Cardiovascular Diseases
Miocardical Infarction
Myocardial infarction (MI) or acute myocardial infarction (AMI), commonly known as a heart attack, is the interruption of blood supply to part of the heart, causing some heart cells to 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 lipids (like cholesterol) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, can cause damage or death (infarction) of heart muscle tissue (myocardium).
Classical symptoms of acute myocardial infarction include sudden 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. Approximately one quarter of all myocardial infarctions are silent, without chest pain or other symptoms. A heart attack is a medical emergency, and people experiencing chest pain are advised to alert their emergency medical services because prompt protection with an external defibrillator can save your life from primary ventricular fibrillation which occurs unexpectedly in 10% of all myocardial infarctions especially during the first hours of symptoms. Contemporary treatment of many myocardial infarctions can result in survival and even good outcomes. While it is true that certain less amenable cases are very massive and rapidly fatal "widowmakers", it is also true that in small attacks with limited damage and optimal treatment the heart muscle can be salvaged.
Heart attacks are the leading cause of death for both men and women all over the world. Important risk factors are previous cardiovascular disease (such as angina, a previous heart attack or stroke), older age (especially men over 40 and women over 50), tobacco smoking, high blood levels of certain lipids (triglycerides, low-density lipoprotein or "bad cholesterol") and low levels of high density lipoprotein (HDL, "good cholesterol"), diabetes, high blood pressure, obesity, chronic kidney disease, heart failure, excessive alcohol consumption, the abuse of certain drugs (such as cocaine and methamphetamine), and chronic high stress levels.
Immediate treatment for suspected acute myocardial infarction includes oxygen, aspirin, and sublingual glyceryl trinitrate (colloquially referred to as nitroglycerin and abbreviated as NTG or GTN). Pain relief is also often given, classically morphine sulfate. However, a 2009 review about the use of high flow oxygen for treating myocardial infarction found its administration increased mortality and infarct size, calling into question the recommendation for its routine use.
The patient will receive a number of diagnostic tests, such as an electrocardiogram (ECG, EKG), a chest X-ray and blood tests to detect elevations in cardiac markers (blood tests to detect heart muscle damage). The most often used markers are the creatine kinase-MB (CK-MB) fraction and the troponin I (TnI) or troponin T (TnT) levels. On the basis of the ECG, a distinction is made between ST elevation MI (STEMI) or non-ST elevation MI (NSTEMI). Most cases of STEMI are treated with thrombolysis or if possible with percutaneous coronary intervention (PCI, angioplasty and stent insertion), provided the hospital has facilities for coronary angiography. NSTEMI is managed with medication, although PCI is often performed during hospital admission. In patients who have multiple blockages and who are relatively stable, or in a few extraordinary emergency cases, bypass surgery of the blocked coronary artery is an option.
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; severe myocardial infarction may lead to heart failure, but not necessarily.
Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA)
Classification
There are two basic types of acute myocardial infarction, (1) transmural MI- IS associated with atherosclerosis involving major coronary artery. It can be subclassified into anterior,posterior or inferior. (2) subendocardial MI- involves small area, in the subendocardial wall of the left ventricle,ventricular septum,papillary muscles.
Clinically, myocardial infarction is further subclassified into ST elevation MI versus non ST elevation MI based on ECG changes.
Signs and symptoms
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 even sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.
Women and older patients experience atypical symptoms more frequently than their male and younger counterparts. Women also have more symptoms compared to men (2.6 on average vs 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms which 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.
Approximately half of all MI patients have experienced warning symptoms such as chest pain prior to the infarction.
Approximately one fourth of all myocardial infarctions are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms or at autopsy without a prior history of related complaints. 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 connected to nerves of the host. In diabetics, 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.
Prevention
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 patients with heart disease, and limitation of alcohol intake.
Patients 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.
- Omega-3 fatty acids, commonly found in fish, have been shown to reduce mortality post-MI. While the mechanism by which these fatty acids decrease mortality is unknown, it has been postulated that the survival benefit is due to electrical stabilization and the prevention of ventricular fibrillation. However, further studies in a high-risk subset have not shown a clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids.
Legal implications
At common law, a myocardial infarction is generally a disease, but may sometimes be an injury. This has implications for no-fault insurance schemes such as workers' compensation. A heart attack is generally not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. Additionally, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person who has suffered from a myocardial infarction may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.
