RA pressure waveforms as a means for describing right ventricular diastolic stiffness

Abstract

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 are needed to determine if exercise-induced changes in RA pressure can unmask structural or pressure induced changes in RV diastolic function.