Heart Attack

Heart Attack



Definition of Heart Attack:

Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, results from the partial interruption of blood supply to a part of the heart muscle, causing the heart cells to be damaged or die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of cholesterol and fatty acids and white blood cells in the wall of an artery. The resulting is chemia (restriction in blood supply) and ensuing oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).

Typical symptoms of acute heart attack include sudden retrosternal chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety (often described as a sense of impending doom). Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue. A sizeable proportion of heart attack (22–64%) are “silent”, that is without chest pain or other symptoms.

Among the diagnostic tests available to detect heart muscle damage are an electrocardiogram (ECG), echocardiography, cardiac MRI and various blood tests. The most often used blood markers are the creatine kinase-MB (CK-MB) fraction and the troponin levels. Immediate treatment for suspected acute heart attack includes oxygen, aspirin, and sublingual nitroglycerin.

Most cases of heart attack with ST elevation on ECG (STEMI) are treated with reperfusion therapy, such as percutaneous coronary intervention (PCI) or thrombolysis. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although PCI may be required if the patient’s risk warrants it. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes mellitus, may benefit from bypass surgery (CABG). The European Society of Cardiology guidelines in 2011 proposed treating the blockage causing the myocardial infarction by PCI and performing CABG later when the patient is more stable. Rarely CABG may be preferred in the acute phase of myocardial infarction, for example when PCI has failed or is contraindicated.

Ischemic heart disease (which includes myocardial infarction, angina pectoris and heart failure when preceded by myocardial infarction) was the leading cause of death for both men and women worldwide in 2004. Important risk factors are previous cardiovascular disease, older 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 and obesity, chronic kidney disease, excessive alcohol consumption, the abuse of illicit drugs (such as cocaine and amphetamines), and chronic high stress levels.

Classification

There are two basic types of acute heart attack 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 5 – Myocardial infarction associated with CABG
    • Type 4a – Myocardial infarction associated with PCI
    • Type 4b – Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy

Cause of Heart Attack:

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 heart attack rate (compared with other more relaxed time frames) for people who are physically very 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 heart attack. 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 Heart Attack:

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 heart attack 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 heart attacks.

Women and older 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 heart attack 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.

At least one-fourth of all heart attacks 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 heart attacks 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 Heart Attack:

Heart attack 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 heart attack include:

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 heart attack. 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 heart attack mediate their risk via other factors. For example, the effect of education is partially based on its effect on income and marital statu.

Diagnosis of Heart Attack:

Medical societies recommend that the physician confirm that a patient is at high risk for heart attack 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 heart attack 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 an echocardiogram 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 heart attack; a patient is diagnosed with heart attack if two (probable) or three (definite) of the following criteria are satisfied:

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

Prevention from Heart Attack:

The risk of a recurrent heart attack 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 Heart Attack:

Heart attack treatment involves salvaging as much myocardium as possible and to prevent further complications, thus the phrase “time is muscle”. Oxygen, aspirin, and nitroglycerin are usually administered as soon as possible. Morphine was classically used if nitroglycerin was not effective however it may increase mortality in the setting of NSTEMI. A 2009 and 2010 review of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.

Antiplatelet agents

Aspirin has been shown to markedly reduce mortality and thus should be taken as soon as possible in those without an allergy to it. Aspirin has an antiplatelet effect which inhibits formation of further thrombi (blood clots) that clog arteries. Chewing is the preferred method of administration, so that it can be absorbed quickly. Dissolved soluble preparations or sublingual administration can also be used. U.S. guidelines recommend a dose of 162–325 mg. Australian guidelines recommend a dose of 150–300 mg. Additionally, the antiplatelet agent clopidogrel improves outcomes in those who will be conservatively managed or undergo percutaneous coronary intervention. It however may worsen outcomes in those who need urgent coronary artery bypass surgery.

Nitroglycerin

Nitroglycerin is used in the treatment of ACS/IHD to relieve anginal symptoms. It is associated with the decrease in myocardial stress due to peripheral vasodilation. The decrease of stress also decreases oxygen demand of the heart. The first line treatment for symptomatic relief of angina is sub-lingual nitroglycerin. Other formulations such as spray and IV can also be used. In the body nitroglycerin donates three nitric oxide molecules, which activate a second messenger system leading to release of calcium ions. The release of calcium ions leads to a relaxation of vascular smooth muscles and vasodilation. Nitroglycerin should not be given if any phosphodiesterase type 5 inhibitors such as Viagra, Cialis, Stondra, and Levitra have been taken by the casualty within the previous 24–48 hours as the combination of the two could cause a serious drop in blood pressure. It should not be given to patients with systolic blood pressure (SBP) less than 90mmHg or 30mmHg or more below baseline.

Beta Blockers

β-blockers have been extensively studied in acute MI. Despite thousands of studies, no consensus has yet been reached as to their efficacy in preventing complications or decreasing mortality. Logically this means that any treatment effect that exists is most likely small and risks and benefits of use in the ER should be weighed carefully. However, in theory β-blockers decrease the effect of the sympathetic nervous system on the heart. Since it is known that the sympathetic nervous system increases the heart rate and blood pressure in order to increase the cardiac output. Hence its blockage spares the heart the extra work load.

Heparin

Unfractionated heparin and enoxaparin result in similar outcomes at one year post MI.

Myocardial Energy Metabolism Regulator

Mildronate is a clinically used pharmacological preconditioning agent and anti-ischemic drug. It acts as a myocardial energy metabolism regulator by inhibiting fatty acid oxidation, and the carnitine biosynthesis and transport pathways, in particular gamma-butyrobetaine dioxygenase and carnitine acetyltransferase. By regulating the effective carnitine concentration, treatment with mildronate shifts the myocardial energy metabolism from fatty acid oxidation to the more favourable glucose oxidation under ischemic conditions.

Reperfusion

The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era. Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery.

Individuals without ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.

The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding.

At least 10% of patients with STEMI do not develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as “aborting” the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.

Rehabilitation

Additional objectives are to prevent life-threatening arrhythmias or conduction disturbances. This requires monitoring in a coronary care unit and protocolised administration of antiarrhythmic agents. Antiarrhythmic agents are typically only given to individuals with life-threatening arrhythmias after a myocardial infarction and not to suppress the ventricular ectopy that is often seen after a myocardial infarction.

Cardiac rehabilitation aims to optimize function and quality of life in those afflicted with a heart disease. This can be with the help of a physician, or in the form of a cardiac rehabilitation program.

Physical exercise is an important part of rehabilitation after a myocardial infarction, with beneficial effects on cholesterol levels, blood pressure, weight, stress and mood. Some patients become afraid of exercising because it might trigger another infarct. Patients are stimulated to exercise, and should only avoid certain exerting activities. Local authorities may place limitations on driving motorised vehicles. In most cases, the advice is a gradual increase in physical exercise during about 6–8 weeks following an MI. If it doesn’t feel too hard for the patient, the advice about exercise is then the same as applies to anyone else to gain health benefits, that is, at least 20–30 minutes of moderate exercise on most days (at least five days per week) to the extent of getting slightly short of breath.

Some people are afraid to have sex after a heart attack. Most people can resume sexual activities after 3 to 4 weeks. The amount of activity needs to be dosed to the patient’s possibilities.