Coronary artery disease (CAD) is the leading cause of myocardial infarction (MI), commonly known as a heart attack. CAD is characterized by the narrowing or blockage of coronary arteries due to atherosclerosis. This process reduces blood flow to the heart muscle. When blood flow is critically reduced or completely blocked, it results in myocardial infarction. This article explains the detailed mechanisms by which CAD causes MI.
Pathophysiology of Coronary Artery Disease
Atherosclerosis Development
Atherosclerosis is the main pathological process in CAD. It begins with endothelial injury due to factors such as high blood pressure, smoking, diabetes, and high cholesterol. This injury causes dysfunction of the endothelial cells lining the arteries.
Low-density lipoprotein (LDL) cholesterol penetrates the damaged endothelium. It undergoes oxidation and triggers an inflammatory response. Immune cells like macrophages engulf oxidized LDL, becoming foam cells. Foam cells accumulate and form fatty streaks—the earliest visible lesions in atherosclerosis.
Plaque Formation and Progression
Over time, fatty streaks evolve into fibrous plaques. These plaques consist of a lipid core covered by a fibrous cap made of smooth muscle cells and collagen. As plaques enlarge, they narrow the arterial lumen, restricting blood flow. The stability of the plaque’s fibrous cap is crucial.
Chronic inflammation weakens the cap, making plaques vulnerable to rupture. Plaque rupture exposes thrombogenic material such as collagen and tissue factor to the bloodstream.
Mechanisms of Myocardial Infarction in CAD
Plaque Rupture and Thrombosis
The most common cause of MI is plaque rupture. When the fibrous cap of an atherosclerotic plaque ruptures, the exposed inner core triggers platelet adhesion and activation. This initiates thrombus (clot) formation at the site.
The thrombus can partially or completely occlude the coronary artery. Complete occlusion stops blood flow to the downstream myocardium, causing ischemia. If prolonged, ischemia leads to necrosis of the heart muscle—this is myocardial infarction.
Coronary Artery Spasm
In some cases, MI occurs due to intense vasospasm of a coronary artery. This spasm can reduce blood flow transiently or persistently. Vasospasm often occurs near atherosclerotic plaques due to endothelial dysfunction. Although less common than thrombosis, coronary spasm is a recognized cause of MI, especially in variant angina (Prinzmetal angina).
Embolism and Other Causes
Rarely, myocardial infarction results from coronary artery embolism, which may occur due to thrombi formed elsewhere in the heart or bloodstream. Coronary dissection and other mechanical causes can also lead to MI but are less frequently linked to CAD.
Ischemic Cascade and Myocardial Injury
Coronary Blood Flow and Oxygen Supply
The myocardium depends on continuous oxygen delivery through coronary arteries. When CAD reduces or blocks coronary blood flow, myocardial oxygen supply drops. The heart muscle has limited oxygen reserves and high metabolic demand, making it vulnerable to ischemia.
Ischemia and Cellular Changes
Within seconds of occlusion, myocardial cells suffer from lack of oxygen. Cellular metabolism shifts from aerobic to anaerobic glycolysis, producing less energy and lactic acid. This causes cellular acidosis and dysfunction of ion pumps.
Without oxygen, cells cannot maintain ionic gradients, leading to calcium overload and cell membrane damage. If ischemia persists beyond 20-30 minutes, irreversible cell injury occurs, leading to necrosis.
Infarct Development and Remodeling
The area of myocardium affected by ischemia is called the infarct zone. Necrotic myocardial cells trigger inflammation and recruitment of immune cells. Over days to weeks, dead tissue is replaced by fibrous scar tissue. This scarring impairs the contractile function of the heart and can lead to heart failure if extensive.
Clinical Presentation of Myocardial Infarction in CAD
Typical Symptoms
Patients with MI often experience severe chest pain described as pressure, squeezing, or heaviness. Pain may radiate to the arm, neck, jaw, or back. Other symptoms include shortness of breath, sweating, nausea, and dizziness.
Electrocardiogram Changes
ECG is critical for diagnosis. ST-segment elevation myocardial infarction (STEMI) occurs when there is full-thickness myocardial injury. Non-ST elevation myocardial infarction (NSTEMI) involves partial thickness injury. ECG changes reflect the extent and location of ischemia.
Cardiac Biomarkers
Elevated cardiac enzymes such as troponins and creatine kinase-MB confirm myocardial cell injury. Troponins are highly specific and sensitive markers for MI.
Risk Factors Linking CAD to Myocardial Infarction
Modifiable Risk Factors
Hyperlipidemia: High LDL cholesterol promotes plaque formation.
Hypertension: Increases arterial wall stress and endothelial injury.
Smoking: Accelerates atherosclerosis and promotes thrombosis.
Diabetes mellitus: Causes endothelial dysfunction and inflammation.
Obesity and sedentary lifestyle: Contribute to metabolic syndrome.
Non-Modifiable Risk Factors
Age: Risk increases with advancing age.
Genetics: Family history of premature CAD increases susceptibility.
Gender: Males have higher risk earlier in life, but risk in females increases after menopause.
Preventing Myocardial Infarction in Patients with CAD
Lifestyle Modifications
Healthy diet, regular exercise, smoking cessation, and weight control reduce CAD progression and MI risk.
Pharmacological Treatments
Medications used to stabilize plaques and prevent MI include:
- Statins: Lower cholesterol and stabilize plaques
- Antiplatelet agents: Aspirin reduces clot formation risk
- Beta-blockers: Decrease myocardial oxygen demand
- ACE inhibitors and ARBs: Improve endothelial function and reduce remodeling
Interventional Procedures
In some cases, percutaneous coronary intervention (PCI) with stent placement or coronary artery bypass grafting (CABG) is necessary to restore blood flow and reduce MI risk.
Conclusion
Coronary artery disease causes myocardial infarction primarily through the process of atherosclerosis leading to plaque formation, rupture, and thrombosis. This blocks coronary blood flow, causing ischemia and irreversible myocardial injury.
Understanding these mechanisms helps guide prevention, early detection, and treatment strategies to reduce the burden of MI worldwide.
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