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Coronary Heart Disease Information
Coronary heart disease, or atherosclerotic coronary artery disease, is the number one killer in the United States and worldwide. Every minute, an American dies of coronary heart disease. It is responsible for more than one in five deaths and nearly 700,000 deaths per year in the United States. More than 10 times the number of women die each year from cardiovascular disease than from breast cancer. Coronary heart disease afflicts nearly 13 million Americans and the prevalence rises steadily with age; thus, the aging of the US population promises to increase the overall burden of coronary heart disease.
Risk Factors for Coronary Artery Disease
Epidemiologic studies have identified a number of important risk factors for coronary artery disease. The vast majority of patients with coronary heart disease have some identifiable risk factor. These include a positive family history (the younger the onset in a first-degree relative, the greater the risk), male gender, blood lipid abnormalities, diabetes mellitus, hypertension, physical inactivity and obesity, and cigarette smoking. Smoking remains the number one preventable cause of cardiovascular disease worldwide. Although smoking rates have declined in the United States in recent decades, 21% of women and 25.7% of men smoke. According to the World Health Organization, 1 year after quitting, the risk of coronary heart disease decreases by 50%. Various interventions, including physician counseling, formal smoking cessation programs, nicotine replacement therapy, and bupropion, have been shown to increase the likelihood of successful cessation (see Health Maintenance & Disease Prevention).
Overwhelming evidence indicates that hypercholesterolemia and other lipid abnormalities provide an important modifiable risk factor for coronary heart disease. Risk increases progressively with higher levels of low-density lipoprotein (LDL) cholesterol and declines with higher levels of high-density lipoprotein (HDL) cholesterol. Composite risk scores, such as the Framingham score (see Table 28–2), provide estimates of 10-year probability of development of coronary heart disease that can guide primary prevention strategies.
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Although many atherosclerotic plaques remain stable or progress only gradually, others may rupture, often related to the inflammatory process and metalloproteinase activity. The rupture causes turbulent flow, extrusion of lipids and fatty gruel, and exposure of tissue factor that result in a cascade of events culminating in intravascular thrombosis. The outcome of these events is determined in large part by whether the vessel becomes occluded, which depends on the lesion anatomy as well as the balance of pro- and antithrombotic and pro- and antifibrinolytic forces. The result may be partial or complete vessel occlusion (causing the symptoms of unstable angina or myocardial infarction), or the plaque may become restabilized, often with more severe stenosis. Transient occlusion and/or embolization of platelet and thrombin debris, which may result in elevation in serum troponin, predispose to clinical events and portend a worse prognosis.
Several features are associated with enhanced plaque vulnerability, including a higher lipid content, a higher concentration of macrophages, especially in the plaque shoulder, and a very thin fibrous cap. Lesions with these characteristics are often relatively early lesions that can be responsible for acute myocardial infarction or sudden death as the first manifestation of coronary disease. Such lesions may occur in up to 50% of cases. This abrupt progression explains why most infarctions do not occur at the site of preexisting critical stenosis. Conversely, the relatively greater reduction in clinical events than in lesion severity in lipid-lowering treatment trials is probably explained by the stabilization of these early nonfibrotic lesions
List of Coronary Heart Disease
Angina Pectoris
Acute Coronary Syndromes
Acute Myocardial Infarction
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