Evaluating CMR

Evaluating CHD risk

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For decades, CHD risk has been evaluated using regression equations derived from observational studies. To date, one of the best known risk prediction systems is based on the Framingham Heart Study (8). The Framingham risk score was designed to estimate the absolute risk of developing CHD in a middle-aged white population sample (9). The Framingham Heart Study developed a simplified coronary prediction model based on blood pressure, cholesterol, and LDL cholesterol categories proposed by the Fifth Joint National Committee on Hypertension (JNC-V) and the National Cholesterol Education Program-Adult Treatment Panel II (NCEP-ATP II) (10-12). Previous NCEP-ATP II (10) and JNC-V guidelines for managing individual risk factors estimated overall risk by adding categorical risk factors. However, this approach did not estimate total risk based on risk factors graded according to severity. In comparison, the Framingham Heart Study developed a model of graded risk factors that is more accurate than the simple addition of categorical risk factors (8).

In interpreting CHD risk estimates, the traditional Framingham model predicted total CHD risk, which included angina pectoris, recognized and unrecognized myocardial infarction (MI), coronary insufficiency (unstable angina), and CHD deaths (13, 14). However, in accordance with several clinical trials (15-17) that defined major coronary events (acute MI and CHD deaths) as the primary coronary endpoints, the Framingham investigators also provided estimates for “hard” CHD (MI and CHD deaths) endpoints (8).

Reference

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8. Wilson PW, D'Agostino RB, Levy D, et al. Prediction of coronary heart disease using risk factor categories. Circulation 1998; 97: 1837-47.

9. Lohman T.G. RAF, Martello R. Anthropometric Standardization Reference Manual, Champaign IL, Human Kinetics. 1988.

10. National Cholesterol Education Program. Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). Circulation 1994; 89: 1333-445.

11. Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II). JAMA 1993; 269: 3015-23.

12. The fifth report of the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure (JNC V). Arch Intern Med 1993; 153: 154-83.

13. Anderson KM, Wilson PW, Odell PM, et al. An updated coronary risk profile. A statement for health professionals. Circulation 1991; 83: 356-62.

14. Kannel WB, Feinleib M, McNamara PM, et al. An investigation of coronary heart disease in families. The Framingham offspring study. Am J Epidemiol 1979; 110: 281-90.

15. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994; 344: 1383-9.

16. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland Coronary Prevention Study Group. N Engl J Med 1995; 333: 1301-7.

17. Sacks FM, M.A. P, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels: Cholesterol And Recurrent Events Trial Investigators. N Engl J Med 1996; 1001-9.

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