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Cardiopulmonary exercise test to detect cardiac dysfunction from pulmonary vascular disease
Mona Alotaibi1, Jenny Z Yang1, Demosthenes G Papamatheakis1
1Division of Pulmonary, Critical Care and Sleep Medicine, University of California, San Diego Healthcare, 200 West Arbor Drive, San Diego, CA, 92103-8378, USA.
Insights
Cardiopulmonary exercise testing (CPET) accurately detects inadequate stroke volume (SV) augmentation in pulmonary vascular disease. CPET
Area of Science:
- Cardiology
- Pulmonary Medicine
- Exercise Physiology
Background:
- Pulmonary vascular disease can cause cardiac dysfunction, leading to characteristic findings on cardiopulmonary exercise testing (CPET).
- Assessing stroke volume (SV) augmentation during exercise is crucial for identifying cardiac limitations in patients with pulmonary vascular disease.
Approach:
- Correlated CPET-derived O2·pulse ratio (O2·pulseAT/O2·pulserest) with right heart catheterization (RHC)-derived SV ratio (SVAT/SVrest) in patients with suspected pulmonary vascular disease.
- Evaluated the sensitivity and specificity of the O2·pulse ratio to detect diminished SV augmentation, comparing it with echocardiography-derived peak tricuspid regurgitant velocity (TRVpeak).
Key Points:
- CPET-derived O2·pulseAT/O2·pulserest strongly correlated with RHC-derived SVAT/SVrest (r=0.72, p<0.0001).
- The O2·pulse ratio demonstrated superior accuracy (AUROC 0.92) in detecting deficient SV augmentation compared to TRVpeak (AUROC 0.69).
- An O2·pulseAT/O2·pulserest ratio below 2.6 showed 92.6% sensitivity and 66.7% specificity for inadequate SV augmentation.
Conclusions:
- CPET is more accurate than echocardiography for detecting impaired SV augmentation in pulmonary vascular disease.
- CPET-derived O2·pulse ratio serves as a valuable noninvasive tool for screening patients at risk for pulmonary vascular disease, including those with persistent dyspnea post-pulmonary embolism.
Background:
Cardiac dysfunction from pulmonary vascular disease causes characteristic findings on cardiopulmonary exercise testing (CPET). We tested the accuracy of CPET for detecting inadequate stroke volume (SV) augmentation during exercise, a pivotal manifestation of cardiac limitation in patients with pulmonary vascular disease.
Methods:
We reviewed patients with suspected pulmonary vascular disease in whom CPET and right heart catheterization (RHC) measurements were taken at rest and at anaerobic threshold (AT). We correlated CPET-determined O2·pulseAT/O2·pulserest with RHC-determined SVAT/SVrest. We evaluated the sensitivity and specificity of O2·pulseAT/O2·pulserest to detect SVAT/SVrest below the lower limit of normal (LLN). For comparison, we performed similar analyses comparing echocardiographically-measured peak tricuspid regurgitant velocity (TRVpeak) with SVAT/SVrest.
Results:
From July 2018 through February 2023, 83 simultaneous RHC and CPET were performed. Thirty-six studies measured O2·pulse and SV at rest and at AT. O2·pulseAT/O2·pulserest correlated highly with SVAT/SVrest (r = 0.72, 95% CI 0.52, 0.85; p < 0.0001), whereas TRVpeak did not (r = -0.09, 95% CI -0.47, 0.33; p = 0.69). The AUROC to detect SVAT/SVrest below the LLN was significantly higher for O2·pulseAT/O2·pulserest (0.92, SE 0.04; p = 0.0002) than for TRVpeak (0.69, SE 0.10; p = 0.12). O2·pulseAT/O2·pulserest of less than 2.6 was 92.6% sensitive (95% CI 76.6%, 98.7%) and 66.7% specific (95% CI 35.2%, 87.9%) for deficient SVAT/SVrest.
Conclusions:
CPET detected deficient SV augmentation more accurately than echocardiography. CPET-determined O2·pulseAT/O2·pulserest may have a prominent role for noninvasive screening of patients at risk for pulmonary vascular disease, such as patients with persistent dyspnea after pulmonary embolism.
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