Myocardial Infarction

Definition of Myocardial Infarction

Myocardial infarction (from Latin: Infarctus myocardii, MI) or acute myocardial infarction (AMI) is the medical term for an event commonly known as a heart attack. It happens when blood stops flowing properly to part of the heart and the heart muscle is injured due to not enough oxygen. Usually this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called “acute” if it is sudden and serious.

A person having an acute myocardial infarction usually has sudden chest pain that is felt behind the breast bone and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64 percent, the person does not have chest pain or other symptoms. These are called “silent” myocardial infarctions.

Important risk factors are previous cardiovascular disease, old age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, the use of cocaine and amphetamines, and chronic high stress levels. The two main ways to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle. Common blood tests are creatine kinase (CK-MB) and troponin. ECG testing is used to differentiate between two types of myocardial infarctions based on the shape of the tracing. When the ST section of the tracing is higher than the baseline it is called an ST-elevation myocardial infarction (STEMI) which usually requires more aggressive treatment.

Immediate treatments for a suspected myocardial infarction include aspirin, which prevents further blood from clotting, and sometimes nitroglycerin to treat chest pain and oxygen. STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG). Ischemic heart disease, which includes myocardial infarction, angina and heart failure when it happens after myocardial infarction, was the leading cause of death for both men and women worldwide in 2011.

Classification

There are two basic types of acute myocardial infarction based on pathology:

Transmural: associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area’s blood supply. In addition, on ECG, ST elevation and Q waves are seen.

Subendocardial: involving a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.

In the clinical context, a myocardial infarction can be further subclassified into a ST elevation MI (STEMI) versus a non-ST elevation MI (non-STEMI) based on ECG changes. The phrase heart attack is sometimes used incorrectly to describe sudden cardiac death, which may or may not be the result of acute myocardial infarction. A heart attack is different from, but can be the cause of, cardiac arrest, which is the stopping of the heartbeat, and cardiac arrhythmia, an abnormal heartbeat. It is also distinct from heart failure, in which the pumping action of the heart is impaired; however severe myocardial infarction may lead to heart failure. A 2007 consensus document classifies myocardial infarction into five main types:

Type 1 – Spontaneous myocardial infarction related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
Type 2 – Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anaemia, arrhythmias, hypertension, or hypotension
Type 3 – Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new LBBB, or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
Type 4 – Associated with coronary angioplasty or stents:
Type 4a – Myocardial infarction associated with PCI
Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy
Type 5 – Myocardial infarction associated with CABG

Cause of Myocardial Infarction

Heart attack rates are higher in association with intense exertion, be it psychological stress or physical exertion, especially if the exertion is more intense than the individual usually performs. The period of intense exercise and subsequent recovery is associated with about a 6-fold higher myocardial infarction rate (compared with other more relaxed time frames) for people who are very physically fit. For those in poor physical condition, the rate differential is over 35-fold higher. One observed mechanism for this phenomenon is increased pulse pressure, which increases stretching of the arterial walls. This stretching results in significant shear stress on atheromas, which results in debris breaking loose from these deposits. This debris floats through the blood vessels, eventually clogging the major coronary arteries.

Acute severe infection, such as pneumonia, can trigger myocardial infarction. A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis. While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor. Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.

There is an association of an increased incidence of a heart attack in the morning hours, more specifically around 9 a.m. Some investigators have noticed that the ability of platelets to aggregate varies according to a circadian rhythm, although they have not proven causation.

Signs and Symptoms of Myocardial Infarction

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn. Levine’s sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.

Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.

Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea (shortness of breath), weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. Women may also experience back or jaw pain during an episode.

At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent myocardial infarctions vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.
The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other non-catastrophic differentials include gastroesophageal reflux and Tietze’s syndrome.

Risk Factors for Myocardial Infarction

Myocardial infarction results from atherosclerosis. Smoking appears to be the cause of about 36% of coronary artery disease and obesity 20%. Lack of exercise has been linked to 7-12% of cases. Job stress appear to play a minor role accounting for about 3% of cases.

Risk factors for myocardial infarction include:

Age
Sex: At any given age men are more at risk than women, particularly before menopause, but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women.
Diabetes mellitus (type 1 or 2)
High blood pressure
Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides
Tobacco smoking, including secondhand smoke
Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not the ozone.
Family history of ischaemic heart disease or myocardial infarction particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a ‘premature’ myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).
Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
Lack of physical activity.
Psychosocial factors including, low socio-economic status, social isolation, negative emotions and stress increase the risk of myocardial infarction and are associated with worse outcomes after myocardial infarction. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI.
Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
Oral contraceptive pill – women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.
Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis, whether elevated homocysteine in the normal range is causal is contentious.

Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but non-specific marker for inflammation. Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician’s discretion in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.

Inflammation in periodontal disease may be linked to coronary heart disease, and, since periodontitis is very common, this could have great consequences for public health. Serological studies measuring antibody levels against typical periodontitis-causing bacteria found that such antibodies were more present in subjects with coronary heart disease. Periodontitis tends to increase blood levels of CRP, fibrinogen and cytokines; thus, periodontitis may mediate its effect on MI risk via other risk factors. Preclinical research suggests that periodontal bacteria can promote aggregation of platelets and promote the formation of foam cells. A role for specific periodontal bacteria has been suggested but remains to be established. There is some evidence that influenza may trigger an acute myocardial infarction.

Baldness, hair greying, a diagonal earlobe crease (Frank’s sign) and possibly other skin features have been suggested as independent risk factors for MI. Their role remains controversial; a common denominator of these signs and the risk of MI is supposed, possibly genetic.
Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile. Non-modifiable risk factors include age, sex, and family history of an early heart attack, which is thought of as reflecting a genetic predisposition. To understand epidemiological study results, it is important to note that many factors associated with MI mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital status.

Diagnosis of Myocardial İnfaction

Medical societies recommend that the physician confirm that a patient is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient’s history, physical exam, ECG and cardiac biomarkers suggest the likelihood of a problem.

The diagnosis of myocardial infarction can be made after assessing patient’s complaints and physical status. ECG changes, coronary angiogram and levels of cardiac markers help to confirm the diagnosis. ECG gives valuable clues to identify the site of myocardial damage while coronary angiogram allows visualization of narrowing or obstructions in the heart vessels. At autopsy, a pathologist can diagnose a myocardial infarction based on anatomopathological findings.

A chest radiograph and routine blood tests may indicate complications or precipitating causes and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on anechocardiogram are also suggestive of a myocardial infarction. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation,Technetium (99mTc) sestamibi (i.e. a “MIBI scan”) or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiologic or pharmacologic stress. Thallium may also be used to determine viability of tissue, distinguishing whether non-functional myocardium is actually dead or merely in a state of hibernation or of being stunned.

WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:

Clinical history of ischaemic type chest pain lasting for more than 20 minutes
Changes in serial ECG tracings
Rise and fall of serum cardiac biomarkers such as creatine kinase-MB fraction and troponin

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers. According to the new guidelines, a cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.

Prevention from Myocardial İnfarction

The risk of a recurrent myocardial infarction decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:

Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, however the risk of hemorrhage is increased.
Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically stable patients, particularly in patients with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling post-MI.
Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other (“pleiotropic”) effects that may prevent myocardial infarction in addition to their effects on blood lipids.
The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone is another option that is sometimes preferable to eplerenone due to cost.
Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease. In high-risk people there is no clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. And they may increase risk in some groups.
Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.

Treatment of Myocardial Infarction

An MI requires immediate medical attention. Treatment attempts to salvage as much myocardium as possible and to prevent further complications, hence the phrase “time is muscle”. Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI. Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use. Other analgesics such as nitrous oxide are of unknown benefit. Early treatment of heart attack patients with an inexpensive beta-blocker drug called metoprolol, while in transit to the hospital, can significantly reduce damage to the heart during a myocardial infarction.

STEMI

Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner. If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended. If after fibrinolysis there is significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes then rescue PCI is indicated emergently. After PCI people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).