken using the standard instruments and techniques. Degree of obesity was estimated based on the body mass index (BMI): subjects with BMI ≥ 25kg/m 2 were considered overweight [ 33 ]. Data on family history of myocardial infarction, personal medical history (hypertension, diabetes mellitus, hypercholesterolemia, disorders of thyroidea, etc), oral contraceptive use, the presence of stressful events (death, stress in the family, financial stress, stress at work, etc) in the previous 12 months, use of tobacco, coffee and alcohol were collected. Participants were considered as smokers if they regularly smoked at least one cigarette per day or approximately 30 g of tobacco per month for one year. Participants were classified as current smokers if they had smoked at least one cigarette every day for the last 12 months, and as former smokers if at least one year passed since smoking cessation.

Data on alcohol consumption were related to the regular intake of any amounts of these beverages. Participants were also questioned about the frequency of alcohol consumption anytime during lifetime (never, sometimes, every day), quantity of alcohol (standard bottle of beer, as well as a glass of wine and a shot of spirits were used as measures of consumption), age at the time of the beginning of consumption (< 20 years, ≥ 20 years), duration of consumption (< 30 years, ≥ 30 years), cessation of consumption, the duration of abstinence (≤ 10 years, > 10 years). Also, participants were questioned about the habit of drinking alcohol during the last 10 years before the onset of the present illness: the frequency of consumption (daily, weekly, monthly) and the amount of consumption (bottle of 500 ml for beer, glass of 200 ml for wine, shot of 50 ml for spiriths) for 11 types of alcoholic beverages (rakija, cognac, brandy, vodka, whiskey, liqueur, vermouth, white wine, rose wine, red wine and beer). Based on the data on the frequency and amount of consumption, the average individual daily intake for each type of alcoholic beverage was determined. If significant changes in the consumption had happened during the observed period, habits before the change were recorded. Participants were classified as daily drinkers if they had drinked at least one drink every day for the last 12 months, and as former drinkers if at least one year passed since drinking cessation.

The total daily amount of consumption for each drink item was calculated and then finally converted into „pure”alcohol using food consumption tables [ 34 ]. In Serbia, a „standard”drink is any drink that contains about 13 grams of „pure”alcohol [ 34 ]. Daily quantity of alcohol consumption was categorized based on the total amount of pure alcohol per day (g), into two groups (≤ 13, > 13).

Binge drinking was defined as the consumption of 5+ standard drinks for men and 4+ standard drinks for women on one occasion at least once a month during the last year preceding the onset of the myocardial infarction for cases and the current illness for controls.

Statistical analysis

A descriptive analysis was performed for categorical variables by using absolute and relative frequencies. Differences were analyzed using the univariate logistic regression model between subgroups of age, gender, place of residence, education level, marital status, body mass index, oral contraceptive use, history of diabetes mellitus, hypertension, hypercholesterolemia, disorders of thyroidea, stressful events, family history of myocardial infarction, cigarette smoking and coffee consumption. Additionally, the univariate logistic regression model was used for analysis of characteristics of patients with acute myocardial infarction and their controls, according to alcohol consumption history.

Univariate and multivariate logistic regression models were performed to estimate the odds ratio (OR) with 95% confidence interval (95% CI) in order to assess the relationships between alcohol consumption and myocardial infarction occurrence. Multivariate logistic regression analysis was used to estimate the adjusted odds ratio with the aim of determining the independent risk factors for myocardial infarction associated with a history of alcohol consumption. Adjustment was made for all variables that were related to myocardial infarction in univariate analyses at a p value of <0.10 (body mass index, positive personal medical history for diabetes mellitus, hypertension, hypercholesterolemia, and disorders of thyroidea, family history of myocardial infarction, stressful events, and tobacco use). Model fit was assessed by the Hosmer-Lemeshow test of goodness of fit and Cox and Snell’s and Nagelkerke’s Pseudo R square measures, together with the calculation of the area under the ROC curve. A test for linear trend in risk was based on the logistic regression model. For binge drinking only, we performed subgroup analyses to explore further the effects of age, gender and place of residence, as the variables known from literature data as possible confounders for the association between alcohol consumption and acute myocardial infarction, although these variables were matched in the present study. Statistical significance was considered when p<0.050. All statistical analyses were conducted using the Statistical Package for Social Sciences software (SPSS Inc, version 20.0, Chicago, IL).

Participant characteristics

The case group with acute myocardial infarction and control group each consisted of 187 participants ( Table 1 ). Cases and controls were individually matched by gender, age and place of residence. More than 50% of cases and controls were ≤ 65 years old. The mean age of cases was 63.2 years (standard deviation = 10.5), and the mean age of controls was 63.9 years (standard deviation = 10.4). A total of 72.7% of participants were from urban areas.

P, probability value (according to univariate logistic regression analysis).

* For retiree the occupation before retirement was shown.

Cases and controls did not differ significantly in occupation, employment, education level, marital status, oral contraceptive use, coffee consumption. Significantly more participants were overweight (body mass index ≥ 25kg/m 2 ) among cases than in controls ( p = 0.043). Data from personal medical history showed that cases significantly more frequently had diabetes ( p < 0.001), hypertension ( p = 0.003) and hypercholesterolemia ( p < 0.001). Disorders of thyroidea were more frequently recorded in cases than controls ( p = 0.088. Presence of myocardial infarction in family history was significantly more common in cases (58.3%) than in controls (41.7%), p = 0.002. Stressful event was present in 79.7% cases and 62.0% controls ( p < 0.001). Cases and controls were significantly different in cigarette smoking habits (63.6% cases versus 51.3% controls, p = 0.021).

Among participants who had ever consumed alcohol, a higher proportion of cases than controls had body mass index ≥ 25kg/m 2 ( p = 0.025), diabetes mellitus ( p = 0.022), hypertension ( p = 0.002), hypercholesterolemia ( p = 0.002), stressful events ( p = 0.027), and family history of myocardial infarction ( p = 0.045) ( Table 2 ). Among participants who had never consumed alcohol, a higher proportion of cases than controls had diabetes mellitus ( p = 0.001), hypercholesterolemia ( p = 0.001), stressful events ( p = 0.001), family history of myocardial infarction ( p = 0.011), and smoking ( p = 0.041).

* For retiree the occupation before retirement was shown

Alcohol consumption and myocardial infarction

The history of alcohol consumption in patients with acute myocardial infarction and their controls was not significantly different: the percentage of those that were not consuming alcohol was slightly higher in controls (49.7%) than in cases (45.5%) ( Table 3 ). Our study found that 24.6% of cases and 20.3% of controls first started drinking alcohol before the age of 20 years, and that average duration of consumption for both groups was 30 years or more. All of the patients who regularly used alcohol consumed more than one type of drink. Of all alcoholic beverages, the most commonly used were spirits (especially rakija, a fruit brandy that normally has 40% alcohol content, but home-produced can be typically 50% to 80%, even going as high as 90%) both in cases (44.4%) and controls (42.2%). But, the risk of myocardial infarction associated with types of alcoholic beverages was similar among patients who reported drinking beer, wine, spirits, or mixed beverages. Although average amount of beer (> 1 bottle) consumed per day was more common in cases than in controls, these differences were not statistically significant. Compared to non-drinkers, cases and controls did not differ significantly in the use of certain types of alcoholic beverages. The intensity of alcohol consumption (the total amount of pure alcohol consumed per day) was higher in cases than in controls, but without statistical significance. The habit of drinking at least one drink every day was reported by 14.4% of cases and 11.8% of controls. Compared to non-drinkers, the habit of binge drinking on one occasion at least once a month during the last year preceding the onset of the myocardial infarction for cases and the current illness for controls was significantly more common in cases (25.1%) than in controls (12.8%): adjusted OR = 2.2 (95%CI = 1.2–4.2, p = 0.017), p for trend = 0.015. No significant differences were observed in the risk of acute myocardial infarction by the history of cessation of alcohol consumption and duration of abstinence.

Abbreviations: OR, Odds Ratio; CI, Confidence Interval; P, Probability value (according to logistic regression analysis); P trend , trend in risk (according to logistic regression model).

* Adjusted for body mass index, positive personal medical history for diabetes mellitus, hypertension, hypercholesterolemia, and disorders of thyroidea, family history of myocardial infarction, stressful events, and tobacco use

† Reference category

‡ A standard drink is defined as 13 g alcohol

|| Binge drinking was defined as the consumption of 5+ standard drinks for men and 4+ standard drinks for women on one occasion at least once a month during the last year preceding the onset of the myocardial infarction for cases and the current illness for controls.

Analysis of binge drinking by age, gender and place of residence revealed that the increase of risk for acute myocardial infarction was associated with older age (adjusted OR = 5.1, 95%CI = 1.7–15.1, p for trend = 0.010), male gender (adjusted OR = 2.3, 95%CI = 1.1–5.2, p for trend = 0.028) and rural place of residence (adjusted OR = 4.8, 95%CI = 1.3–18.5, p for trend = 0.033) ( Table 4 ).

Abbreviation: P trend , trend in risk (according to logistic regression model).

* According to multivariate logistic regression analysis

† Adjusted for body mass index, positive personal medical history for diabetes mellitus, hypertension, hypercholesterolemia, and disorders of thyroidea, family history of myocardial infarction, stressful events, and tobacco use

‡ Binge drinking was defined as the consumption of 5+ standard drinks for men and 4+ standard drinks for women on one occasion at least once a month during the last year preceding the onset of the myocardial infarction for cases and the current illness for controls

|| Reference category.

Our study showed that binge drinking is significantly associated with the increased risk for acute myocardial infarction, especially in older people, males and those living in the countryside.

Until today, a few investigators have specifically examined the influence of binge drinking on myocardial infarction occurrence. Our results (for binge drinking: OR = 2.2, 95%CI = 1.2–4.2) were consistent with some previous studies [ 27 – 31 ] that showed that binge drinking was associated with an increased risk of acute myocardial infarction. Also, a nationwide representative cohort of 50,000 Swedish male conscripts of 18–20 years of age indicated, through a 1969–2004 follow-up, that binge drinking and high alcohol consumption significantly increased the risk of total myocardial infarction (1.71, 95%CI = 1.24–2.35), but non-significantly increased the risk for fatal myocardial infarction (2.23, 95%CI = 0.81–6.53) [ 35 ]. Nevertheless, some epidemiological studies have found that heavy alcohol consumption was associated with a decreased risk of coronary heart disease [ 36 , 37 ]. During an average follow up of 4.36 years, Chinese men aged 45–81 years, who consumed >40 grams of ethanol per time with ≥5 times per week, had a significantly decreased risk of coronary heart disease (HR = 0.73, 95%CI = 0.54–1.00) compared with non-drinkers [ 37 ]. Contrary to that, a case-crossover study of 250 incident acute myocardial infarction cases in Switzerland found no evidence that the effect of binge drinking was significant [ 38 ]. Also, a recent a case-crossover study in Iran showed that alcohol abuse was not an acute trigger associated with significantly increased risk of myocardial infarction [ 39 ]. Possible explanations for the differences in results of these studies could include differences both in the characteristics of respondents (in terms of age, gender, occupation, comorbidity) and in the study design (in terms of the differences in selection of the cases with myocardial infarction and their controls, choice of the reference category for assessment of alcohol consumption, etc).

Drinking of alcoholic beverages in Serbia is considered a socially acceptable behavior [ 40 ]. The high prevalence of alcohol use (especially spirits) in our study is, inter alia, a consequence of considering alcohol use a part of tradition, customs and culture. Also, 16% of the general population in Serbia practiced excessive drinking per occasion (binge drinking) at least once per month [ 40 ]. In our case-control study, binge drinking was reported by 25.1% of cases and 12.8% of controls, which is, according to the available literature data, a larger percentage than in most of the countries in the region [ 41 , 42 ]. In the United States of America, the overall prevalence of binge drinking among adults aged ≥18 years was 17.1% in 2010 [ 43 ]. Potential mechanisms for a detrimental effect of binge drinking on acute myocardial infarction risk include increased fluctuations in blood pressure (either an acute increase or sustained hypertension after cessation of drinking) [ 44 , 45 ], together with heightened platelet activation and adverse changes in the balance of fibrinolytic factors, ventricular arrhythmia [ 46 ], direct damage to heart muscle cells (alcoholic cardiomyopathy) [ 47 ], as well as the unfavorable effects on lipid profile reported in some studies (such as increase of low-density lipoprotein levels, and no increase in high-density lipoprotein levels) [ 48 ], although the evidence is inconsistent [ 49 ].

The relationship between binge drinking and risk of acute myocardial infarction seems to be associated with older age, male gender and with life in the countryside in our study. Similarly, the “INTERHEART” study recorded that binge drinking related to myocardial infarction, especially in older people in developed countries [ 26 ]. Information about potential mechanisms linking diverse patterns of drinking to diverse risk of myocardial infarction by age, gender and place of residence is limited. Heavy episodic drinking is frequently reported by elderly, male and those with lower levels of education, who may be particularly at risk because of age-related increases in comorbidities and medication use [ 50 , 51 ]. Additionally, women had, on average, a very low level of alcohol consumption and there were only small differences in incidence of myocardial infarction between drinkers and non-drinkers [ 29 ].

The findings of numerous epidemiological studies that indicated a protective effect of moderate alcohol consumption on the occurrence of myocardial infarction were not confirmed in our study. Tavani et al [ 18 ] noted that the consumption of alcoholic drinks was inversely related to non-fatal myocardial infarction, irrespective of the type of drink, and depended on the duration of alcohol consumption. People who consumed alcohol for 40 years or more had a 60% lower risk of developing the disease, and those who regularly consumed alcoholic beverages, one to three glasses a day, had a two times lower risk of myocardial infarction [ 18 ]. Schröder et al [ 15 ] observed that consumption of up to 30 g of alcohol per day was inversely related to the onset of non-fatal myocardial infarction after controlling for potential confounding factors. Alcohol consumption of up to 20 g / day including wine, beer and brandy, significantly reduced the risk of myocardial infarction, while higher alcohol intake did not substantially reduce the risk [ 15 ]. Two nested case-control studies in the United States, which included women enrolled in the Nurses Health Study and men enrolled in the Health Professionals Follow-Up Study, found that the frequency of alcohol consumption was significantly associated with a reduced risk of acute myocardial infarction [ 52 ]. The lowest risk was recorded in people who consumed alcohol most frequently (3–7 drinks per week) and those who consumed the highest quantities (30g / day and more). Similar results were observed in studies in Spain, Costa Rica, France and Northern Ireland [ 53 – 55 ]. A large meta-analysis which included 240 studies showed that a daily intake of alcohol in the amount of 50 g / day had a protective effect for myocardial infarction (RR = 0.87, 95% CI = 0.54–0.90), while intake of 100 g / day was associated with an increased risk (RR = 1.13; 95% CI = 1.06–1.21) [ 56 ]. This meta-analysis found that the daily intake of 72 g/day was the limit in amount of consumed alcohol for which significant protective effect was still recorded, while the amount of 89 g / day was the value from which a significantly increased risk began [ 56 ].

The relationship between alcohol consumption and myocardial infarction remains controversial. Differences between the results obtained in some studies can partly be explained with different methodology that was used, but also with differences in the characteristics of study groups (some studies are limited to specific groups of subjects such as employed patients or patients after rehabilitation, or focused on older patients, while other focus on younger and healthier patients). Although our case-control study was hospital-based, data in available literature show that the frequency of alcohol consumption found in our respondents was similar to the pattern of alcohol consumption across the entire population [ 40 , 41 ]. A possible reason for the absence of substantial differences is the fact that comorbidity was not a reason for exclusion from the study (among the controls there were probably illnesses associated with alcohol consumption, e.g. trauma). Also, in our study among those who used alcohol there were significantly more persons with obesity and hypertension among cases than among controls, while those differences were not significant in non-drinkers. In addition, our study did not include the most severe patients with myocardial infarction, as they died shortly after admission to the hospital, so there was no alcohol consumption data available. Future epidemiological analytical studies are needed to clarify the impact of not only pure ethanol but also non-alcoholic ingredients in alcoholic beverages on the occurrence of myocardial infarction.

Limitations of the study

Our study has several strengths. Firstly, this study presented detailed qualitative and quantitative data on alcohol consumption over a period of 10 years before the onset of the disease. Secondly, based on the intake of certain types of beverages, we estimated the average daily intake of pure alcohol in our study. In addition, the former drinkers (regardless of the duration of abstinence) were excluded from the reference group which might have minimized bias to some extent. But, our study has some limitations. The limitation of this study might be that the definitions of alcohol consumption (such as differences in the definition of alcohol use, categories of the frequency and intensity of alcohol consumption, as well as the differences in the quality of alcoholic beverages or "standard" drink) somewhat differed from the definitions that were used in some other studies, so the comparison of findings was sometimes difficult [ 25 ]. The response rate of 100%, as well as the fact that the interview was always conducted by a medical doctor, could partly reduce the shortcomings of our case-control study. Also, although we estimate that the underreporting of alcohol consumption in this study was not a problem, because drinking in Serbia is a traditionally accepted habit, we cannot preclude the possible existence of recall bias when doing a retrospective study of alcohol use and myocardial infarction. The limitation of the study is the lack of information on the consumption of alcohol in periods of high sensitivity (such as puberty, pregnancy, lactation). In addition to the well-known shortcomings of case control studies, a further limitation of the study was the relatively small sample size. We acknowledge that failure in both determining previous use of medications among cases and controls and compliance to a recommended treatment might have led to a less accurate assessment of risk for myocardial infarction, but in this study there was no suitable data for this. As in many other studies, our list of potential confounders was not complete and we cannot exclude the possibility that some unmeasured confounders (such as dietary factors, socio-economic status) might explain the results of this study.

Conclusions

Our study is one of the few in which binge drinking was found to be a risk factor for acute myocardial infarction. Binge drinking is frequent among older aged, men and those living in the countryside, and needs to be addressed in understanding the health risks. But, this study confirms that the relationship between alcohol consumption and myocardial infarction is quite complex and further analytical epidemiological studies are needed to clarify the observed association.

Supporting information

Funding statement.

This work was supported by the Ministry of Education and Science of Republic of Serbia, through contract no. 175042. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Data Availability

• Heart attack

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Coping and support, preparing for your appointment.

Ideally, a health care provider should screen you during regular checkups for risk factors that can lead to a heart attack.

A heart attack is often diagnosed in an emergency setting. If you've had or are having a heart attack, care providers will take immediate steps to treat your condition. If you're able to answer questions, you may be asked about your symptoms and medical history.

Diagnosis of a heart attack includes checking blood pressure, pulse and temperature. Tests are done to see how the heart is beating and to check overall heart health.

Tests to diagnose a heart attack include:

• Electrocardiogram (ECG or EKG). This first test done to diagnose a heart attack records electrical signals as they travel through the heart. Sticky patches (electrodes) are attached to the chest and sometimes the arms and legs. Signals are recorded as waves displayed on a monitor or printed on paper. An electrocardiogram (ECG) can show if you are having or have had a heart attack.
• Blood tests. Certain heart proteins slowly leak into the blood after heart damage from a heart attack. Blood tests can be done to check for these proteins (cardiac markers).
• Chest X-ray. A chest X-ray shows the condition and size of the heart and lungs.
• Echocardiogram. Sound waves (ultrasound) create images of the moving heart. This test can show how blood moves through the heart and heart valves. An echocardiogram can help identify whether an area of your heart has been damaged.
• Coronary catheterization (angiogram). A long, thin tube (catheter) is inserted into an artery, usually in the leg, and guided to the heart. Dye flows through the catheter to help the arteries show up more clearly on images made during the test.
• Cardiac computed tomography (CT) or Magnetic resonance imaging (MRI). These tests create images of the heart and chest. Cardiac CT scans use X-rays. Cardiac MRI uses a magnetic field and radio waves to create images of your heart. For both tests, you usually lie on a table that slides inside a long tubelike machine. Each test can be used to diagnose heart problems. They can help show the severity of heart damage.

More Information

• Cardiac catheterization
• Chest X-rays
• Coronary angiogram
• Echocardiogram
• Electrocardiogram (ECG or EKG)
• Stress test

Each minute after a heart attack, more heart tissue is damaged or dies. Urgent treatment is needed to fix blood flow and restore oxygen levels. Oxygen is given immediately. Specific heart attack treatment depends on whether there's a partial or complete blockage of blood flow.

Medications

Medications to treat a heart attack might include:

• Aspirin. Aspirin reduces blood clotting. It helps keep blood moving through a narrowed artery. If you called 911 or your local emergency number, you may be told to chew aspirin. Emergency medical providers may give you aspirin immediately.
• Clot busters (thrombolytics or fibrinolytics). These drugs help break up any blood clots that are blocking blood flow to the heart. The earlier a thrombolytic drug is given after a heart attack, the less the heart is damaged and the greater the chance of survival.
• Other blood-thinning medicines. A medicine called heparin may be given by an intravenous (IV) injection. Heparin makes the blood less sticky and less likely to form clots.
• Nitroglycerin. This medication widens the blood vessels. It helps improve blood flow to the heart. Nitroglycerin is used to treat sudden chest pain (angina). It's given as a pill under the tongue, as a pill to swallow or as an injection.
• Morphine. This medicine is given to relieve chest pain that doesn't go away with nitroglycerin.
• Beta blockers. These medications slow the heartbeat and decrease blood pressure. Beta blockers can limit the amount of heart muscle damage and prevent future heart attacks. They are given to most people who are having a heart attack.
• Blood pressure medicines called angiotensin-converting enzyme (ACE) inhibitors. These drugs lower blood pressure and reduce stress on the heart.
• Statins. These drugs help lower unhealthy cholesterol levels. Too much bad (low-density lipoprotein, or LDL) cholesterol can clog arteries.

Surgical and other procedures

If you've had a heart attack, a surgery or procedure may be done to open a blocked artery. Surgeries and procedures to treat a heart attack include:

Coronary angioplasty and stenting. This procedure is done to open clogged heart arteries. It may also be called percutaneous coronary intervention (PCI). If you've had a heart attack, this procedure is often done during a procedure to find blockages (cardiac catheterization).

During angioplasty, a heart doctor (cardiologist) guides a thin, flexible tube (catheter) to the narrowed part of the heart artery. A tiny balloon is inflated to help widen the blocked artery and improve blood flow.

A small wire mesh tube (stent) may be placed in the artery during angioplasty. The stent helps keep the artery open. It lowers the risk of the artery narrowing again. Some stents are coated with a medication that helps keep the arteries open.

• Coronary artery bypass grafting (CABG). This is open-heart surgery. A surgeon takes a healthy blood vessel from another part of the body to create a new path for blood in the heart. The blood then goes around the blocked or narrowed coronary artery. It may be done as an emergency surgery at the time of a heart attack. Sometimes it's done a few days later, after the heart has recovered a bit.

Cardiac rehabilitation

Cardiac rehabilitation is a personalized exercise and education program that teaches ways to improve heart health after heart surgery. It focuses on exercise, a heart-healthy diet, stress management and a gradual return to usual activities. Most hospitals offer cardiac rehabilitation starting in the hospital. The program typically continues for a few weeks or months after you return home.

People who attend cardiac rehab after a heart attack generally live longer and are less likely to have another heart attack or complications from the heart attack. If cardiac rehab is not recommended during your hospital stay, ask your provider about it.

• Coronary artery bypass surgery
• Extracorporeal membrane oxygenation (ECMO)

Clinical trials

Explore Mayo Clinic studies  testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition.

To improve heart health, take the following steps:

• Exercise. Regular exercise helps improve heart health. As a general goal, aim for at least 30 minutes of moderate or vigorous physical activity five or more days a week. If you've had a heart attack or heart surgery, you may have activity restrictions. Ask your health care provider what's best for you.
• Eat a heart-healthy diet. Avoid or limit foods with a lot of saturated fat, trans fats, salt and sugar. Choose whole grains, fruits, vegetables, and lean proteins, such as fish and beans.
• Maintain a healthy weight. Too much weight strains the heart. Being overweight increases the risk of high cholesterol, high blood pressure and diabetes.
• Don't smoke. Quitting smoking is the most important thing you can do to improve heart health. Also, avoid being around secondhand smoke. If you need to quit, ask your provider for help.
• Limit alcohol. If you choose to drink alcohol, do so in moderation. For healthy adults, that means up to one drink a day for women and up to two drinks a day for men.
• Get regular health checkups. Some of the major risk factors for a heart attack — high blood cholesterol, high blood pressure and diabetes — don't cause early symptoms.
• Manage blood pressure, cholesterol and blood sugar. Ask your provider how often you need to have your blood pressure, blood sugar and cholesterol levels checked.
• Control stress. Find ways to help reduce emotional stress. Getting more exercise, practicing mindfulness and connecting with others in support groups are some ways to ease stress.

Having a heart attack is scary. Talking about your feelings with your care provider, a family member or a friend might help. Or consider talking to a mental health care provider or joining a support group. Support groups let you connect with others who have been through similar events.

If you feel sad, scared or depressed, tell your care provider. Cardiac rehabilitation programs can help prevent or treat depression after a heart attack.

Sex after a heart attack

Some people worry about having sex after a heart attack. Most people can safely return to sexual activity after recovery. But talk to your care provider first. When you can resume sex may depend on your physical comfort, emotional readiness and previous sexual activity.

Some heart medications can affect sexual function. If you're having problems with sexual dysfunction, talk to your care provider.

A heart attack usually is diagnosed in an emergency setting. However, if you're concerned about your risk of a heart attack, talk to your care provider. A cardiovascular risk assessment can be done to determine your level of risk.

You may be referred to a doctor trained in heart diseases (cardiologist).

Here's some information to help you prepare for your appointment.

What you can do

When you make the appointment, ask if there's anything you need to do in advance, such as restrict your diet. You might need to avoid food or drink for a while before a cholesterol test, for example.

Make a list of:

• Your symptoms, including any that seem unrelated to heart disease, and when they began
• Family history of heart problems, including heart disease, stroke, high blood pressure, diabetes or early heart attacks
• Important personal information, including recent major stresses or recent life changes
• All medications, vitamins and other supplements you take, including doses
• Questions to ask your provider

Take a friend or relative along, if possible, to help you remember the information you're given.

Some questions to ask your provider about heart attack prevention include:

• What tests do I need to determine my current heart health?
• What foods should I eat or avoid?
• What's an appropriate level of physical activity?
• How often should I be screened for heart disease?
• I have other health conditions. How can I best manage these conditions together?
• Are there brochures or other printed material that I can have? What websites do you recommend?

Don't hesitate to ask other questions.

What to expect from your doctor

Your health care provider is likely to ask you questions, including:

• How severe are your symptoms?
• Are they constant or do they come and go?
• What, if anything, seems to improve your symptoms?
• If you have chest pain, does it improve with rest?
• What, if anything, worsens your symptoms?
• If you have chest pain, does strenuous activity make it worse?
• Have you been diagnosed with high blood pressure, diabetes or high cholesterol?

What you can do in the meantime

It's never too early to make healthy lifestyle changes, such as quitting smoking, eating healthy foods and becoming more active. These are important steps in preventing heart attacks and improving overall health.

Oct 09, 2023

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