PATHOPHYSIOLOGY, INVESTIGATIONS, AND MANAGEMENT OF UNSTABLE ANGINA: A REVIEW

Unstable angina pectoris is a phenomenon that disrupts the early recovery phase of acute myocardial infection, the emergence of new ischemic symptoms, the development of more severe pain, usually at rest, or the formation of intermittent ischemic events. ۔ Acute myocardial infarction is the most serious complication of unstable angina pectoris, which can affect up to 25% of patients within three months of the onset of symptoms. Physically, changes in ECG and hemodynamics usually occur before the onset of pain. The following hemodynamic changes and an increase in oxygen demand in the already ischemic heart respond positively, leading to further instability in unstable angina. Hemodynamic changes may be the result of abnormal stress response or excessive chemotherapeutic discharge. While coronary spasm may play a role in the pathogenesis of unstable angina, other factors such as bleeding in the wall of the atherosclerotic plaque, peripheral embolization, alteration, or platelet aggregation in the coronary artery from nearby soft cholesterol "abscess". Feedback should also be considered. Along with medications such as nitrates, calcium antagonists, and warnings, beta-adrenergic blockers are used to stimulate coronary and peripheral vasodilation and reduce cardiac effort. Treatment with aortic counter-pulsating balloons is recommended for those who have failed to respond to pharmacological treatment. Emergency surgery should be performed voluntarily. The full clinical and pathological compatibility of unstable angina pectoris is still unknown. Future issues will revolve around further investigations into entity procedures, treatment and prevention. The purpose of this review is to explain the pathophysiology of unstable angina, highlight changes in ECG in the assessment of unstable angina, and improve the outcome of patients with unstable angina. Consider the need to strengthen the coordination of care within the team.