Increase in paced heart rate reduces muscle sympathetic nerve activity in heart failure patients treated with cardiac resynchronization therapy.

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To test the hypothesis that acute increased biventricularly (BiV) paced heart rate (pHR) results in decreased muscle sympathetic nerve activity (MSNA), and that dyssynchronous pacing (AAI) attenuates this effect, in heart failure patients receiving cardiac resynchronization therapy (CRT). Fourteen CRT patients (NYHA II-III, 12 males, mean EF 28 ± 14%) were recruited. Three different pHRs (50-90 b.p.m.) were randomly programmed in BiV- and AAI-pacing modes. Muscle sympathetic nerve activity (total sympathetic nerve activity/min (units) and number of bursts/100 RR) were recorded from the peroneal nerve using a microelectrode. In addition, cardiac output (CO) and mean blood pressure (mBP) were measured. With BiV pacing, the total MSNA/min was lower at 70 b.p.m. (-7 ± 21%, P = 0.18) and 90 b.p.m. (-29 ± 18%, P = 0.01) compared with at 50 b.p.m. (280 ± 180 U). Similarly, bursts/100RR decreased with increased BiV pHR. Cardiac output (3.7 L/min at 50 b.p.m., +12 ± 12% at 70 b.p.m., and +18 ± 19% at 90 b.p.m.) and mBP (78 ± 11 mmHg at 50 b.p.m., +6 ± 6% at 70 b.p.m. and +11 ± 8% at 90 b.p.m.) increased significantly at elevated pHRs in BiV-pacing mode. The effect on MSNA, CO, and mBP was less pronounced in AAImode but we found no significant differences between the pacing modes. Increased pHR acutely reduces MSNA and improves haemodynamics in HF patients treated with CRT with no evident differences between BiV- and AAI-pacing modes. Further studies are warranted to guide the programming of basic pHR in CRT patients.