Aetiology
The etiology or causes of myocardial infarction, commonly known as a heart attack, can be attributed to various factors. The primary cause of myocardial infarction is the obstruction of blood flow to the heart muscle. This obstruction is typically due to the formation of a blood clot or atherosclerosis, a condition characterized by the buildup of fatty plaques in the arteries. Here are some key factors involved in the etiology of myocardial infarction :-
1) Atherosclerosis :- Atherosclerosis is a gradual process where plaque, consisting of cholesterol, fat, calcium, and other substances, accumulates in the walls of the coronary arteries that supply blood to the heart. Over time, these plaques can narrow the arteries, reducing blood flow and increasing the risk of a heart attack.
2) Coronary artery disease (CAD) :- CAD refers to the narrowing or blockage of the coronary arteries, which are responsible for supplying oxygen and nutrients to the heart muscle. When the arteries become significantly narrowed due to atherosclerosis, it can lead to inadequate blood flow and oxygen supply, resulting in a myocardial infarction.
3) Thrombosis :- Sometimes, a blood clot or thrombus can form within a coronary artery, partially or completely blocking blood flow. Thrombosis is often associated with the rupture of an atherosclerotic plaque. If the clot becomes large enough to completely occlude the artery, it can lead to a heart attack.
4) Spasm of coronary arteries :- In some cases, the coronary arteries may undergo sudden constriction or spasm, causing a temporary reduction in blood flow. This constriction can be triggered by various factors such as emotional stress, exposure to cold, smoking, or certain medications. If the spasm is severe and prolonged, it can result in myocardial infarction.
5) Risk factors :- Several risk factors can contribute to the development of myocardial infarction. These include age, gender (men are generally at higher risk), family history of heart disease, smoking, high blood pressure (hypertension), high cholesterol levels, diabetes, obesity, sedentary lifestyle, and unhealthy diet.
Pathogenesis
The pathogenesis, or the process by which acute myocardial infarction (MI) develops, involves several stages that lead to the formation of a blood clot and subsequent ischemic injury to the heart muscle. Here is an overview of the pathogenesis of acute MI :-
1) Atherosclerosis :- The underlying cause of most cases of acute MI is atherosclerosis. This process involves the gradual buildup of fatty plaques within the walls of the coronary arteries, which supply blood to the heart muscle. Atherosclerosis is influenced by various risk factors such as high blood pressure, high cholesterol, smoking, diabetes, and genetic predisposition.
2) Plaque rupture or erosion :- Within an atherosclerotic plaque, there is a fibrous cap that separates the lipid-rich core of the plaque from the bloodstream. Plaque rupture or erosion occurs when the fibrous cap becomes weak or disrupted, exposing the lipid core to the circulating blood.
3) Thrombosis formation :- When the plaque ruptures or erodes, it exposes substances that promote blood clotting, such as collagen and tissue factor, to the bloodstream. Platelets are activated at the site of plaque disruption and aggregate to form a clot, known as a thrombus, on top of the plaque. This thrombus can partially or completely obstruct the coronary artery, leading to reduced blood flow to the heart muscle.
4) Coronary artery occlusion :- If the thrombus is large enough or if the coronary artery is already narrowed due to underlying atherosclerosis, it can cause a complete occlusion of the artery. This leads to a sudden and significant reduction or cessation of blood flow to the downstream heart muscle.
5) Ischemia and necrosis :- The occlusion of the coronary artery results in ischemia, a lack of oxygen and nutrients supply to the affected region of the heart muscle. Without adequate blood flow, the heart muscle cells (myocytes) begin to undergo irreversible damage and necrosis (cell death). This area of necrotic tissue is referred to as an infarct.
6) Inflammatory response :- The necrotic tissue triggers an inflammatory response within the affected area. Inflammatory cells, such as neutrophils and macrophages, migrate to the site of injury and release pro-inflammatory substances. This inflammatory response further damages the heart tissue.
Types of infarcts
In acute myocardial infarction (MI), there are two main types of infarcts that can occur based on the extent and distribution of the affected area within the heart muscle. These types are :-
1) Transmural (or ST-segment elevation) MI :- Transmural MI involves the full thickness or entire wall of the heart muscle being affected. It occurs when a coronary artery supplying a specific region of the heart becomes completely occluded, leading to the complete blockage of blood flow to that area. This type of MI is often associated with ST-segment elevation on an electrocardiogram (ECG). Transmural MI typically results in a larger infarct size and carries a higher risk of complications.
2) Subendocardial (or non-ST-segment elevation) MI :- Subendocardial MI affects the inner layer or subendocardium of the heart muscle. It occurs when there is a partial or temporary reduction in blood flow to the affected region, resulting in ischemia. The blood flow may be partially restored before irreversible damage occurs, leading to a smaller infarct size compared to transmural MI. Subendocardial MI is often associated with non-ST-segment elevation on an ECG. However, it's important to note that subendocardial MI can progress to transmural MI if left untreated or if blood flow remains compromised.
Clinical features
Acute myocardial infarction (MI) presents with a range of clinical features, which can vary in severity and duration among individuals. The following are the common clinical features associated with acute MI :-
1) Chest pain or discomfort :- Chest pain is the hallmark symptom of acute MI. It is typically described as a severe, crushing, or squeezing sensation in the chest. The pain may radiate to the left arm, neck, jaw, back, or shoulder. The chest pain of MI is often prolonged and not relieved by rest or nitroglycerin.
2) Shortness of breath :- Many individuals experiencing acute MI may feel breathless or have difficulty breathing. Shortness of breath can occur at rest or with minimal exertion and is often associated with a feeling of suffocation or inability to get enough air.
3) Diaphoresis (excessive sweating) :- Profuse sweating, particularly cold and clammy skin, is a common feature of acute MI. The sweatiness may be more pronounced compared to normal sweating.
4) Nausea and vomiting :- Some individuals may experience nausea, vomiting, or a general feeling of discomfort in the upper abdomen. These symptoms can occur due to the activation of the autonomic nervous system during an acute MI.
5) Fatigue and weakness :- Unexplained fatigue, weakness, or a sense of impending doom may be present in acute MI. These symptoms can be attributed to the inadequate supply of oxygen-rich blood to the heart muscle.
6) Palpitations :- Some individuals may perceive abnormal or irregular heartbeats during an acute MI. Palpitations can manifest as a sensation of rapid, pounding, or skipping heartbeats.
7) Dizziness and lightheadedness :- Reduced blood flow to the brain can lead to feelings of dizziness, lightheadedness, or fainting in acute MI. These symptoms may be accompanied by a drop in blood pressure.
Diagnosis
The diagnosis of acute myocardial infarction (MI) involves a combination of clinical evaluation, symptoms assessment, physical examination, and diagnostic tests. Here are the key components of the diagnostic process for acute MI :-
1) Medical History and Physical Examination :- The healthcare provider will take a detailed medical history, including symptoms, risk factors, and relevant medical conditions. They will also perform a physical examination to assess vital signs, heart sounds, and signs of cardiac distress.
2) ECG changes :- Diagnosing acute myocardial infarction (MI) through ECG changes involves analyzing specific patterns and alterations in the electrocardiogram (ECG) tracing. Here are the key ECG changes that can help in the diagnosis of acute MI :-
a) ST-Segment Elevation :- ST-segment elevation is a hallmark ECG finding in ST-segment elevation myocardial infarction (STEMI), which is a type of acute MI. ST-segment elevation indicates significant myocardial injury and ischemia. The elevated ST segment is observed above the baseline in one or more leads and signifies the area of the heart affected by the infarction.
b) T-Wave Changes :- T-wave changes often accompany ST-segment elevation or depression in acute MI. The T-wave may become peaked, inverted, or exhibit biphasic morphology, depending on the location and extent of the infarct.
c) Q-Waves :- Q-waves are deep, wide, and abnormal QRS complexes that occur in the ECG after an acute MI. Q-waves indicate myocardial necrosis and represent permanent scar tissue. The presence of pathological Q-waves is an important criterion for diagnosing MI and can help determine the location of the infarct.
d) ST-Segment Depression :- ST-segment depression can occur in certain types of acute MI, such as non ST segment elevation myocardial infarction (NSTEMI) or when there is reciprocal ST-segment depression in leads opposite to the infarct location. ST-segment depression suggests subendocardial ischemia or injury.
e) Other ECG Changes :- Other ECG findings that may be observed in acute MI include bundle branch blocks, atrioventricular (AV) block, and arrhythmias such as ventricular tachycardia or fibrillation. These changes may occur due to the extent of myocardial damage or ischemia.
3) Serum markers :- The diagnosis of acute myocardial infarction (MI) can be supported by evaluating specific serum markers that are released into the bloodstream following myocardial cell injury or necrosis. The most commonly used cardiac biomarkers for diagnosing acute MI are cardiac troponins (troponin I or troponin T). Here's how serum markers aid in the diagnosis of acute MI :-
a) Troponins :- Troponins are proteins found in cardiac muscle cells, and their release into the bloodstream indicates myocardial damage. Troponin levels rise within a few hours of the onset of myocardial injury, peak within 24 to 48 hours, and can remain elevated for several days. Elevated troponin levels, when interpreted in the appropriate clinical context, are highly suggestive of acute MI.
• Troponin I (cTnI) or Troponin T (cTnT) levels above the diagnostic cutoff are considered indicative of myocardial injury. The cutoff values may vary depending on the assay used.
• High-sensitivity troponin assays have improved sensitivity and can detect even minor myocardial injury. They allow for earlier detection and monitoring of troponin levels over time.
b) Creatine Kinase-MB (CK-MB) :- CK-MB is another enzyme released into the bloodstream following myocardial injury. Historically, CK-MB was widely used for diagnosing acute MI, but it has been largely replaced by troponins due to their higher specificity and sensitivity. Elevated CK-MB levels can still be observed in some cases and may be used in conjunction with troponin measurements for diagnostic confirmation.
• The CK-MB levels rise within a few hours, peak around 12 to 24 hours, and return to normal within 48 to 72 hours.
c) Other Biomarkers :- In addition to troponins and CK-MB, other serum markers may provide supportive evidence for the diagnosis of acute MI, such as:
• Myoglobin :- Myoglobin is an oxygen-binding protein found in cardiac and skeletal muscle. Elevated myoglobin levels can be observed in the early hours following myocardial injury. However, myoglobin lacks specificity and sensitivity compared to troponins and is more commonly used as a rule-out test in combination with other markers.
• Lactate Dehydrogenase (LDH) :- LDH is an enzyme found in many tissues, including the heart. LDH levels may be elevated in acute MI, but they lack specificity and sensitivity for diagnosing MI and are therefore not commonly used.
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