Ischemic heart disease (IHD) is characterized by an imbalance in myocardial oxygen supply and demand primarily as a result of atherosclerotic plaques in coronary arteries and endothelial dysfunction-associated vasoconstriction and thrombus formation.16 It can be considered in two broad categories: chronic coronary artery disease (CAD), i.e., stable angina pectoris; and acute coronary syndromes (ACS), i.e., unstable angina pectoris and MI, each with a distinct pathogenesis.
Chronic CAD is associated with subintimal deposition of atheromas in coronary arteries.16 Its principal clinical manifestation is chronic stable angina pectoris. Atherosclerotic plaques in patients with chronic stable angina are overlaid by a thick, fibrous cap that resists disruption, but that reduces vessel lumen diameter and causes inappropriate vasoconstriction resulting in acute myocardial ischemia and chest pain at reproducible workloads, e.g., walking up a flight of stairs.16
All patient with chronic CAD require aggressive lipid lowering therapy and BP control and focused therapy intended to reduce oxygen demand governed by heart rate, contractility, and ventricular wall stress: (1) β1-adrenoceptor antagonists reduce heart rate and contractility, Ca2+ channel blocking agents decrease cardiac contractility and systemic vascular resistance, and (3) nitric oxide donors decrease preload and dilate peripheral capacity veins.3,5,6,16 Nitroglycerin is used to treat acute symptoms.
Acute coronary syndromes are caused by the rupture of unstable atherosclerotic plaques that results in vasoconstriction, platelet aggregation, and thrombus formation, which lead to acute myocardial ischemia and, potentially, irreversible myocardial injury (myocyte necrosis).16 The principal clinical manifestation of ACS is unstable angina pectoris (UA) characterized by increased frequency and severity of chest pain that may occur even at rest.16 Patients with UA are at high risk for MI.
An unstable plaque that abruptly ruptures and partially occludes the lumen of a coronary artery causes non-ST elevation MI (NSTEMI).16 Because there is a persistent prothrombotic surface at the site of plaque rupture, the patient is at high risk for recurrent ischemia. The goals of prevention and treatment of both UA and NSTEMI are (1) to relieve ischemic symptoms, i.e., β1-adrenoceptor antagonists; and (2) to prevent additional thrombus formation, i.e., antiplatelet agents and/or an anticoagulant.3,6,9,16
Complete coronary artery occlusion, unless perfusion is reestablished, leads to ST elevation MI (STEMI).16 The treatment of STEMI is the same as that of UA and NSTEMI. When pharmacological strategies are sufficient to reestablish perfusion patients with STEMI require coronary artery bypass grafts or percutaneous coronary intervention, i.e., balloon angioplasty or stent implantation.16 Ischemia-induced electrical instability of the myocardium can lead to sudden cardiac death.
The functional consequences of MI vary greatly among patients; consequently, post-MI therapeutic regimens are individualized and include (1) aspirin (clopidogrel if aspirin is contraindicated); (2) aspirin and another anti-platelet agent following percutaneous coronary intervention; (3) a β1-adrenoceptor antagonist; (4) an ACE inhibitor for patients with HF, hypertension, and diabetes; (5) an aldosterone antagonist for patients with left ventricular dysfunction; and (6) lipid-lowering agents.16