Stable ischemic heart disease (SIHD) is a major public health concern in most developed nations and has become a leading cause of death and disability in high- as well as low- and middle-resource 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 Globally, CAD accounts for 7.4 million deaths annually, and in the United States, it is responsible for one in seven deaths per year, which in 2013 totaled approximately 370,200 fatalities.3 Despite advancements in the identification of atherosclerotic risk factors and effective therapies for primary and secondary prevention, it is estimated that annually 660,000 Americans are hospitalized or die from an initial MI, 305,000 suffer from recurrent MI, and an additional 160,000 individuals develop a clinically silent MI.3 In these patients, the transition from a clinically stable coronary atherosclerotic substrate to an acute life-threatening event remains a focus of intense investigation spanning genetic, basic, translational, and epidemiologic avenues of scientific exploration.4 In addition, there is an imprecise temporal and biological boundary on the other end of the clinical spectrum from acute coronary syndrome (ACS) to SIHD. This chapter reviews methods for diagnosing CAD, the clinical profile of patients affected by SIHD, and predictive models for assessing risk to inform treatment. Findings from contemporary landmark clinical trials that have influenced the use of specific medical, percutaneous, surgical, and hybrid treatments will also be discussed.
OVERVIEW OF STABLE ISCHEMIC HEART DISEASE
Etiology and Classification
Myocardial ischemia is mediated by an imbalance between oxygen supply and demand at the cardiomyocyte cellular level (see Chap. 34). 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. However, CBF is impaired even in the absence of epicardial CAD in several other disease states, including severe aortic valve disease with left ventricular hypertrophy (LVH), systemic hypertension, idiopathic dilated cardiomyopathy, and hypertrophic cardiomyopathy. In patients with LVH, ischemia may result from a combination of inadequate capillary density, pathologic changes within small intramyocardial arteries and arterioles, reduced coronary flow reserve (CFR), systolic compressive forces, and markedly elevated diastolic pressures within the vulnerable subendocardium. Nonobstructive epicardial CAD may nevertheless result in endothelial dysfunction and impaired CFR, which is a major mechanism underlying the expression of microvascular angina. A primary reduction in myocardial oxygen supply following intraluminal thrombus formation and/or epicardial constriction underlies the development of ACSs (Table 43–1). There are other, nonatherosclerotic causes of abrupt reductions in CBF, including spontaneous dissection and embolization. Chronic reductions in oxygen supply may also occur with severe, diffuse, and extensive CAD, resulting in myocardial hibernation. Oxygen supply can also be reduced in the setting of severe anemia or ...