Epidemiology
Chronic Stable Coronary Artery DiseaseChronic Stable Coronary Artery Disease
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Normal Lab Values
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- If the diagnosis of CAD is in question after the history, physical examination, and resting electrocardiogram, stress testing is the next step in most patients.
- In patients with an abnormal baseline electrocardiogram or known CAD, the initial stress test should use cardiac imaging.
- Long-term medical treatment in most patients with known CAD should include aspirin, a lipid-lowering drug, an angiotensin-converting enzyme inhibitor, and a β-blocker.
- Medical therapy of chronic angina is directed toward restoration of the myocardial oxygen supply/demand balance and prevention of platelet aggregation.
- Restenosis following PCI is dramatically reduced by the use of drug-eluting stents.
- CABG is preferred over PCI in patients with severe multivessel disease, patients with diabetes, and patients with a reduced left ventricular ejection fraction.
CAD most often consists of atherosclerotic disease of the major epicardial coronary arteries. Other causes of impairment of coronary blood flow, including systemic vasculitis, drug-induced vascular spasm, thromboembolism, valvular disease, hypertrophic cardiomyopathy, and spontaneous coronary artery dissection, may present similarly and should be considered in the differential diagnosis of a patient presenting with myocardial ischemia or infarction.
Chronic stable CAD is the most common type of ischemic heart disease, comprising more than half of symptomatic patients. The annual incidence of exertional angina is approximately 200 per 100,000 persons older than 30 years. Although approximately 17 million persons in the United States have angina, many do not seek attention for their chest pain, underscoring the importance of public and patient education.
Myocardial ischemia produces a cascade of responses directly related to the duration of ischemia. The first manifestations of the imbalance in the myocardial oxygen supply and demand equilibrium are biochemical, consisting of lactate production, acidosis, and impaired glucose utilization. As the duration and intensity of ischemia increase, diastolic dysfunction occurs, then systolic dysfunction, followed by electrocardiographic abnormalities and, lastly, symptoms of angina pectoris.
Symptomatic ischemia is manifested principally as classic angina pectoris or a constellation of complaints consisting of chest discomfort or pain in the chest, shoulder, back, neck, or arm. Rarely, it may be characterized as toothache or jaw pain. Classic angina is exacerbated by physical activity or emotional stress and relieved by rest and nitroglycerin. In addition to typical angina, symptoms of ischemia may include “anginal equivalents,” such as shortness of breath with exertion, atypical chest pain, or chest discomfort occurring at rest. Atypical chest pain is chest discomfort that is not precipitated by exertion, relieved by rest, or responsive to nitroglycerin. In addition, atypical chest pain may have an unusual pattern of pain distribution or radiation and associations of the pain to activity, rest, or time of day are variable. Some patients with coronary disease are asymptomatic but have evidence of ischemia on electrocardiogram or imaging; these patients are considered to have silent ischemia.
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