Pre-clinical cardiovascular disease and surrogate end-points in hypertension: does race influence target organ damage independent of blood pressure?

OBJECTIVES

To examine the adequacy of available evidence that: 1) left ventricular hypertrophy (LVH) and its regression influence the rate of cardiovascular events in hypertension; 2) carotid artery wall thickening and discrete plaque have comparable significance to LVH; and 3) black hypertensive patients have greater target organ damage than white hypertensives, independent of blood pressure and other relevant covariates.

DESIGN AND METHODS

Statistical, epidemiologic, and treatment trial literature concerning ECG and echocardiographic LVH and carotid ultrasound findings was reviewed to address the above three questions.

RESULTS

Results of seven electrocardiographic and ten echocardiographic studies (total of 20,000 subjects) show consistently higher risks of morbid events in individuals with LVH as compared to those without (odds ratios 1.4 to 5.4). Available data (five studies, 1544 subjects) suggest that morbid events occur in a greater proportion of individuals in whom LVH progresses (13% to 59%) than in whom it regresses (7% to 12%). Results of four studies using carotid ultrasound (n = 9570) show consistently higher rates of subsequent cardiovascular events in individuals with carotid wall thickening, discrete atherosclerotic plaque or arterial stenosis than those without; however, data are only available from one study regarding the relation between longitudinal change in carotid ultrasound findings and subsequent events. Of the available echocardiographic studies comparing black and white hypertensive patients, most (7 out of 9) show higher LV wall thickness in blacks, with no consistent difference with regard to LV mass.

CONCLUSIONS

LVH satisfies strict criteria to establish a fully adequate surrogate endpoint for morbid events in hypertension more fully than do carotid arterial findings. It has not yet been fully established whether black-white differences in hypertensive target organ damage are independent of blood pressure or other factors.