Diastolic Blood Pressure Control: How Low Is Too Low?

Ari Mosenkis, MD; Raymond R. Townsend, MD

Disclosures

It is well established that controlling hypertension through the use of antihypertensive agents reduces morbidity and mortality. It has been further demonstrated that lowering systolic blood pressure (SBP) as well diastolic blood pressure (DBP) confers benefit.[1] In the late 1970s, reexamination of Framingham data revealed that whereas there is no level of SBP lowering that does not incrementally improve outcomes, such may not be the case for DBP.[2] Subsequently, numerous analyses have been performed demonstrating the J-shaped curve, with increased mortality and coronary events in the groups of subjects whose DBPs were lowered below 65-85 mm Hg.[3,4,5] Many of these analyses were, however, based on small numbers of cases. Three explanations have been offered to explain this phenomenon. One is that diastolic hypotension is frequently noted in conditions such as cardiomyopathy or malignancy and that some of the patients who exhibited this phenomenon may just have been sicker. Another explanation is that low DBP is really a marker for widened pulse pressure, which is an indicator of increased arterial stiffness and atherosclerosis. Finally, some have suggested that diastolic hypotension reduces coronary filling pressures, thereby inducing endocardial ischemia.

In practice, isolated diastolic hypotension is a relatively uncommon complication of antihypertensive therapy. On the contrary, many patients are inadequately treated and have both SBP and DBP above the recommended targets. One group where diastolic hypotension may complicate therapy is the elderly. In elderly persons, a common variant of hypertension is isolated systolic hypertension with a wide pulse pressure and normal or even low diastolic pressure. Although numerous studies, notably the Systolic Hypertension in the Elderly Program (SHEP), have demonstrated the considerable benefits of treating this form of hypertension, DBP lowering is an inevitable consequence of such treatment. This reality raises some important questions: At what point in the treatment of isolated systolic hypertension does the potential harm of low DBP outweigh the benefit of lowering SBP? Is the increased event rate associated with diastolic hypotension a result of treatment, or is it seen even in those patients treated with placebo?

To address these issues, Somes and colleagues[6] reanalyzed the data from the SHEP trial. They found a higher incidence of cardiovascular disease events in those patients with isolated systolic hypertension whose DBPs were lowered to <70 mm Hg. In those patients whose DBPs were reduced to below 55 mm Hg, the relative risk of cardiovascular events nearly doubled. There are some problems with these data because, again, the numbers of patients who achieved DBP <55 mm Hg were small and a careful reading of this study suggests that levels of 45 mm Hg were not deleterious. These phenomena were noted in the treatment arm but not the placebo arm. It is not clear whether the increased event rate associated with low DBP in the treatment arm was a direct result of diastolic hypotension or, rather, the result of some subclinical disease that was unmasked by antihypertensive therapy. Importantly, the event rate in those patients in the active treatment arm with diastolic hypotension was still lower than the event rate of patients in the placebo arm. The authors conclude that patients who achieve DBP levels of about 55-60 mm Hg deserve more careful monitoring and more aggressive treatment of other cardiovascular risk factors.

Based on these results we recommend treating patients with isolated systolic hypertension to lower SBP to <140 mm Hg, as recommended by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure.[7] Caution should reign when DBP hovers around 56-60 mm Hg because (as far as we can currently tell) that is the point at which risk may approach benefit. As always, it remains prudent to offer such patients aggressive control of their other cardiovascular risk factors.

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