What’s in the Works for Refractory Hypertension Beyond Drugs and Diet?


Debbie L. Cohen, MD, Renal Division, University of Pennsylvania School of Medicine, 210 White Building, Philadelphia, PA 19104
E-mail: cohendl@mail.med.upenn.edu

Refractory hypertension is extremely frustrating to manage for both the physician and the patient. Often, when drug therapy is exhausted, the physician is left with limited options. Nondrug therapy options include implantation of the CVRx (Rheos) device (Minneapolis, MN), catheter-based radiofrequency ablation of the renal sympathetic nerves, and use of the Resp-E-Rate device (InterCure, Inc, New York, NY).

Enhanced external counterpulsation (EECP) is a technique gaining popularity that is used to treat patients with coronary artery disease who are nonrevascularizable and are considered to have refractory angina.1 An earlier model of EECP was first developed in China in 1983 for patients with angina. Based on this model, the current technique of EECP was developed using electrocardiographic-gated, sequentially inflated pneumatic compression cuffs.2 The current model of EECP consists of three pneumatic compression cuffs applied to each of the patient’s legs. Cuffs are wrapped around the patient’s legs and, using compressed air, sequential pressure (300 mm Hg) is applied from the lower legs to the lower and upper thighs in early diastole to propel blood back to the heart. The mechanism is synchronized with the patient’s electrocardiogram such that with each cardiac cycle, pressure is sequentially applied distally to proximally in early diastole (diastolic augmentation) and retrograde aortic diastolic blood flow.1 At end diastole, pressure is simultaneously released from all cuffs, resulting in systolic unloading and afterload reduction.3 The degree of hemodynamic effect is monitored by the ratio of systolic to diastolic pressures, monitored by finger plethysmography. A usual course of EECP consists of 35 one-hour sessions. The mechanism by which EECP transmits its hemodynamic effect is similar to an intra-aortic balloon pump (IABP). The degree of diastolic augmentation produced is comparable with that of IABP. EECP also increases venous return and cardiac preload through the compression of capacitance veins, leading to increased right atrial pressure, pulmonary capillary wedge pressure, cardiac index, and cardiac output.4 Other noninvasive studies have also shown increased stroke volume and cardiac output, decreased systemic vascular resistance, and relative bradycardia.5

An interesting study was recently presented at the Council for High BP Research Meeting.6 Karia and colleagues studied 100 consecutive patients (58 normotensive and 42 hypertensive) with angina and coronary artery disease. Both groups received 40 one-hour EECP sessions. The change in systolic blood pressure (BP) in normotensive vs hypertensive patients was −2±14 mm Hg vs −25±11 mm Hg. Similarly, the change in diastolic BP in normotensive vs hypertensive patients was −1±11 mm Hg vs −7.5±9 mm Hg. Analysis with stratification of BP resulted in a more enhanced response to EECP with higher baseline BP.

EECP may present an interesting noninvasive treatment option for patients with refractory hypertension, although the exact mechanism for lowering BP is not fully understood. However, one contraindication to using EECP is a BP >180/110 mm Hg, since under these circumstances, EECP could produce diastolic BP that exceeds acceptable limits.7 There is increasing interest in this technique for the treatment of chronic nonrevascularizable angina patients, with many programs now establishing programs. More research is needed in this area, but it presents an interesting opportunity to be tested in a randomized clinical trial of refractory hypertension.