Key result
COPD patients without significant resting pulmonary hypertension had a significantly steeper mPAP/cardiac output slope during exercise compared to controls (6.9 vs 3.7 mmHg/L/min, p=0.007).
Why the study?
Pulmonary hypertension is common in COPD and linked to poor prognosis; researchers hypothesized that abnormal exercise pulmonary hemodynamics affect exercise capacity even without significant resting PH.
Do COPD patients without significant resting pulmonary hypertension exhibit abnormal pulmonary hemodynamics during exercise compared to controls?
Observational (n=52)
No
Do COPD patients without significant resting pulmonary hypertension exhibit abnormal pulmonary hemodynamics during exercise compared to controls?
Absolute Event Rate: 6.9% vs 3.7%
p-value: p=0.007
Even without significant pulmonary hypertension at rest, COPD patients exhibit abnormal pulmonary hemodynamics during exercise that correlate with reduced exercise capacity.
Abnormal exercise hemodynamics may occur in COPD without resting PH; hypothesis-generating for impact on capacity and need for prospective trials.
Background Pulmonary hypertension (PH) is a frequent complication in COPD and it is associated with decreased exercise capacity and poor prognosis. We hypothesized that even in COPD patients without significant PH at rest, abnormal pulmonary hemodynamics during exercise affect exercise capacity. Methods Consecutive COPD patients with clinically indicated right heart catheterization and resting mean pulmonary arterial pressure (mPAP) < 25mmHg and age- and sex-matched controls without chronic lung disease who underwent clinical work-up including invasive hemodynamic assessment during exercise were retrospectively analyzed. Chi-square tests were used to evaluate differences between groups for categorical data and Fisher’s exact test or Mann-Whitney-U-tests for continuous variables. Associations were analyzed with Spearman rank correlation tests. Results We included n=26 COPD patients (female/male: 16/10, 66±11yr, FEV1: 56±25 %predicted) and n=26 matched controls (FEV1: 96±22 %predicted). At rest, COPD patients presented with slightly increased mPAP (21 (18-23) vs. 17 (14-20) mmHg, p=0.022), and pulmonary vascular resistance (PVR) (2.5 (1.9-3.0) vs. 1.9 (1.5-2.4) WU, p=0.020) as compared to controls. During exercise, COPD patients reached significantly higher mPAP (47 (40-52) vs. 38 (32-44) mmHg, p=0.015) and PVR (3.1 (2.2-3.7) vs. 1.7 (1.1-2.9) WU, p=0.028) values despite lower peak exercise level (50 (50-75) vs. 100 (75-125) Watt, p=0.002). The mPAP/cardiac output slope was increased in COPD vs. controls (6.9 (5.5-10.9) vs. 3.7 (2.4-7.4) mmHg/L/min, p=0.007) and negatively correlated with both peak oxygen uptake (r=-0.46, p=0.007) and 6-minute walk distance (r=-0.46, p=0.001). Conclusion Even in the absence of significant PH at rest, COPD patients reveal characteristic abnormalities in pulmonary hemodynamics during exercise, which may represent an important exercise-limiting factor.
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Sassmann et al. (2022) conducted an observational in COPD (n=52). COPD vs. Matched controls without chronic lung disease was evaluated on mPAP/cardiac output slope (mmHg/L/min) (p=0.007). COPD patients without significant resting pulmonary hypertension had a significantly steeper mPAP/cardiac output slope during exercise compared to controls (6.9 vs 3.7 mmHg/L/min, p=0.007).
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