Introduction: Pulmonary vascular distensibility associates with right ventricular function and clinical outcomes in patients with unexplained dyspnea and pulmonary hypertension. Alpha distensibility coefficient is determined from a non-linear fit to multipoint pressure-flow plots. The study aims were 1) to create and test a user-friendly tool to standardize analysis of exercise hemodynamics including distensibility and 2) to investigate changes in distensibility following treatment in patients with pulmonary arterial hypertension. Methods: Participants with repeat exercise right heart catherization and PAH were identified from the University of Arizona PH Registry (n=29). Single-beat analysis was used to quantify right ventricular function including the coupling ratio and diastolic stiffness. Prototypes of the iCPET calculator were developed using Matlab, Python and RShiny to analyze exercise hemodynamics and alpha distensibility coefficient, α (%/mmHg) from multi-point pressure flow plots. Interclass coefficients were calculated for inter-platform and interobserver variability in alpha. Results: No significant bias in the intra-platform (Matlab vs RShiny: ICC: 0.996) or inter-observer (ICC: 0.982) comparison of alpha values. Participants with PAH had a significant decrease in afterload at follow-up (p<0.05) but no significant change in alpha distensibility. At follow-up, participants with a resting mean PA pressure < 25 mmHg had no change in pressure, resistance or alpha distensibility. Alpha distensibility significantly correlated with PA compliance at both the index and follow-up visit. Discussion: The iCPET calculator standardizes alpha distensibility calculations. In this retrospective cohort, alpha distensibility did not change despite a decrease in pulmonary vascular afterload (PVR and mPAP) at follow-up after treatment with pulmonary vasodilators.
Introduction Exercise‐induced changes in right atrial (RA) pressure associates with morality in patients with pulmonary hypertension (PH). Increased right ventricular (RV) diastolic stiffness impairs right ventricular filling during atrial contraction. Right atrial waveforms consist of the a‐wave (atrial contraction) and v‐wave (RA passive filling), as well as x and y descents representing atrial relaxation and ventricular filling, respectively. Ventricular distensibility has been associated with the difference between the x‐ and y‐descents (x‐y difference) in RA pressure. A positive x‐y difference correlates with increased ventricular stiffness. The study aim was to investigate the relationship between RA pressure waveforms and RV diastolic function in patients with pulmonary arterial hypertension (PAH). We hypothesized that exercise‐induced increases in RA pressure associate with increased RV diastolic stiffness and a positive x‐y difference. Methods Participants (n = 52) with a right heart catheterization (RHC) and invasive cardiopulmonary exercise test were selected from the University of Arizona Pulmonary Hypertension Registry. Resting (REST) and peak exercise (EX) measurements of RA pressure (RAP), pulmonary artery pressure (PAP), cardiac output (CO), and heart rate (HR) were analyzed. Raw RA waveforms were analyzed to identify the a‐wave, v‐wave, and x‐ and y‐descents using a custom MATLAB program. Single‐beat methods were used to calculate end‐diastolic elastance (Eed) a measure of RV stiffness. Wilcoxon signed‐rank test was used test differences between rest and exercise conditions (R version 4.0.3). Data is presented as mean ± standard deviation or median [IQR]. A p< 0.05 is considered significant. Results Forty‐three participants with pulmonary arterial hypertension diagnosis (age: 53 ± 13, sex: 73% female) and 9 participants without PH (age: 61 ± 13 years, sex: 100% female) were included. At rest, patients with pulmonary hypertension have increased PAP (37 ± 11 vs 16 ± 5 mmHg, p < 0.001) but no significant differences in RAP (2.7 [0.5‐4.7] vs 0.1 [‐0.1 – 3.0] mmHg, p = 0.4). There is a non‐significant increase in Eed (0.61 [0.34‐0.93] vs. 0.31 [0.26‐0.53] mmHg/ml, p = 0.07) compared to controls. At peak exercise (PAH: 20 [10‐50] W and controls: 30 [10‐60] W), RA pressure significantly increased (Figure 1A). Participants with PAH had an exercise‐induced increase in RA x‐descent (Figure 1B) and y‐descent (Figure 1C). There was an exercise‐induced decrease in the x‐y descent in participants with PAH but not Controls (Figure 1D). The x‐y difference did not correlate with resting Eed at rest (p = 0.58) or peak exercise (p = 0.22). Discussion/Conclusion Exercise significantly increased average RA, x‐descent, and y‐descent pressure. The RA x‐y difference did not correlate with end‐diastolic elastance, another measure of ventricular stiffness. Overall, exercise decreased the x‐y difference in participants with PAH that suggests an exercise‐induced increase in ventricular distensibility. Further investigations...
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