Faculty Opinions recommendation of Determinants and prognostic value of pulmonary arterial pressure in patients with chronic heart failure.

Author(s):  
Jean-Luc Vachiery
2010 ◽  
Vol 31 (18) ◽  
pp. 2280-2290 ◽  
Author(s):  
Thibaud Damy ◽  
Kevin M. Goode ◽  
Anna Kallvikbacka-Bennett ◽  
Christian Lewinter ◽  
James Hobkirk ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
David S Olshan ◽  
Rohan Bhat ◽  
Robyn Farrell ◽  
Mark Schoenike ◽  
Liana Brooks ◽  
...  

Introduction: The post-exercise recovery period poses advantages over the within-exercise period for acquisition of hemodynamic measurements because of attenuated respirophasic changes, ability to time measurements precisely relative to peak exercise, and increased feasibility of multi-modality data acquisition (i.e. echocardiographic imaging). While several studies have linked rest and exercise hemodynamic measurements to outcomes, the prognostic significance of recovery hemodynamics in patients with dyspnea on exertion remains unknown. Hypothesis: Impaired recovery of mean pulmonary arterial pressure (mPAP) following exercise predicts poor clinical outcomes. Methods: Upright incremental ramp cycle ergometry cardiopulmonary exercise testing with invasive hemodynamic monitoring was performed in patients referred for evaluation of exertional dyspnea. mPAP was obtained at rest, peak exercise, and at two-minutes following peak exercise. In addition, maximum workload was recorded for each patient. mPAP elevation at recovery versus baseline, indexed to peak workload, was determined. Cox regression was performed using the primary outcome of heart failure event-free survival. Results: Among 272 patients with dyspnea on exertion and preserved LVEF [age 61 (IQR 49 – 70), 47% male, BMI 29 kg/m 2 (25 – 34), exercise duration 8.1 minutes (6.9 – 9.2), peak workload 91 watts (71 – 121)] we observed an increase in mPAP from 17 (14– 20) to 33 (28 – 41) mmHg with a fall in mPAP to 22 (18 – 29) at 2 minutes of recovery. Median mPAP elevation at recovery versus baseline mPAP, indexed to peak workload, was 0.057 (0.031 – 0.101) mmHg/W. Persistently elevated mPAP, indexed to peak workload, was associated with future risk of HF hospitalization or death both in unadjusted analysis (Cox hazard ratio 1.53 for every standard deviation increase, p=0.003), and when adjusted for age, sex, and BMI (HR 1.40, p=0.025). Conclusions: Among patients with dyspnea on exertion undergoing invasive hemodynamic evaluation during exercise, persistently elevated mPAP following exercise predicts future heart failure event-free survival and may be more feasible to estimate non-invasively than measures obtained at peak exercise.


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