We assessed the feasibility of achieving acute, sustained blood pressure reductions through the use of cardiac pacing algorithms delivered via standard dual-chamber pacing based on introducing short atrio-ventricular (AV) delays (SAVD). Eighteen hypertensive subjects (57.3 ± 9.8 years old; 10 male and 8 female) with average initial systolic and diastolic blood pressures of 151.2 ± 17.6/92.2 ± 12.7 mmHg already scheduled to undergo an invasive electrophysiology procedure were included in this study. Pacing sequences were applied for ∼1-minute intervals with AV delays of 80, 40, 20 and 2 ms, while making high fidelity blood pressure measurements. Average reductions of 19.6 ± 7.7 mmHg in systolic pressure and 4.3 ± 3.8 mmHg in diastolic pressure (P < .001 each) were demonstrated with 2 ms AV delay pacing. Initial SBP reductions were followed by rebound effects which diminished the SBP reducing effects of SAVD pacing, likely due to baroceptor activation causing increased peripheral resistance. This effect was eliminated by intermittent introduction of longer AV delay pacing which modulated the baroreflexes. These findings provide the rationale and evidence underlying recent data showing significant and long-term blood pressure reductions in response to this cardiac neuromodulation therapy in hypertensive patients despite medical therapy.

我们评估了通过采用标准的双室起搏器提供的心脏起搏器算法实现急性，持续性血压降低的可行性，该算法基于引入短暂的房室（AV）延迟（SAVD）。这项研究包括了18位高血压受试者（57.3±9.8岁； 10位男性和8位女性），其平均初始收缩压和舒张压平均为151.2±17.6 / 92.2±12.7 mmHg，已经计划进行侵入性电生理检查。起搏序列间隔约1分钟，AV延迟分别为80、40、20和2 ms，同时进行高保真血压测量。收缩压平均降低19.6±7.7 mmHg，舒张压平均降低4.3±3.8 mmHg（P2毫秒AV延迟起搏证明了每个<0.001）。最初的SBP降低后是反弹效应，这减弱了SAVD起搏的SBP降低效应，这可能是由于气压感受器激活导致周围阻力增加所致。间歇性引入较长的AV延迟起搏可消除压力反射，从而消除了这种影响。这些发现提供了依据和最新的数据基础的证据，这些数据表明尽管进行了药物治疗，但对高血压患者的这种心脏神经调节治疗产生了显着的长期血压降低。