Yang Bing, Wang Yue, Zhang Fengxiang, Ju Weizhu, Chen Hongwu, Mika Yuval, Aviv Ricardo, Evans Steven J, Burkhoff Daniel, Wang Jie, Chen Minglong
Cardiology Division, the First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China.
Academy of Clinical and Translational Research, Jiangsu Province, The First Affiliated Hospital of Nanjing Medical University, Nanjing, P. R. China.
J Am Soc Hypertens. 2018 May;12(5):381-391. doi: 10.1016/j.jash.2018.03.004. Epub 2018 Mar 21.
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.
我们评估了通过基于引入短房室(AV)延迟(SAVD)的标准双腔起搏所传递的心脏起搏算法来实现急性、持续性血压降低的可行性。本研究纳入了18名高血压患者(年龄57.3±9.8岁;男性10名,女性8名),这些患者已计划接受侵入性电生理检查,其平均初始收缩压和舒张压分别为151.2±17.6/92.2±12.7 mmHg。在进行高保真血压测量时,以80、40、20和2毫秒的AV延迟,按约1分钟的间隔应用起搏序列。2毫秒AV延迟起搏显示收缩压平均降低19.6±7.7 mmHg,舒张压平均降低4.3±3.8 mmHg(每项P<0.001)。初始收缩压降低后出现反跳效应,这减弱了SAVD起搏对收缩压的降低作用,可能是由于压力感受器激活导致外周阻力增加。通过间歇性引入较长AV延迟起搏来调节压力反射,这种效应得以消除。这些发现为近期的数据提供了理论依据和证据,这些数据表明,尽管进行了药物治疗,但这种心脏神经调节疗法仍能使高血压患者的血压显著且长期降低。