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. 2000 Jun;5(2):167-73.
doi: 10.1023/A:1009884820941.

Incidence and Epidemiology of Heart Failure


Incidence and Epidemiology of Heart Failure

W B Kannel. Heart Fail Rev. .


Epidemiologic data from the Framingham Study provide insights into the population burden of heart failure (CHF), its prognosis and modifiable risk factors that promote it. In the general population CHF is chiefly the end stage of hypertensive, coronary and valvular cardiovascular disease. It is a major and growing problem in most affluent countries because of aging populations of increased size, and the prolongation of the lives of cardiac patients by modern therapy. Once clinically manifest, CHF, despite recent innovations in therapy, carries an unacceptably high mortality rate. In the Framingham Study, median survival is only 1.7 y for men and 3.2 y for women, with only 25% of men and 38% of women surviving 5 y. This is a mortality rate 4-8 times that of the general population of the same age. This poor outlook is observed for all etiologies of CHF and sudden death is a prominent feature of the mortality. Based on population attributable risks, hypertension has the greatest impact, accounting for 39% of CHF events in men and 59% in women. Despite its much lower prevalence in the population (3-10%) myocardial infarction also has a high attributable risk in men (34%) and women (13%). Valvular heart disease only accounted for 7-8% of CHF. Hypertension increased the age and risk factor adjusted hazard of CHF 2-fold in men and 3-fold in women, with a greater impact of the systolic than diastolic blood pressure. Diabetes increased CHF risk 2-8 fold with risk ratios twice as large in women as men. About 19% of CHF cases have diabetes. It accounted for 6-12% of the CHF in the Framingham Study cohort. Dyslipidemia characterized by a high total/HDL cholesterol ratio, but not the total cholesterol alone was a risk factor for CHF. An enlarged heart on X-Ray, ECG-LVH, a reduced vital capacity and rapid heart rate usually signified deteriorating cardiac function. CHF risk associated with ECG-LVH was independent of X-Ray cardiomegaly but risk was further augmented when both coexist. Echocardiographic left ventricular hypertrophy signifies a high risk of CHF proportional to the degree of increase in left ventricular mass without a critical value that delineates compensatory from pathological hypertrophy. Risk of CHF in persons predisposed by hypertension, diabetes or cardiac conditions varies over a 10-fold range depending on the aforementioned modifiable risk factors and indicators of deteriorating left ventricular function. Using multivariate risk formulations it is possible to identify 20% of the population from which 70% of the CHF will evolve. Those in the upper quintile of multivariate risk are good candidates for echocardiographic testing to delineate those needing aggressive preventive measures to delay the onset of CHF. Therapy of CHF must begin with treatment of presymptomatic left ventricular dysfunction to reverse the dysfunctional maladaptive changes.

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