PE Survivors May Benefit from Exercise Rehabilitation

Acute PE is associated with ~100,000 deaths annually in the U.S. One-third of patients recovering after an acute PE have persistent symptoms and quality of life problems including exercise impairment. The causes are not well understood.

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A research team at Mass General led by Aaron Baggish, MD, director of the Cardiovascular Performance Program, and Ido Weinberg, MD, director of the Vascular Medicine Fellowship, set out to examine exercise capacity and cardiopulmonary function among massive and submassive PE survivors. In a study published in the Journal of the American Heart Association, they discovered that impaired exercise capacity was associated with deconditioning and not cardiopulmonary dysfunction, highlighting a greater need for cardiac rehabilitation following PE.

This prospective, longitudinal, repeated-measures study began with the hypothesis that acute PE survivors would have impairments to exercise capacity that would be explained by cardiopulmonary dysfunction. To test this hypothesis, the team evaluated cardiopulmonary status and function, as well as exercise capacity in 20 (3 massive and 17 submassive) PE patients at one- and six-month points following the index event. An acute PE response team used computed tomography to confirm PE diagnosis.

At diagnosis, all patients with electrocardiographic evidence of RV strain also had echocardiographic RV dysfunction. In total, 17 patients showed signs of RV dysfunction as defined by either an abnormal RV FAC, S′ or TAPSE.

At a one- and six- month follow-up, researchers conducted a cardiovascular work-up using biomarkers, comprehensive resting transthoracic echocardiography (TTE) and CPET, which measures functional capacity (defined by peak oxygen consumption). Statistical analyses determined any association between RV dilation and dysfunction and RV/pulmonary vascular coupling (as classified by NYHA class) and exercise capacity through peak VO2 with <80% of maximum predicted.

Most survivors experienced persistent exertional symptoms and objective impairments in peak exercise capacity up to six months after the event. Functional capacity was similar at one-month and six-month follow-up. All patients who reported excessive dyspnea during physical activity at one-month remained affected at six-months. Peak VO2 values at one to six months were correlated and impaired exercise capacity remained similar (12/20). Notably, among patients with persistent RV dysfunction at six months, compared to patients with normal RV function, no difference in peak VO2 was found. Therefore, the researchers conclude that the prevalence of physical activity symptoms and VO2 impairment among survivors does not appear to be caused by cardiopulmonary dysfunction, but by deconditioning.

CPET and Cardiac Rehabilitation

CPET is an established independent predictor of long-term outcomes in patients with cardiovascular disease. This has been found in recent studies of acute MI, coronary artery bypass grafting and ischemic heart disease, but not following acute PE. There is also not a lot of longitudinal data on functional capacity post PE and there is no guidance on participation in exercise post PE.

CPET is currently the standard of care for managing numerous cardiovascular diseases including CAD and heart failure. Given the findings of this study, the researcher advocate using CPET as a tool for assessment of post-PE functional capacity because it can measure response to exercise and delineate sources of exercise limitation. It could also be used to tailor therapy among massive and submassive PE survivors.

Specifically, the researchers recommend exploring the use of exercise training as part of a cardiac rehabilitation program because it may offer tremendous benefit for acute PE survivors, as it benefits patients following other acute coronary syndromes.

Further studies are needed to evaluate the impact of cardiac rehabilitation on clinical outcomes.

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