Chronic ischemic heart disease from coronary artery atherosclerosis remains a chief public health concern in most industrialized nations and has become a leading cause of death and disability in developing countries.1 Thrombosis complicating an atherosclerotic plaque is the proximate cause of acute myocardial infarction (MI) in patients with coronary artery disease (CAD) and represents the leading cause of death for men and women worldwide.2 As a result of improved survival rates following MI, the size of the patient population living with chronic CAD is increasing. For example, in the United States, it is estimated that 470,000 individuals suffer a recurrent MI yearly.3 In these patients, the transition from a clinically stable coronary syndrome to an acute life-threatening event remains largely unpredictable despite substantial gains in the understanding of the pathobiology of atherosclerosis.4 Traditional (eg, history) and contemporary (eg, advanced imaging) methods of diagnosis and risk stratification are used to initiate treatment strategies. This chapter provides a framework for the evaluation and management of patients with chronic CAD. Conclusions from landmark clinical trials that have influenced the application of medical, percutaneous, and surgical treatments will be discussed.
Etiology and Classification
Myocardial ischemia is mediated by an imbalance between oxygen supply and demand at the cellular (myocyte) level (see Chap. 54). Coronary atherosclerosis impairs coronary blood flow (CBF) via a variety of mechanisms and is the dominant cause of angina under conditions of elevated myocardial oxygen demand, such as exercise or emotional stress. CBF is impaired in several other disease states, including severe aortic valve disease with left ventricular hypertrophy (LVH), hypertension, idiopathic dilated cardiomyopathy, and hypertrophic cardiomyopathy, even in the absence of epicardial CAD. In patients with LVH, ischemia may result from a combination of inadequate capillary density, pathologic changes within small intramyocardial arteries and arterioles, reduced CBF reserve, systolic compressive forces, and markedly elevated diastolic pressures within the vulnerable subendocardium. A primary reduction in myocardial oxygen supply following intraluminal thrombus formation and/or epicardial constriction underlies the development of acute coronary syndromes. Reduced oxygen supply in the chronic setting may derive from severe anemia or hemoglobin disorders. The major determinants of myocardial oxygen demand, namely heart rate, wall stress, and contractility, can singularly or in combination trigger an ischemic cascade in a vulnerable patient.
For over two centuries, it has been recognized that cardiac angina can be effectively diagnosed by a careful patient interview. William Herberden is credited with the initial description of angina in 1772 in his chapter entitled, "Pectoris Dolor," from his Commentaries on the History and Cure of Diseases.5 Remarkably, several elements from this original characterization remain pertinent to the management of CAD today. Herberden correctly identified that certain descriptive features of angina, such as the occurrence of chest pain at rest, portend a particularly grave prognosis.
The Canadian Cardiovascular Society (CCS) classification, now more than 3 decades old, ...