The pathophysiology behind the progression of angina pectoris is inadequate demand and supply of blood and transition of aerobic metabolism to anaerobic metabolism in cells of myocardia.
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The most common manifestation of myocardial ischemia is stable angina pectoris. Symptoms include a pain or pressure sensation in the chest, which may radiate to the left arm, shoulder, or jaw. Symptoms occur upon exertion and emotional stress and are relieved with sublingual nitroglycerin. The goals of treatment are to reduce or eliminate symptoms and prevent complications, such as myocardial infarction, left ventricular failure, and life-threatening arrhythmias. Treatment consists of lifestyle modifications, medication therapy, and, in some cases, revascularization.
Stable angina pectoris (SAP) is the most common manifestation of myocardial ischemia. Myocardial ischemia occurs when the oxygen demand of the heart exceeds the supply. There are three factors that determine myocardial oxygen demand—heart rate, contractility, and intra-myocardial wall tension, with the latter considered the most important.1 Oxygen demand increases in response to an increase in heart rate or an increase in left ventricular preload or afterload. A higher end-diastolic volume will raise left ventricular preload, and increased systolic blood pressure and/or arterial stiffness will increase left ventricular afterload and consequently myocardial oxygen demand. Blood supply to the heart can become compromised through atherosclerotic plaque buildup and/or coronary artery spasm. Often patients will have both.2