Background/Aims: The value of the Framingham equation in predicting cardiovascular risk in African Americans and patients with chronic kidney disease (CKD) is unclear. The purpose of the study was to evaluate whether the addition of CKD and race to the Framingham equation improves risk stratification in hypertensive patients. Methods: Participants in the ALLHAT were studied. Those randomized to doxazosin, older than 74 years, and those with a history of coronary heart disease were excluded. Two risk stratification models were developed using Cox proportional hazards models in a two-thirds developmental sample. The first model included the traditional Framingham risk factors. The second model included the traditional risk factors plus CKD, defined by estimated glomerular filtration rate categories, and stratification by race (black vs non-black). The primary outcome was a composite of fatal coronary heart disease, nonfatal myocardial infarction, coronary revascularization, and hospitalized angina. Results: There were a total of 19,811 eligible subjects. In the validation cohort, there was no difference in C-statistics between the Framingham equation and the ALLHAT model including CKD and race. This was consistent across subgroups by race and sex and among those with CKD. One exception was among Non-Black women where the C-statistic was higher for the Framingham equation (0.68 vs 0.65, P =.02). In addition, net reclassification improvement was not significant for any subgroup based on race and sex, ranging from -5.5% to 4.4%. Conclusion: The addition of CKD status and stratification by race does not improve risk prediction in high-risk hypertensive patients.
|Original language||English (US)|
|Journal||American Heart Journal|
|State||Published - Dec 2012|
Bibliographical noteFunding Information:
None of the authors reports a conflict of interest with regard to the content of this paper. Dr Davis has consulted for Amgen, Forest Pharmaceuticals, and Takeda; and has received honoraria from Takeda. Dr Brown has consulted for Merck. Dr Henriquez has received honoraria from Astra-Zeneca, Boehringer Ingelheim, Forest Pharmaceuticals and Novartis. Dr Rahman has received honoraria from Boehringer Ingelheim. Dr Sweeney has received a research grant from Novartis. Dr Wong has consulted for Novartis, and has received research grants from Forest Pharmaceuticals, Merck, and Novartis. Drs Baraniuk, Colon, Cuyjet, Dart, Drawz, Graumlich, Moloo, Saklayen, Simmons, and Stanford have no financial interests to disclose.
Funding/Support—This study was supported by contract NO1-HC-35130 with the National Heart, Lung, and Blood Institute (NHLBI) and by a Career Development Award to PED (1K23DK087919). ALLHAT investigators received contributions of study medications supplied by Pfizer (amlodipine besylate and doxazosin mesylate), AstraZeneca (atenolol and lisinopril), and Bristol-Myers Squibb (pravastatin), and financial support provided by Pfizer.