Enhanced External Counterpulsation in Patients With Heart Failure: A Multicenter Feasibility Study

Ozlem Soran, MD, Bruce Fleishman, MD, Theresa Demarco, MD, William Grossman, MD, Virginia M. Schneider, RN, Karen Manzo, RN, Paul-André de Lame, MD, Arthur M. Feldman, MD, PhD


CHF. 2002;8(4) 

In This Article


The present study showed that when carefully applied and monitored, the application of 35 1-hour daily sessions of EECP over approximately 7 weeks was safe and well-tolerated in patients with relatively stable heart failure and no fluid overload. Although EECP treatments were limited by arrhythmias in some patients, there were no clinically significant problems associated with the administration of EECP in this group of patients with symptomatic heart failure. Furthermore, adverse events that were seen in patients outside the EECP treatment sessions could not be attributed to EECP itself but rather were expected consequences of the disease. Although it had been intended to enroll patients who were stable and presumably NYHA class II-III, the median ejection fraction of the population was 23%, consistent with clinical trials enrolling NYHA class II-IV heart failure patients.

The results of the present study, albeit in a small population and in the absence of a control group, also suggest that EECP can provide short- and long-term benefits to selected patients with chronic stable heart failure. These benefits, consisting of significant and persistent increases in exercise capacity (peak oxygen uptake and exercise duration), were observed 1 week after the end of the 35-session EECP treatment period and were still present at the 6-month follow-up. It appears that the study subjects benefited from EECP to a similar degree, regardless of the ischemic or nonischemic etiology of their heart failure.

While a diminution in the ischemic burden in patients with ischemic heart failure may explain the salutary effects in patients with coronary disease, the mechanism of the beneficial effects of EECP in patients with idiopathic cardiomyopathy remains less obvious. Patients with dilated cardiomyopathy have lower perfusion pressure resulting in decreased coronary flow and insufficient oxygen supply at the cellular level secondary to ventricular hypertrophy. By increasing perfusion pressure and decreasing cardiac work, EECP might improve oxygen supply and promote the recovery of otherwise non-functional areas of the myocardium.

Other possible mechanisms of benefit from EECP in heart failure include the effects of EECP on endothelial function. One such effect is an increase in nitric oxide,[12,13] with subsequent coronary and systemic vasodilation.

Alternatively, EECP has been shown also to decrease levels of endothelin-1, a potent endothelium-derived vasoconstrictor that is felt to contribute to the pathogenesis of heart failure.[13,14]