White-coat hypertension and the development of sustained hypertension

For 50 years, hypertension has been recognized as the most significant risk factor for the development of symptomatic cardiovascular disease in Western society. One half of patients who develop myocardial infarction and approximately two thirds of those who develop cardiovascular accidents have antecedent hypertension. There is a large body of data confirming that this risk can be significantly reduced by adequate therapy. Despite this overwhelming public health imperative, the diagnosis and treatment of hypertension remain difficult.

According to recent American Heart As­sociation data, 32% of Americans (65,000,000 people) have hypertension, and only one third of these are being appropriately treated. Thirty percent (almost 20,000,000 people) are un­aware they have the disease, and an additional 36% (nearly 24,000,000 people) are inadequately treated. Several well-documented rea­sons for this dramatic public health failure exist, including issues related to access to care, poor compliance with pharmacotherapy and lifestyle modifications, and the reluctance of physicians and patients to commit to a lifetime of therapy on the basis of 1 or 2 sphygmomanometer readings.

One factor that contributes to this reluctance to treat is the notion that “white-coat hypertension” (WCHT), an intermittent rise in blood pressure in a medical setting that is not reflected in a less stressful ambulatory environment, might not be pathologic. This concept is addressed in the present study by Ugajin and colleagues. The authors followed 777 initially normotensive adult pa&shy;tients, including more than 100 patients with WCHT, for approximately 8 years. The sustained normotensive (SNT) group and the WCHT group were not distinguished by age or comorbidities, although the WCHT group was slightly more hypertensive in the ambulatory environment (121/73 mm Hg vs 115/70 mm Hg; P < .001) and slightly more likely to be men (P < .03). Over the course of the study, 47% of those with WCHT and 22% of those with SNT developed overt hypertension or were started on antihypertensive medications, a difference that was highly significant (with an adjusted odds ratio of developing hypertension for the WCHT co&shy;hort of 2.86; P < .001). These differences remained highly significant, even after adjustment for initial ambulatory blood pressure measurements.

It is, of course, easy to critique any study of this type. Follow-up was imperfect: 15% of the subjects initially enrolled and characterized did not complete the study, the number of subjects with WCHT was relatively small (and substantially less than those with SNT), and the groups were imperfectly matched (male gender and obesity, both factors that predict the development of hypertension over time in any normotensive cohort, were disproportionately represented in the WCHT group). Although the authors made a good-faith effort to quantify the blood pressure measurements, the data were self-reported (albeit using a semiautomatic device), and the mean of a variable number of determinations was used to define the blood pressure of an individual subject, which might have introduced some ill-defined bias.

These concerns aside, the study was thoughtfully conducted, and the re&shy;sults are worthy of our consideration. What is clear is that an intermittent rise in blood pressure, even in a stressful situation, is not without significance. In approximately 50% of cases, this transient rise in blood pressure predicts the development of sustained hypertension. It therefore must de&shy;mand attention, certainly in the form of careful ongoing monitoring and focused dietary and lifestyle recommendations. What is unclear is whether patients with WCHT have a worse or different prognosis than the matched group of SNT subjects or a cohort of patients who have sustained modest hypertension. Equally unclear is whether subjects with WCHT have a different biologic (or genetic) form of hypertension.