Pathophysiological Approach of Myocardial Infarction: A Review

Abstract

Coronary artery disease (CAD) is the primary cause of myocardial infarction (MI), which is defined by a decreased or stopped blood supply to a portion of the heart myocardium, resulting in cardiac cell death. Because CAD robs the heart of oxygen supply, it frequently presents as silently or with symptoms like radiating chest pain to the shoulder, arm, neck, or jaw. Elevated cardiac troponins and ECG alterations are involved in the diagnosis. MI is caused by prolonged blockage of a major coronary artery; collateral circulation, hemodynamics, and residual blood flow all affect the size of the infarct. Atherosclerosis, thrombosis, and plaque erosion are the primary causes of ST-elevation MI (STEMI) and non-ST-elevation MI (NSTEMI). Male pattern baldness, advancing age, a family history of the condition, high cholesterol, smoking, hypertension, diabetes, obesity, and stress are risk factors for MI. Aortic dissection, drug misuse, and anomalies in the heart are further causes. Anaerobic respiration and lactate buildup are the results of tissue oxygen deprivation, which starts both reversible and irreversible phases of Myocardial infarction. Oxidative stress and endothelial dysfunction, in conjunction with inflammation and susceptible plaques, worsen the development of MI. Significant MI risks are highlighted by epidemiological research on smoking, obesity, diabetes, hypertension, and socioeconomic variables. Other factors include family history and genetic predisposition. Given that MI continues to be a major cause of morbidity and death worldwide, an understanding of its pathophysiology and risk factors is essential for both prevention and intervention. To lessen the effects of this terrible illness, effective strategies require prompt intervention and thorough risk factor control.