ISCHEMIC MYOCARDIUM: PATHOPHYSIOLOGY, DIAGNOSIS AND MANAGEMENT

Аннотация

Ischemic myocardium results from insufficient coronary blood flow, leading to myocardial hypoxia and metabolic disturbances. The primary cause is atherosclerotic coronary artery disease (CAD), which contributes to chronic coronary syndromes (CCS) and acute coronary syndromes (ACS), including unstable angina, NSTEMI, and STEMI. This review explores the pathophysiological mechanisms, clinical presentation, diagnostic modalities, and management strategies for ischemic myocardium. It also discusses emerging therapies, including PCSK9 inhibitors, anti-inflammatory treatments, and regenerative medicine approaches. A multidisciplinary approach integrating medical therapy, lifestyle interventions, and revascularization techniques remains essential in reducing cardiovascular morbidityand mortality. Introduction: Cardiovascular disease remains the leading cause of death worldwide, with ischemic myocardium playing a central role in the pathogenesis of ischemic heart disease (IHD). The primary mechanism involves an imbalance between myocardial oxygen supply and demand due to coronary artery obstruction, endothelial dysfunction, and microvascular disease. Understanding the underlying pathophysiology, early detection, and evidence-based management strategies is essential toimproving patient outcomes. Pathophysiology ofIschemic Myocardium Ischemic myocardium results from reduced perfusion, leading to metabolic derangements and myocardial injury. Key pathophysiological events include: Atherosclerosis and Coronary Obstruction Endothelial Dysfunction: Early-stage atherosclerosis is characterized by reduced nitric oxide (NO) production and increased expression of pro-inflammatory cytokines, adhesion molecules (ICAM-1, VCAM-1), and oxidized LDL. Plaque Formation and Progression: Macrophage infiltration and smooth muscle cell proliferation lead to fibrous cap formation,increasing therisk ofrupture. Plaque Rupture and Thrombosis: Exposure of thrombogenic plaque components triggers platelet aggregation and thrombus formation,precipitating ACS. Ischemic Cascadeand CellularInjury Early Ischemia: Reduced oxygen supply shifts myocardial metabolism to anaerobic glycolysis, leading toATP depletion, lactic acid accumulation, and intracellularacidosis. Myocyte Dysfunction: Impaired Na+/K+ ATPase activity results in intracellular sodium and calcium overload,disruptingmyocardial contractilityand increasing therisk of arrhythmias. 501 INTERNATIONAL MULTIDISCIPLINARY JOURNAL FOR RESEARCH & DEVELOPMENT SJIF2019:5.2222020:5.5522021:5.6372022:5.4792023:6.5632024:7,805 eISSN:2394-6334 https://www.ijmrd.in/index.php/imjrd Volume12,issue02(2025) Irreversible Myocardial Necrosis: Prolonged ischemia (>20-30 minutes) leads to cardiomyocyte death, inflammation,and fibrosis,contributing to heart failure (HF). Microvascular Dysfunction: Patients with ischemia with non-obstructive coronary arteries (INOCA) exhibit microvascular dysfunction due to endothelial and smooth muscle abnormalities, impairing vasodilation and coronary flow reserve. Clinical Presentationof ChronicCoronary Syndrome (CCS) •Stableangina pectoris (predictable exertionalchest pain,relieved byrest/nitroglycerin). •Symptoms correlate withcoronary stenosis(>70% luminalnarrowing). •Maypresent as silent ischemiain diabetic and elderly patients. DiagnosticApproach Electrocardiography (ECG) (ECG) remains the first-line diagnostictool fordetecting myocardial ischemia and infarction. It provides critical information about ischemic severity, location, and progression. Changes in ECG patterns correlate with the degree of myocardial ischemia and infarction,guidingtreatmentdecisions. Pathophysiology ofECGChanges in Ischemia Myocardial ischemia alters transmembrane ion gradients, particularly potassium (K+) and calcium(Ca2+), affecting depolarization and repolarization. • ST-segment depression (NSTEMI/unstable angina) vs. elevation (STEMI). • T-wave inversions in ischemic territories. Biomarkers of Myocardial Injury. Serum troponins and CK-MB (creatine kinase-MB)are readily detectable and reliable cardiac-specific biomarkers of subclinical myocardial injury. This study explores theroles of cTnI(cardiac troponinI) and CK-MBin hypertrophic cardiomyopathy (HCM) • Cardiac Troponins (I/T): High specificity for myocardial necrosis. • Creatine Kinase-MB (CK-MB): Useful for detecting reinfarction. Invasive Coronary Angiography. Cardiac catheterisation is an invasive diagnostic procedure that provides important information about the structure and function of the heart. It usually involves taking X-rays of the heart's arteries (coronary arteries) using a technique called coronary angiography orarteriography. •Gold standard forhigh-risk patients toevaluate coronary stenosis. Among patients who are candidates for treatment with thrombolytic agents, careful management of blood pressure is critical before and during the administration of alteplase (recombinant tissue plasminogen activator [rtPA]), and for the ens