Michael H. Criqui

Primary Prevention of Coronary Heart Disease: Guidance From Framingham A Statement for Healthcare Professionals From the AHA Task Force on Risk Reduction

The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification.nnThe American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …

Very low cholesterol and cholesterol lowering. A statement for healthcare professionals from the American Heart Association Task Force on Cholesterol Issues.

E pidemiological studies have consistently reported a U-shaped relationship between total cholesterol and all-cause mortality. A recent meta-analysis confirms that at high levels of cholesterol the increase in total mortality is due to a sharply increased risk of cardiovascular death, particularly death from coronary heart disease (CHD). At low levels of cholesterol, where the cardiovascular death rate is low, the increase in total mortality is due to a number of causes, including trauma, cancer, hemorrhagic stroke, and respiratory and infectious diseases. It should also be noted that there is no trend for an increase in total mortality unless the total cholesterol level is less than 160 mg/dL. It is estimated that in the United States less than 10% of middle-aged men and women have serum cholesterol levels below this range. Careful analysis has revealed that a substantial portion of this excess mortality at low levels of cholesterol appears to be caused by poor health at baseline in many persons with lower cholesterol. However, after exclusion of ill persons and early deaths, a residual association between very low cholesterol and mortality persists in some studies. Although this issue clearly requires further evaluation, it is of little current relevance to the prevention of cardiovascular disease in patients or populations. Completed clinical trials of cholesterol lowering have focused on patients with high cholesterol, and investigators have typically reported a modest reduction in cholesterol, so that even after intervention cholesterol remains relatively high. As expected, a decrease in CHD has been observed in these trials. Meta-analyses of trials of cholesterol lowering in patients with established CHD (secondary prevention), in which subjects were at high short-term risk of death from CHD, have demon-