Response to Prehypertension: To Treat or Not To Treat Should No Longer Be the Question

In response to our recent study,¹ Kwatra et al² wrote a Letter to the Editor indicating that we missed the opportunity to emphasize the evidence for pharmacotherapy in this population. We were surprised by this comment, because we repeatedly highlighted in our article the need for an effective pharmacological complement to therapeutic lifestyle intervention only for slowing the rapid progression from prehypertension to hypertension. In fact, we stated that the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure recommendation of therapeutic lifestyle change, which includes weight loss, salt restriction, and eating a healthy diet, for example, Dietary Approaches to Stop Hypertension, had limited adoption in the population.³ We specifically proposed the need for comparative effectiveness research to address this critical issue. We would now like to further document the strong rationale for comparative effectiveness research rather than rapidly moving to pharmacotherapy for the large prehypertensive patient population, which was the focus of our report.

The justification made by Kwatra et al² to treat prehypertension pharmacologically was based on a meta-analysis of randomized, controlled trials and is out of context.⁴ The cited study refers to prehypertensives treated not for arresting the progression of prehypertension to hypertension but rather for reduction in incident stroke among patients with compelling clinical conditions for pharmacotherapy, for example, clinical coronary artery disease, heart failure, type 2 diabetes mellitus, and atrial fibrillation. Of note, an earlier report also documented significant reductions in stroke, as well as myocardial infarction, heart failure, cardiovascular mortality, and all-cause mortality, when nonhypertensive patients with clinical cardiovascular disease received various antihypertensive medications.⁵

We do not believe that these 2 reports on nonhypertensive patients with clinical cardiovascular disease establish a sufficient evidence base for treating the much larger population of clinically uncomplicated prehypertensive patients. However, there is strong justification to explore pharmacological intervention in clinically uncomplicated prehypertensive patients at high risk of future hypertension and clinical cardiovascular events, for example, blacks,⁶ given their accelerated transition from prehypertension to hypertension and their greater risk of cardiovascular disease complications, even in the absence of progression.⁷ We continue to view a pharmacological option to preventing hypertension and cardiovascular events in high-risk prehypertensives without clinical cardiovascular disease as more likely to succeed than therapeutic lifestyle change given the slow and incomplete adoption and maintenance of the latter.

Thus, our decision to recommend comparative effectiveness research rather than immediately and strongly advocating pharmacotherapy as a primary prevention strategy is not an opportunity that we missed. Rather, we believe that the recommendation for comparative effectiveness research is a prudent and necessary next step in building the evidence base required to change the current treatment guidelines and management paradigms for millions of prehypertensive patients without clinical cardiovascular disease.

• © 2012 American Heart Association, Inc.