A plateau pattern of pulmonary arterial pressure during exercise in LVSD patients was associated with increased mortality compared to a linear pattern (HR 8.1; 95% CI 2.7-23.8; P<0.001).
Observational (n=79)
Do pulmonary vascular response patterns during exercise predict exercise capacity and mortality in patients with left ventricular systolic dysfunction?
In patients with LVSD, a plateau pattern in pulmonary arterial pressure during exercise is associated with worse exercise capacity and significantly higher mortality compared to a linear response.
Effect estimate: HR 8.1 (95% CI 2.7 to 23.8)
p-value: p=<0.001
BACKGROUND: Elevated resting pulmonary arterial pressure (PAP) in patients with left ventricular systolic dysfunction (LVSD) purports a poor prognosis. However, PAP response patterns to exercise in LVSD and their relationship to functional capacity and outcomes have not been characterized. METHODS AND RESULTS: Sixty consecutive patients with LVSD (age 60±12 years, left ventricular ejection fraction 0.31±0.07, mean±SD) and 19 controls underwent maximum incremental cardiopulmonary exercise testing with simultaneous hemodynamic monitoring. During low-level exercise (30 W), LVSD subjects, compared with controls, had greater augmentation in mean PAPs (15±1 versus 5±1 mm Hg), transpulmonary gradients (5±1 versus 1±1 mm Hg), and effective pulmonary artery elastance (0.05±0.02 versus -0.03±0.01 mm Hg/mL, P<0.0001 for all). A linear increment in PAP relative to work (0.28±0.12 mm Hg/W) was observed in 65% of LVSD patients, which exceeded that observed in controls (0.07±0.02 mm Hg/W, P<0.0001). Exercise capacity and survival was worse in patients with a PAP/watt slope above the median than in patients with a lower slope. In the remaining 35% of LVSD patients, exercise induced a steep initial increment in PAP (0.41±0.16 mm Hg/W) followed by a plateau. The plateau pattern, compared with a linear pattern, was associated with reduced peak Vo(2) (10.6±2.6 versus 13.1±4.0 mL · kg(-1) · min(-1), P=0.005), lower right ventricular stroke work index augmentation with exercise (5.7±3.8 versus 9.7±5.0 g/m(2), P=0.002), and increased mortality (hazard ratio 8.1, 95% CI 2.7 to 23.8, P<0.001). CONCLUSIONS: A steep increment in PAP during exercise and failure to augment PAP throughout exercise are associated with decreased exercise capacity and survival in patients with LVSD, and may therefore represent therapeutic targets. CLINICAL TRIAL INFORMATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00309790.
Lewis et al. (2011) conducted an observational in Left ventricular systolic dysfunction (n=79). Plateau pulmonary arterial pressure response pattern during exercise vs. Linear pulmonary arterial pressure response pattern was evaluated on Mortality (HR 8.1, 95% CI 2.7 to 23.8, p=<0.001). A plateau pattern of pulmonary arterial pressure during exercise in LVSD patients was associated with increased mortality compared to a linear pattern (HR 8.1; 95% CI 2.7-23.8; P<0.001).