Contrasting haemodynamic effects of exercise and saline infusion in older adults with pulmonary arterial hypertension (original) (raw)

The contemporary population of patients with pulmonary arterial hypertension (PAH) are older, with a high prevalence of cardiovascular risk factors [1], and potentially at risk for left ventricular diastolic dysfunction [2]. Accordingly, the effect of exercise or volume expansion may elicit augmented increases in pulmonary artery wedge pressure (PAWP) [3, 4], in addition to abnormal behaviour of pulmonary artery pressures. In healthy older subjects, exercise-associated increases in PAWP are predictably coupled to decreases in pulmonary arterial compliance (PAC) and pulmonary vascular resistance (PVR), thereby systematically lowering the product of the resistance-compliance relationship (RC-time) [5]. We prospectively examined this physiology in older patients with PAH. Exercise and volume expansion were compared with respect to the response of the PAWP and relationships to pulmonary artery pressures and RC-time. Adults with PAH aged >45 years referred for right heart catheterisation were recruited. Exclusion criteria included left ventricular systolic dysfunction (left ventricular ejection fraction <50%) or ⩾ moderate left-sided valvular heart disease. The local research ethics board approved the study protocol. Participants provided written informed consent. A balloon-tipped fluid-filled catheter was positioned in the pulmonary artery via internal jugular venous access. Right atrial pressure (RAP), pulmonary artery pressures (PAP) and PAWP were recorded at baseline in the supine position and heart rate (HR) was monitored continuously. After baseline, Volume consisted of volume expansion challenge by intravenous infusion of 15 mL•kg −1 of 0.9% sodium chloride solution at 100 mL•min −1. Haemodynamic data were recorded 1 min after completing Volume. Afterwards, participants were transferred to a cycle ergometer in a semi-upright position. Haemodynamic data were acquired at 1, 3 and 5 min at rest (Control) and averaged. Participants then pedalled at self-selected cadence between 60 and 80 xg at constant a work-rate of 15 watts. Haemodynamic data were obtained at 3 min after onset of cycling (Exercise). Analysis intervals consisted of ⩾10 consecutive beats free from premature beats. Calculations included: pulmonary pulse pressure (pulmonary PP; mmHg) = pulmonary artery systolic pressure (PASP) − pulmonary artery diastolic pressure (PADP); transpulmonary gradient (TPG; mmHg) = mean pulmonary artery pressure (mPAP) − PAWP; diastolic pressure difference (DPD; mmHg) = PADP-PAWP; RC-time is calculated as the product of PVR (TPG/(stroke volume×HR)) and PAC (stroke volume/PP), which can be simplified to TPG/(HR×PP). Changes in RAP and PAWP, relative to volume infused, were assessed by the slopes of RAP/volume infused and PAWP/volume infused relations. Data were analysed using SPSS, version 21 (IBM Corp., Armonk, NY, USA) and presented as median and interquartile ranges (IQR). Comparisons of continuous variables between conditions were analysed using related-samples Wilcoxon signed rank test. Two-tailed α level of 0.05 was considered statistically significant. @ERSpublications In this study, among patients with pulmonary arterial hypertension, exercise was more potent in eliciting pulmonary vascular abnormalities and demonstrated paradoxical increase in RC-time https://bit.ly/35Mb0dv