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Coronary heart disease

Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. more...

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Overview

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in caliber.

Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel. As the plaques expand into the lumen of the vessel, they can affect the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.

Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.

As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.

A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.

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Local increases in coronary heart disease mortality - Heart Health - Brief Article
From Nutrition Research Newsletter, 10/1/01

Geographic variations in coronary heart disease (CHD) death rates within the United States have been observed for decades. An excess of CHD mortality in the southern United States was first observed in 1950, and it appears to have persisted over time. The current article reports on geographic patterns of CHD mortality among United States adults 35 years and older, for the period 1985-1995.

The study population consisted of White and African-American adults who resided in the United States. The geographic unit of analysis in this study was the labor market area. Labor market areas consist of one or more counties and define small regions, in which participants in local labor markets both live and work. Labor market areas offer a more theoretically defensible approximation of "communities" than counties or other county aggregates. Labor market areas are relatively large in land area relative to the small areas defined for other types of epidemiological studies, such as analyses of cancer clusters. Each labor market area contains a heterogeneity of microenvironments, including neighborhoods and households. There are 394 labor market areas defined for the United States. Each labor market area comprised at least 100,000 inhabitants in 1990, and hence the land areas of labor market areas tend to be larger in the western United States, which is more sparsely populated.

Death certificates were obtained from the National Center for Health Statistics, and deaths from CHD were defined for this study on the basis of underlying cause of death. County-specific CHD deaths and population counts were summed to the labor market area level of year of death, sex, race, and 10-year age group.

Substantial geographic variation in CHD mortality trends from 1985 to 1995 was evident for adults in each of the race-sex groups analyzed. Mean average annual percentage change values in CHD mortality for labor market areas were -3.1% for White men, -2.8% for White women, -2.1% for Black men, and -2.1% for Black women. Overall, White men experienced the most favorable distribution of local CHD mortality trends. CHD death rates strongly increased from 1985 to 1995 in two labor markets. Moderate increases in CHD death rates were observed for nine labor market areas. Negligible change in CHD mortality among Black women was found for a cluster of labor market areas in the Mississippi River Valley region, parts of rural Texas, and several large cities and their surrounding areas, including New York, San Francisco, Miami, and Buffalo. Black women in the majority of labor market areas (75%) experienced moderate or strong declines in CHD mortality.

Of the 23 labor market areas in which African-American men experienced increased CHD mortality from 1985 to 1995, only one was located outside of the South. Black men in the majority of labor market areas (72%) experienced moderate or strong declines in CHD mortality. Among White women, only one labor market area had a strong increase in CHD mortality from 1985 to 1995. Moderate increases in CHD death rates were experienced by White women in nine additional labor market areas. Moderate and strong declines in CHD mortality were experienced by White women in the majority (86%) of labor market areas. White men in 90% of labor market areas experienced moderate or strong declines in CHD mortality from 1985-1995. There were no labor market areas in which White men experienced strong increases in CHD mortality and only four in which they experienced moderate increases.

The results of this study are consistent with previous reports of widening geographic inequalities in CHD mortality nationwide, unfavorable patterns of CHD mortality in the South, and recent adverse trends in CHD mortality among African-American men. Whereas Black women were about 1.5 times more likely than White women to experience adverse CHD mortality trends, Black men were more than 25 times as likely as White men to experience adverse CHD mortality trends from 1985-1995. In addition, a substantial minority of African-American adults experienced negligible changes in CHD mortality over the study period.

E. Barnett, J. Halverson. Local Increases in Coronary Heart Disease Mortality Among Blacks and Whites in the United States, 1985-1995. Am J Public Health 91(9):1499-1506 (September 2001) [Correspondence: Elizabeth Barnett, Ph.D, MSPH, Office of Social Environment and Health Research, Dept. of Epidemiology and Biostatistics, University of Florida College of Public Health, 13201 Bruce B. Downs Blvd., MDC 56, Tampa, FL 33612-3805. E-mail: ebarnett@hsc.usf.edu].

COPYRIGHT 2001 Frost & Sullivan
COPYRIGHT 2002 Gale Group

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