Key result
Increasing pacing rate to 90 bpm reduces TR regurgitant volume by ~47% while improving cardiac output.
Why the study?
The force-frequency relationship suggests physiologic heart-rate augmentation can enhance contractility and cardiac output, motivating an evaluation of whether pacemaker-programmed heart-rate elevation improves left-ventricular forward pump performance, hemodynamics, and functional tricuspid regurgitation.
Does pacemaker-programmed heart-rate elevation within a normal physiologic range (60 to 90 bpm) improve cardiac output and attenuate severe functional tricuspid regurgitation in patients with chronic bradyarrhythmia?
Does pacemaker-programmed heart-rate elevation within a normal physiologic range (60 to 90 bpm) improve cardiac output and attenuate severe functional tricuspid regurgitation in patients with chronic bradyarrhythmia?
Pacemaker-programmed heart-rate augmentation between 60 and 90 bpm acutely increases cardiac output and markedly reduces regurgitant volume and vena contracta width in patients with chronic bradyarrhythmia and severe functional tricuspid regurgitation.
Acute rate increase may attenuate severe TR and boost output; hypothesis-generating pending randomized trials.
Background After the Fontan procedure, pulmonary blood flow depends on passive venous return; the single ventricle (often the left ventricle) serves as the sole systemic pump and indirectly determines pulmonary flow by maintaining low filling pressures. The force–frequency relationship (Bowditch phenomenon) suggests that, within a physiologic heart-rate range, heart-rate augmentation can enhance myocardial contractility and improve cardiac output. Based on these concepts, we tested whether pacemaker-programmed heart-rate elevation within a normal range could enhance left-ventricular forward pump performance, improve hemodynamics, and improve functional tricuspid regurgitation (TR). Methods Ten consecutive patients with pacemakers for chronic bradyarrhythmia and concomitant severe TR were enrolled. Heart rate was sequentially programmed to 60, 70, 80, and 90 bpm, and TTE was performed at each rate. LVOT and RVOT diameter and Doppler spectra were acquired to evaluate VTIs and cardiac output (CO). TR vena contracta width was measured in two orthogonal planes on RV-foucused four-chamber view (TRVC1, TRVC2). TR regurgitant volume (TRVol) was quantified by PISA method. TRVol-to-stroke volume ratios were calculated (TRVol/LVSV and TRVol/RVSV). Results With pacing rate increased from 60 to 90 bpm, parameters changed consistently. (1) TR severity decreased: TRVol 77.80±58.31, 68.07±53.19, 54.50±42.75, and 40.88±32.86 mL at 60/70/80/90 bpm, respectively (P<0.05). TRVC1 decreased from 14.11±7.03 to 10.62±6.63 mm and TRVC2 from 12.01±2.90 to 7.84±2.79 mm (P<0.05). (2) VTI (surrogate of stroke volume) decreased while CO increased: LVOT-VTI 22.79±3.87, 22.39±4.14, 20.57±3.38, 19.90±4.04 (P<0.05); RVOT-VTI 18.96±3.90, 20.41±4.20, 19.03±3.51, 18.13±3.42 (P<0.05). LVOT-CO increased from 4.10±0.96 to 5.26±1.98 L/min (P<0.05) and RVOT-CO from 7.44±2.40 to 10.38±2.05 L/min (P<0.05). (3) Relative regurgitant burden decreased: TRVol/LVSV decreased from 1.38±1.39 to 0.98±1.06 and TRVol/RVSV from 0.71±0.59 to 0.35±0.25 (P<0.05). Conclusions Within a physiologic pacing range (60–90 bpm), heart-rate augmentation increased CO despite reduced SV and was associated with a marked reduction in TRVol and VC width. The reduction in TR exceeded the rate-related decline in SV, suggesting that pacemaker-based “rate optimization” may represent a feasible minimally invasive hemodynamic strategy for severe functional TR in patients with chronic bradyarrhythmia. Larger studies with follow-up are warranted.
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Li et al. (2026) studied Chronic bradyarrhythmia and concomitant severe functional tricuspid regurgitation (n=10). Pacemaker-programmed heart-rate elevation vs. Baseline pacing at 60 bpm was evaluated on Tricuspid regurgitation regurgitant volume (TRVol) and cardiac output (LVOT-CO and RVOT-CO) (p=<0.05). Increasing pacing rate from 60 to 90 bpm reduced TR regurgitant volume from 77.80 to 40.88 mL and increased LVOT cardiac output from 4.10 to 5.26 L/min (both P<0.05).
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