Why the study?
Is white coat hypertension associated with increased target-organ damage compared to normotension and sustained hypertension?
Is white coat hypertension associated with increased target-organ damage compared to normotension and sustained hypertension?
White coat hypertension is not associated with increased left ventricular mass or carotid atherosclerosis compared to normotension, suggesting it may be a benign condition.
White coat hypertension was associated with no excess target-organ damage; leaves open whether treatment is warranted.
Although white coat hypertension may be present in 20% or more of hypertensive individuals, its prognostic significance is unknown. We compared prognostically relevant measures of target-organ damage among 24 individuals with white coat hypertension and age- and sex-matched groups of sustained hypertensive and normotensive subjects classified by clinical and 24-hour ambulatory blood pressures. Left ventricular and carotid artery structure and function were evaluated by ultrasonography. Left ventricular mass index was similar in white coat hypertensive (82 +/- 17 g/m2) and normotensive (78 +/- 15 g/m2) subjects but was higher in sustained hypertensive subjects (97 +/- 19 g/m2, P < .02 and P < .002, respectively). Similarly, carotid artery intimal-medial thickness was greater in the sustained hypertensive group (0.98 +/- 0.21 mm) than in the white coat hypertensive (0.84 +/- 0.16 mm, P < .05) and normotensive (0.76 +/- 0.18 mm, P < .001) groups. The prevalence of discrete atherosclerotic plaques was higher in the sustained hypertensive group (58%) than in the white coat hypertensive (25%, P < .05) and normotensive (21%, P < .02) groups. Cardiac and carotid structure in individuals with white coat hypertension resemble findings in normotensive subjects and differ significantly from those in age- and sex-matched sustained hypertensive subjects. These findings suggest that white coat hypertension may be a benign condition for which pharmacological intervention may not be necessary, a hypothesis that needs to be tested in longitudinal studies with clinical end points.
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Cavallini et al. (1995) studied this question.
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