Cardiopulmonary Exercise Testing in Patients Following Massive and Submassive Pulmonary Embolism

Mazen S Albaghdadi, David M Dudzinski, Nicholas Giordano, Christopher Kabrhel, Brian Ghoshhajra, Michael R Jaff, Ido Weinberg, Aaron Baggish, Mazen S Albaghdadi, David M Dudzinski, Nicholas Giordano, Christopher Kabrhel, Brian Ghoshhajra, Michael R Jaff, Ido Weinberg, Aaron Baggish

Abstract

Background: Little data exist regarding the functional capacity of patients following acute pulmonary embolism. We sought to characterize the natural history of symptom burden, right ventricular (RV) structure and function, and exercise capacity among survivors of massive and submassive pulmonary embolism.

Methods and results: Survivors of submassive or massive pulmonary embolism (n=20, age 57±13.3 years, 8/20 female) underwent clinical evaluation, transthoracic echocardiography, and cardiopulmonary exercise testing at 1 and 6 months following hospital discharge. At 1 month, 9/20 (45%) patients had New York Heart Association II or greater symptoms, 13/20 (65%) demonstrated either persistent RV dilation or systolic dysfunction, and 14/20 (70%) had objective exercise impairment as defined by a peak oxygen consumption (V˙O2) of <80% of age-sex predicted maximal values (16.25 [13.4-20.98] mL/kg per minute). At 6 months, no appreciable improvements in symptom severity, RV structure or function, and peak V˙O2 (17.45 [14.08-22.48] mL/kg per minute, P=NS) were observed. No patients demonstrated an exercise limitation attributable to either RV/pulmonary vascular coupling, as defined by a VE/VCO2 slope >33, or a pulmonary mechanical limit to exercise at either time point. Similarly, persistent RV dilation or dysfunction was not significantly related to symptom burden or peak V˙O2 at either time point.

Conclusions: Persistent symptoms, abnormalities of RV structure and function, and objective exercise limitation are common among survivors of massive and submassive pulmonary embolism. Functional impairment appears to be attributable to general deconditioning rather than intrinsic cardiopulmonary limitation, suggesting an important role for prescribed exercise rehabilitation as a means toward improved patient outcomes and quality of life.

Keywords: echocardiography; exercise physiology; pulmonary embolism; quality of life.

© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

Figures

Figure 1
Figure 1
Study outline: All patients with acute high‐risk PE who were cared for by the PERT during the time period spanning from February 2014 and February 2015 were screened for eligibility for the present study. *Patients deemed ineligible could not perform exercise because of neurologic or orthopedic issues, or declined to participate in the study. PE indicates pulmonary embolism; PERT, PE Response Team.
Figure 2
Figure 2
Change in New York Heart Association (NYHA) functional class from baseline at 1 and 6 months following acute high‐risk pulmonary embolism.
Figure 3
Figure 3
Changes in 2 estimates of pulmonary artery systolic pressure. A, Tricuspid regurgitant velocity (TRV) and (B) pulmonary artery acceleration time (PAAT) at 1 and 6 months following acute high‐risk pulmonary embolism. *P<0.01 vs baseline. Circles represent outlier data points.
Figure 4
Figure 4
Changes in estimates of right ventricular RV function. A, Tricuspid annular plane systolic excursion (TAPSE), (B) RV free wall velocity (S′), (C) RV fractional area change (FAC), and (D) RV end‐diastolic area (RVEDA) at 1 and 6 months following acute high‐risk pulmonary embolism. *P<0.01 vs baseline. Circles represent outlier data points.
Figure 5
Figure 5
Patterns of cardiopulmonary exercise testing measure of peak VO2 consumption at 1 and 6 months following acute high‐risk pulmonary embolism.

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