Ischemic heart disease (IHD) is a broad term encompassing several closely related syndromes caused by myocardial ischemia—an imbalance between cardiac blood supply (perfusion) and myocardial oxygen and nutritional requirements. Since cardiac myocytes generate energy almost exclusively through mitochondrial oxidative phosphorylation, cardiac function is strictly dependent upon the continuous flow of oxygenated blood through the coronary arteries. Despite dramatic improvements in therapy in the past quarter century, IHD in its various forms remains the leading cause of mortality in the United States and other developed nations, accounting for 7.5 million deaths worldwide each year.
In more than 90% of cases, IHD is a consequence of reduced coronary blood flow secondary to obstructive atherosclerotic vascular disease (Chapter 10). Thus, unless otherwise specified, IHD usually is synonymous with coronary artery disease (CAD). In most cases, the various syndromes of IHD are consequences of coronary atherosclerosis that has been gradually progressing for decades (beginning even in childhood or adolescence). In the remaining cases, cardiac ischemia may be the result of increased demand (e.g., with increased heart rate or hypertension); diminished blood volume (e.g., with hypotension or shock); diminished oxygenation (e.g., due to pneumonia or CHF); or diminished oxygen-carrying capacity (e.g., due to anemia or carbon monoxide poisoning).
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The manifestations of IHD are a direct consequence of the insufficient blood supply to the heart. The clinical presentation may include one or more of the following cardiac syndromes:
Angina pectoris (literally, “chest pain”). Ischemia induces pain but is insufficient to cause myocyte death. Angina can be stable (occurring predictably at certain levels of exertion), can be caused by vessel spasm (Prinzmetal angina), or can be unstable (occurring with progressively less exertion or even at rest).
Myocardial infarction (MI). This occurs when the severity or duration of ischemia is sufficient to cause cardiomyocyte death.
Chronic IHD with CHF. This progressive cardiac decompensation, which occurs after acute MI or secondary to accumulated small ischemic insults, eventually precipitates mechanical pump failure.
Sudden cardiac death (SCD). This can occur as a consequence of tissue damage from MI, but most commonly results from a lethal arrhythmia without myocyte necrosis (see “ ” later in the chapter).
The term acute coronary syndrome is applied to any of the three catastrophic manifestations of IHD—unstable angina, MI, and SCD.
More than 700,000 Americans experience a MI each year, and roughly half of those affected die. As troubling as this toll is, it represents a spectacular advance; since peaking in 1963, the mortality related to IHD in the United States has declined by 50%. The improvement is largely attributed to interventions that have diminished cardiac risk factors (behaviors or conditions that promote atherosclerosis; (Chapter 10), in particular smoking cessation programs, hypertension and diabetes treatment, and use of cholesterol-lowering agents. To a lesser extent, diagnostic and therapeutic advances also have contributed; these include aspirin prophylaxis, better arrhythmia control, establishment of coronary care units, thrombolysis for MI, angioplasty and endovascular stenting, and coronary artery bypass graft surgery. Maintaining this downward trend in mortality will be particularly challenging given the predicted longevity of “baby boomers,” as well as the epidemic of obesity that is sweeping the United States and other parts of the world.