Acute myocardial infarction
by Dr. Md. Asaduzzaman
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Patients with acute myocardial infarction (AMI) usually complain of sudden or gradual onset of discomfort in the anterior chest, which may also be described as heaviness, pressure, or gas.
Diagnosis of AMI is determined by a high clinical suspicion from history and physical examination, in addition to changes in cardiac bio-markers (creatinine kinase MB [CK-MB], troponins, and myoglobin) and electrocardiogram (ECG) findings. Imaging techniques, such as two-dimensional echocardiography, are also useful in demonstrating myocardial dysfunction.
Treatment focuses on limiting the injury to cardiac tissue. Reperfusion therapy should be initiated as early as possible by the use of thrombolytics or percutaneous coronary intervention (PCI). Oxygen, nitrates, analgesic medications, aspirin, β-blockers, and angiotensin-converting enzyme (ACE) inhibitors are the cornerstone medications in the treatment of AMI.
Complications may arise as a result of myocardial damage, leading to arrhythmias, shock, and cardiac failure. These complications must be taken into account when considering treatment.
Cardiac rehabilitation involves preventive strategies to decrease the risk for reinfarction. Strategies include patient and family education; optimal control of comorbid conditions (particularly hypertension, diabetes mellitus, and hyperlipidemia); and lifestyle modification strategies, including smoking cessation, weight management, and physical activity. Maintenance medication is also prescribed, as determined by patient needs.
Definition/Description of Myocardial Infarction
The term myocardial infarction pathologically denotes the death of cardiac myocytes due to extended ischemia, which may be caused by an increase in perfusion demand or a decrease in blood flow. AMI falls in the spectrum of acute coronary syndromes (ACS), which includes unstable angina (UA), non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI).
Persistent elevation of the ST-segment on ECG signifies total occlusion of a coronary artery that causes necrosis of the myocardial tissue. This condition is STEMI. ACS without ST-segment elevation may either be NSTEMI or UA NSTEMI is more severe than UA. In this condition, the ischemia in the cardiac tissue is extensive enough to release cardiac biomarkers (troponin I or T) into the blood, but the occlusion is not as complete enough to cause elevation of the ST-segment.
In the U.S., approximately 500,000 episodes of AMI (30% of ACS cases) occur per year occur. Around 600 in every 100,000 men and 200 in every 100,000 women have an AMI every year.
There is an annual decline in the overall mortality rates among AMI patients in the U.S.
The WHO estimates that 17.1 million people died from coronary artery disease (CAD) in 2004, representing 29% of global deaths.
An epidemiologic study done by the National Registry of Myocardial Infarction (NRMI) from 1990 to 2006 presented the trends in characteristics and mortality of patients with AMI in the U.S., and calculated the mortality rates for AMI in patients who received guideline-based acute therapy.
A study was conducted to estimate the baseline characteristics of 2,515,106 patients previously admitted to 2,157 unique U.S. hospitals from 1990 to 2006 enrolled into the National Registry of Myocardial Infarction. Prevalence was estimated using four methods. By observational data, 1,146,609 (47%) patients presented with STEMI, whereas the remaining were classified as NSTEMI. In 1990, only 14.2% of patients with AMI were classified as NSTEMI; by 2006, the majority of patients (59.1%) were classified as NSTEMI. The percentage of STEMI decreased accordingly. Mean age of AMI increased from 64.1 to 66.4 years. AMI was increasingly diagnosed in women (from 32.4% of cases to 37.0%). Hospital mortality rates overall declined (10.4% to 6.3%), and in each category as well (STEMI, from 11.5% to 8.0%; NSTEMI, from 7.1% to 5.2%). After statistical adjustment for baseline variables, the reductions were more marked: 23.6% overall, 24.2% in STEMI, and 22.6% in NSTEMI. Level of Evidence: Low.
Rupture of high-risk plaque in the coronary arteries is a primary causative factor in the development of AMI. High-risk or vulnerable plaques are covered by a thin fibrous cap, which predisposed these plaques to rupture. Rupture of the thin fibrous cap exposes blood to plaque constituents that contribute to the activation, adhesion, and aggregation of platelets and the production of thrombin, causing subsequent thrombus formation, which occludes the vessels, impedes blood flow, and subsequently leads to the development of AMI. More than 90% of STEMI patients and approximately 35% to 75% of NSTEMI or UA patients have been found to have thrombus formation in their coronary arteries.
Well-established risk factors leading to atherosclerosis and plaque formation include dyslipidemia, smoking, hypertension, diabetes, age, family history, and male gender.
A case-control study of AMI in 52 countries, comprising 15,152 cases and 14,820 controls, was conducted. Among the most important risk factors for AMI in both men and women were were smoking (odds ratio [OR] = 2.87 for current vs never), raised ApoB/ApoA1 ratio (OR = 3.25 for top vs lowest quintile), history of hypertension (OR = 1.91), and diabetes (OR = 2.37)).Level of Evidence: Low.
Less well-established factors include obesity, metabolic syndrome, and chronic kidney disease. Potential triggers for AMI include excessive alcohol intake, excessive physical activity, psychosocial conditions, nonsteroidal anti-inflammatory (NSAID) drug use, and use of illicit drugs such as cocaine and amphetamines.
Increasing age is considered the most significant risk factor for CAD. Individuals aged older than 45 years have an eight times greater risk for AMI (less than 10% of patients who have AMI are aged younger than 45 years) An analysis using data from the VALIANT (VALsartan In Acute myocardial iNfarcTion) randomized, controlled trial (RCT) showed that of 14,703 patients with an AMI in the original trial, 803 patients were aged 18 to 45. The younger patients were compared against 7,715 patients aged greater than or equal to 65 years. The younger patients had less diabetes, hypertension, and history of AMI, and were more likely to be male (88% vs 59.1%), nonwhite (9.6% vs 5%), current smokers (73.7% vs 15.9%), obese (37.9% vs 25.1%), and dyslipidemic at randomization (43.1% vs 32.7%). Adjusted relative risks were higher in the young patients: smoking hazardous risk = 1.6, hypertension hazardous risk = 1.8. Level of Evidence: Low.
The risk for mortality after AMI is higher for older individuals
Cigarette smoking is a major risk factor for atherosclerosis and hence AMI. Risk is directly proportional to the number of cigarettes smoked per day.
Dyslipidemia is one of the most important risk factors.
Elevated serum levels of low-density lipoprotein cholesterol (LDL-C) and non–high-density lipoprotein cholesterol (HDL-C) (other triglyceride-rich lipoproteins) significantly increase the risk of AMI.
A study of 303 patients without a history of AMI or angina, in whom symptoms of AMI began before admission, matched against 297 controls, was conducted to determine the value of non–HDL-C levels in predicting a first nonfatal AMI. The risks were OR = 1.83 for the second quartile, OR = 2.07 for the third quartile, and OR = 2.33 for the fourth quartile.Level of Evidence: Moderate.
HDL-C value less than 40 mg/dL is also a risk factor for atherosclerosis.
Hypertension is associated with a higher risk of AMI
Diabetes mellitus is associated with a higher risk of AM
Individuals with a family history of ischemic heart disease (IHD) in a first-degree relative have a higher risk for AMI
An Italian case control study of 378 men and 129 women with a first nonfatal AMI compared against 297 male and 181 female controls was conducted. The odds ratio for those having one or more first-degree relative with IHD was 2.1; for those with two or more relatives, 3.8. Level of Evidence: Low.
Screening of asymptomatic individuals in the general population for AMI is not applicable; however, a person’s overall risk for CAD can be evaluated by applying his or her cardiac risk factors to risk predication equations that are based on large cohort series such as the Framingham study.
Routine screening for CAD in patients with low or even moderately increased risk for CAD is not advised by the U.S. Preventive Services Task Force (USPSTF). This recommendation includes the routine use of resting ECG, exercise treadmill test (ETT), or electron-beam computerized tomography (EBCT) to screen for evidence of coronary atherosclerosis or prediction of CAD events in persons without significantly increased risk.
The USPSTF concludes that the use of nontraditional risk factors—such as high-sensitivity C-reactive protein (hs-CRP), ankle–brachial index (ABI), leukocyte count, fasting blood glucose level, periodontal disease, carotid intima–media thickness (carotid IMT), coronary artery calcification (CAC) score on EBCT, homocysteine level, and lipoprotein(a) level—to prevent cardiac events in persons without a history of CAD is unproven.
Measures for preventing AMI are the same as those for preventing the development of CAD and include lifestyle modifications (eg, quitting smoking, getting regular exercise, making diet changes), control of comorbidities (eg, hypertension, diabetes mellitus, hypercholesterolemia), and appropriate patient education.
Population at Risk
Physicians should be able to identify patients who are at risk for AMI by the presence of risk factors for CAD (eg, smoking, hypertension, diabetes mellitus, hypercholesterolemia) and initiate appropriate management.
The 10-year risk of CAD occurrence (based on the Framingham point systems provided in Tables 1 and 2) in all patients with two or more risk factors should be calculated. Patients with two or more risk factors who are found to have high 10-year risk would benefit the most from primary prevention.
A prospective cohort study of 6,643 British men aged 40 to 59 years was conducted to establish the predictive accuracy of the Framingham risk score. The study found that 2.8% died from CAD compared with 4.1% predicted (relative overestimation 47%). A fatal or nonfatal CAD event occurred in 10.2% versus a predicted 16.0% (relative overestimation of 57%).Level of Evidence: Low.
It is important to identify patients with CAD and those with risk equivalents to initiate secondary prevention strategies.
Risk equivalents are conditions that, if present, signify that the patient has an absolute risk of having a new CAD event or of having recurrent CAD events in the future. Risk equivalents include clinical atherosclerotic diseases (peripheral arterial disease, carotid artery disease, abdominal aortic aneurysm); diabetes mellitus; and multiple risk factors, wherein the individual has an absolute 10-year risk for major CAD events (AMI and CAD death) of more than 20%.
There are several preventive measures supported by the American College of Cardiology (ACC) and the American Heart Association (AHA).
Smoking cessation for as short as 6 months has been found to lessen the dysfunction of coronary endothelium in AMI patients. Two years after cessation, the risk of AMI drops by 50%.
Alcohol moderation and prevention of illicit drug use are important in the prevention of cardiac conditions.
Physical activity and exercise
Leisure-time physical activity has been associated with a lower risk of AMI among lean, normal-weight, and overweight (BMI 25-25.9) patients. Patients with a BMI of 30 or more have a higher risk of AMI.
Light to moderate leisure time activities performed regularly, such as gardening and walking, are recommended. Sports or other vigorous activities are not necessary.
A study of 5,934 men aged 40 to 59 years, of whom 772 had CAD, was conducted. Risks for all cause and cardiovascular mortality when compared with inactive/occasionally active exercise were light exercise (RR = 0.42), moderate (RR = 0.47), and moderately vigorous/vigorous (RR = 0.63). Level of Evidence: Low.
Physical activity has been found to decrease the risk of CAD by decreasing inflammatory/hemostatic biomarkers (ie, CRP); lowering blood pressure, lipid levels, and BMI; and increasing insulin sensitivity.
A prospective study of 27,055 healthy women followed for a mean of 10.9 years was conducted. There were 979 cardiovascular events. The risk of cardiovascular events decreased linearly with higher levels of activity. Using 200 kcal/week of activity as a reference, relative risk reductions were 27% for the 200 to 599 kcal/week group, 32% for the 600 to 1499 kcal/week group, and 41% for the greater than 1500 kcal/week group.Level of Evidence: Moderate.
Diets rich in soluble fiber, vegetables, fruits, and whole grains, and low in saturated fat and cholesterol should be encouraged.
Management and control of comorbid diseases or risk equivalents:
Hypertension should be managed properly. Patients with CAD should have their blood pressure maintained at less than 130/80 mm Hg. This may be achieved using a multimodal approach, which includes diet modification, lifestyle changes, exercise, and medications.
According to the 2007 ACC/AHA guideline for management of patients with STEMI, for patients with blood pressures greater than or equal to 140/90 mm Hg (or ≥130/80 mm Hg for patients with diabetes or chronic kidney disease), it is recommended to initiate or maintain lifestyle modifications, including weight control; increased physical activity; alcohol moderation; sodium reduction; and emphasis on increased consumption of fresh fruits, vegetables, and low-fat dairy products. For patients with blood pressures greater than or equal to 140/90 mm Hg (or ≥130/80 mmHg for patients with diabetes or chronic kidney disease), it is useful as tolerated, to add hypertension medication, treating initially with β-blockers and/or ACE inhibitors, with the addition of other drugs such as thiazides as needed to achieve goal blood pressure.Level of Evidence: Very low.
Aspirin, 75 to 162 mg/d, as a prophylactic agent, is beneficial for those with a 10-year CAD risk of 6% or more. A large randomized trial involving nearly 40,000 initially healthy women age 45 or above compared 100 mg of aspirin every other day to placebo. At follow-up, there were 477 cardiovascular events in the aspirin group and 522 in the placebo group, representing a nonsignificant 9% decrease. The reduction in risk for stroke was 17% in the aspirin group compared to placebo (RR = 0.84), but there was no significant decrease in risk for nonfatal AMI or cardiovascular death. Gastrointestinal bleeding requiring transfusion was higher in the aspirin group. Level of Evidence: High
A systematic review of six RCTs of aspirin therapy in a total of more than 95,000 patients without previous cardiovascular disease, both women and men, showed that aspirin reduced the risk of a composite of cardiovascular events, including stroke, in women but no significant decrease in AMI or cardiovascular mortality. In men, aspirin was associated with a significant decrease in cardiovascular events and AMI, but there was no significant effect on stroke or cardiovascular mortality. Aspirin increased risk for bleeding in both men and women. Level of Evidence: High.
Treatments that aim to lower LDL-C levels in dyslipidemic patients are effective in preventing AMI. Beneficial LDL-C levels are 80 mg/dL or less in patients with atherosclerosis and 100 mg/dL or less in asymptomatic patients with high risk for CAD. According to the 2007 ACC/AHA guideline for management of patients with STEMI, the recommended LDL-C level should be substantially less than 70 mg/dL
Diabetes control should be appropriate, with HbA1c levels maintained at 6.5% or less. Ideal fasting/preprandial plasma glucose is 110 mg/dL or less, while ideal postprandial plasma glucose is 135 mg/dL or less. According to the 2007 ACC/AHA guideline for management of patients with STEMI, the goal for HbA1c in diabetic patients should be less than 7%.
Patients, their family members, and the community should be educated properly, especially on how to detect and respond to an episode of AMI.
Read more about Acute myocardial infarction from this First Consult monograph:
Prevention | Diagnosis | Differential Diagnosis | Treatment | Resources
More Key Resources
Myocardial Infarction (Quick Reference)
Ferri: Ferri’s Clinical Advisor 2013, 1st ed.
Signs & Symptoms
The History: Major Symptoms Associated With Cardiac Disease
Bonow: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 9th ed.
Nonacute coronary syndrome anginal chest pain
Agarwal M – Med Clin North Am – 01-MAR-2010; 94(2): 201-16
Pathophysiology of acute myocardial infarction
Burke AP – Med Clin North Am – 01-JUL-2007; 91(4): 553-72; ix
Evaluation of myocardial abnormalities and ischemia (includes Images)
Chandarana H – Radiol Clin North Am – 01-JUL-2010; 48(4): 771-82
Evaluation of the patient with acute chest pain (includes Images)
Goldberg A – Radiol Clin North Am – 01-JUL-2010; 48(4): 745-55
Treatment & Management
Treatment of Acute Myocardial Infarction (includes Figure and Tables)
Bope and Kellerman: Conn’s Current Therapy 2012, 1st ed.
Management of ST-segment elevation myocardial infarction in EDs
Diercks DB – Am J Emerg Med – January 2008; 26(1); 91-100
Acute ST-segment elevation myocardial infarction: Critical care perspective
Karve AM – Crit Care Clin – 01-OCT-2007; 23(4): 685-707, v
Management of non-ST-Segment elevation myocardial infarction
Van Horn SE – Med Clin North Am – July 2007; 91(4); 683-700
Management of ST-segment elevation myocardial infarction: Comparison of the updated guidelines from North America and Europe
Thomas D – Am Heart J – November, 2009; 158(5); 695-705
Adjunct therapy in STEMI intervention (includes Images and Tables)
Mehta S – Cardiol Clin – 01-FEB-2010; 28(1): 107-25
Challenges in oral antiplatelet therapy: ST-segment elevation myocardial infarction (includes Table)
Dauerman HL – Am J Cardiol – 7-SEP-2009; 104(5 Suppl): 39C-43C
Office management after myocardial infarction
Aronow WS – Am J Med – 01-JUL-2010; 123(7): 593-595
Trends in the age adjusted mortality from acute ST segment elevation myocardial infarction in the United States (1988-2004)
Movahed M – Am J Cardiol – October 15, 2009; 104(8); 1030-1034
Epidemiology of myocardial infarction
Roger VL – Med Clin North Am – 01-JUL-2007; 91(4): 537-52; ix
Heart Attack: Warning Signs and Tips on Prevention
Managing Your Heart Attack
Managing Your Heart Attack: For Women
Stress Test Used to Predict Heart Attack Risk
Focused Updates: Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction and Guidelines on Percutaneous Coronary Intervention (2009)
Source: American College of Cardiology Foundation and the American Heart Association
Aspirin for the Prevention of Cardiovascular Disease: Recommendation Statement (2009)
US Preventive Services Task Force
Universal Definition of Myocardial Infarction (2007)
Source: American College of Cardiology
Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction (2008)
American College of Cardiology and the American Heart Association
Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction (2007)
Source: American Heart Association and the American College of Cardiology
Detection and Management of Post-myocardial Infarction Depression (2009)
Source: American Academy of Family Physicians
Guideline for Percutaneous Coronary Intervention (2011)
Source: American College of Cardiology (ACC)/American Heart Association (AHA)/Society for Cardiovascular Angiography .)
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