Ruminations About Renal Denervation.

Abstract

Renal artery denervation has captured the imagination of cardiologists as few recent technologies have done.1 The underlying pathophysiological construct seemed persuasive because evidence of sympathetic overactivity in the genesis of hypertension and heart failure has been clearly documented. Moreover, initial nonrandomized studies using different catheter systems in patients with hypertension deemed treatment resistant almost uniformly found large drops in office blood pressure measurements. The initial assessment of those very impressive results was surprisingly noncritical in many parts of the world in which the procedure was adopted into clinical practice. Subsequently, the neutral results of the SYMPLICITY-HTN 3 trial (Renal Denervation in Patients With Uncontrolled Hypertension),2 which was the first to incorporate a “sham procedure” control arm, came as a stunning surprise to some and generated a wide spectrum of responses, including denial, disbelief, abrogation of the entire concept, a critique of several technical and operator-dependent issues, and an increasing awareness of the power of placebo, regression to the mean, and methods of assessing blood pressure control. As is so often the case after the initial furor, it is a time for sober reflection, and a more circumspect view of renal artery denervation has been adopted that in turn has led to the design of more sophisticated ongoing trials. Since the first studies, there is now a much greater understanding of resistant hypertension. Many of these lessons came from the SYMPLICITY HTN-3 trial.2 First, reports of the prevalence of resistant hypertension may have been greatly exaggerated. When studied rigorously, it appears that poor adherence is the root cause of the majority of cases initially felt to be resistant hypertension.3 The salutary role of aldosterone blockade in many instances of resistant hypertension has also now been fully appreciated. Partnership with dedicated hypertension experts based …