Abstract

Pacing to increase resting heart rate (HR) is commonly employed in order to improve hemodynamics and cardiac output (CO), particularly in post-operative setting when right ventricle (RV) dysfunction is present. We tested if right atrial (RA) pacing improves RV hemodynamics acutely, and if the degree of baseline RV dysfunction modifies this relationship. We prospectively enrolled adult subjects with known or suspected pulmonary arterial hypertension (PAH) who underwent elective right heart catheterization between January 2013 and April 2016. RV pressure-volume (PV) analysis was performed with conductance catheters. RV volumes were calibrated by cardiac MRI same day. After measuring baseline PV data, a bipolar pacing wire was positioned in the RA and rate set to 80 to 90 beats per minute (bpm). Rate was increased in steps of 20 bpm. PV loops were recorded at end-expiration after 1 minute in each group: 80-99, 100-119, and 120-139 bpm. Parametric data were analyzed by Repeated Measures ANOVA, and non-parametric data were analyzed by Friedman Test. Baseline hemodynamic predictors of CO were analyzed by Repeated Measures simple linear regression. Twenty-three subjects were included in this analysis. Baseline mean RA pressure was 7 ± 3 mmHg with pulmonary vascular resistance of 5.2 ± 4.1 wood units. As HR increased with RA pacing, stroke volume (SV) declined in each pacing group (68±22, 61±19, 54±21 mL, respectively; p<0.001) with increase in CO (5.5±1.9, 6.2±1.9, 6.6±2.5 L/min; p<0.001). The dP/dt maximum increased (429, 490, 549 mmHg/s; p<0.001); however, RV-pulmonary arterial coupling (Ees/Ea) fell with pacing (0.97 vs 0.84 vs 0.78, p=0.009). No baseline hemodynamic parameter or measure of RV function modified the relationship between CO and RA pacing. Between-subject data had large variation; exclusion of non-PAH subjects (n=6) did not alter results. As heart rate increases with RA pacing, RV contractility and CO increase modestly at the expense of cardiac efficiency.

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