What is the clinical evidence from this study?

Study design: RCT. Population: Heart failure (n=10). Intervention: Increased biventricularly paced heart rates (pHRs) vs. Baseline/lower paced heart rate (60 bpm). Primary outcome: Right ventricular (RV) haemodynamics including RV+dP/dt, filling pressures, and cardiac output (p=<0.001).

October 14, 2010Open Access

Acute haemodynamic effects of increase in paced heart rate in heart failure patients recorded with an implantable haemodynamic monitor

Q: What are the key findings of this study?

Increasing biventricularly paced heart rate from 60 to 100 bpm significantly increased RV+dP/dt and cardiac output (P<0.001) while decreasing filling pressures in heart failure patients.

Key Result

Increasing biventricularly paced heart rate from 60 to 100 bpm significantly increased RV+dP/dt and cardiac output (P<0.001) while decreasing filling pressures in heart failure patients.

Study Design

Type

RCT (n=10)

Randomization

Randomly programmed

Structured PICO

Does increasing biventricularly paced heart rate improve right ventricular haemodynamics in heart failure patients with an implantable haemodynamic monitor?

Population

10 male heart failure patients (NYHA II-III) with an implantable haemodynamic monitor, mean age 65 years, undergoing acute pacing interventions.

Intervention

Seven biventricularly paced heart rates (60-120 bpm in steps of 10), randomly programmed and maintained for 60 s at rest.

Comparator

Spontaneous, sinus-driven heart rate increase during symptom-limited bicycle exercise, and baseline/lower paced heart rates.

Outcome

Right ventricular haemodynamics including RV systolic and diastolic pressures, estimated pulmonary artery diastolic (ePAD) pressure, RV+dP/dt, and cardiac output.surrogate

In heart failure patients with CRT, increasing paced heart rate between 60 and 100 bpm acutely improves right ventricular contractility and cardiac output while lowering filling pressures.

Main Result

p-value: p=<0.001

Abstract

AIMS: The aim of this study was to investigate the acute effects of different biventricularly paced heart rates (pHRs) on right ventricular (RV) haemodynamics in heart failure (HF) patients with an implantable haemodynamic monitor (IHM). METHODS AND RESULTS: At rest, seven pHRs, range 60-120 bpm (steps of 10), were randomly programmed and maintained for 60 s in 10 patients (male, 65±12 years, New York Heart Association II-III). Right ventricular systolic (RVSP) and diastolic pressures, estimated pulmonary artery diastolic (ePAD) pressure, and RV+dP/dt were recorded beat-to-beat using the IHM. Cardiac output (CO) was estimated from the RV pressure waveforms and arterial blood pressure was measured (Portapres®). To compare the haemodynamic effects of increased pHR at rest to that of spontaneous, sinus-driven heart rate (HR) increase, patients also performed a symptom-limited bicycle exercise. At rest, RV+dP/dt increased significantly with elevated pHR (P, main effect, 00 bpm. At a pHR of 100 bpm, ePAD was 1.4 mmHg lower compared with 60 bpm (P<0.01). Cardiac output increased gradually with elevated pHR at rest (P<0.001). Both total peripheral and estimated pulmonary arterial resistance significantly decreased with increased pHR. During exercise-induced maximum HR increase, RV+dP/dt, ePAD, and CO were all significantly higher compared with the corresponding pHR at rest. CONCLUSION: During cardiac resynchronization therapy in HF patients, the force frequency relationship is present in the RV, as increasing the pHR in the range 60-100 bpm results in decreased filling pressures and increased CO.