Study provides new insights on exercise limitations in patients with ventricular assist devices

Why don't patients with ventricular assist devices (VADs) get better improvement in exercise tolerance? Increases in key internal heart pressures appear to be the answer, reports a study in the ASAIO Journal, official journal of ASAIO. The journal is published in the Lippincott portfolio by Wolters Kluwer.

While VADs pump more oxygenated blood in response to exercise, the impact on exercise capacity is limited by increased pressures in the left ventricle and pulmonary artery, according to new research led by Professor Guy A. MacGowan, MD, FACC, of Freeman Hospital, Newcastle upon Tyne (U.K), and the Institute of Genetic Medicine at Newcastle University. The findings might point to ways of making VADs more responsive to the demands of physical activity.

New insights on exercise hemodynamics in patients with VADs

Ventricular assist devices are mechanical devices that can help pump blood in people with weakened hearts, typically due to heart failure. The devices may be used as a bridge to heart transplantation or sometimes on an indefinite basis.

As patients live longer with VADs, the focus has shifted to other issues, including exercise capacity. In a recent study, Prof. MacGowan and colleagues found that the improvement in exercise capacity after VAD placement was only about 40 percent of the predicted value. In contrast to patients with heart transplants, physical activity does not improve over time in patients with VADs.

In the new study, the researchers assessed hemodynamic responses to exercise in 20 patients with the HeartWare VAD, which takes over the pumping action of the left ventricle. Key pressures within the heart were measured during heart catheterization. Responses to exercise in patients with the left ventricular assist device were compared to those of 22 patients with heart failure managed by medications. The two groups had similar heart pressures at rest.

During exercise, the VAD patients had a higher cardiac index, indicating increased pumping of oxygenated blood from the left ventricle. They also had a trend toward higher peak oxygen consumption, which normally reflects increased exercise capacity. In heart failure patients without VADs, the cardiac index and heart rate were the only factors affecting oxygen consumption.

In contrast, for patients with VADs, oxygen consumption was also affected by two key pressures measured in the pulmonary artery, which carries deoxygenated blood from the heart to the lungs. These increased pressures – the pulmonary artery pressure and pulmonary wedge pressure – limited the increases in exercise capacity from increased pumping ability.

"This shows that passive elevation of pulmonary pressures due to increased left ventricular filling pressures is a significant cause of exercise intolerance in VAD patients," Prof. MacGowan and coauthors write. Even though the VAD increases cardiac output during exercise, the high left ventricular filling pressure limits any further increase in pulmonary artery pressures – and thus limits the ability to increase exercise capacity.

Could changing the way VADs pump blood improve their ability to respond to the demands of exercise?

A mechanism to reduce filling pressures in response to exercise could benefit exercise capacity. Future designs of VADs should consider exercise responsiveness, and future studies should study enhanced afterload reduction as a strategy to reduce left ventricular filling pressure elevations with exercise."

Prof. Guy A. MacGowan and colleagues