Grassi Guido, Seravalle Gino, Bertinieri Giovanni, Stella Maria Luisa, Turri Carlo, Mancia Giuseppe
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano -Bicocca, Ospedale San Gerardo, Monza, Milan, Italy.
Hypertension. 2002 Apr;39(4):886-91. doi: 10.1161/01.hyp.0000013265.48954.a5.
Provoked premature ventricular contractions (PVCs) evoke, in concomitance with an early and late blood pressure fall and overshoot, an early sympathoexcitation and a later period of sympathoinhibition, respectively. The present study was designed to examine whether in healthy subjects this is the case for spontaneous PVCs. Because of their pathophysiological relevance for arrhythmogenesis, it was also designed to determine whether the sympathetic responses are different from those seen in essential hypertension and congestive heart failure. In 14 untreated mild essential hypertensives (EH; age, 53.8+/-2.6 years; mean+/-SEM), 20 untreated congestive heart failure patients (CHF; age, 56.7+/-2.5 years; New York Heart Association class, II or III), and 16 age-matched healthy subjects (control) in Lown class <II, we evaluated the blood pressure (Finapres), heart rate (ECG), and muscle sympathetic nerve traffic (MSNA; by microneurography) responses to isolated monofocal PVCs. MSNA, quantified as bursts/100 heart beats, was significantly increased in EH (57.8+/-3.8, P<0.05) and CHF patients (77.7+/-4.0, P<0.01) compared with controls (44.6+/-4.4). In controls, the PVC-induced blood pressure fall and overshoot were accompanied by a sympathoexcitation (144.2+/-14%), followed by a period of sympathoinhibition (average duration, 12043+/-985 ms). The responses were similar in EH but not in CHF, in whom the magnitude of the sympathoexcitation and particularly the duration of the subsequent sympathoinhibition were strikingly reduced (average reduction, -46.1 and -72.8%, respectively). The most important factor accounting for this reduction appeared to be an altered baroreflex response to the PVC-induced BP changes. These data demonstrate that the MSNA responses to spontaneous PVCs are similar in controls and EH but markedly impaired in CHF, presumably because of the baroreflex alteration. This may represent an important factor for the genesis of the life-threatening ventricular arrhythmias that characterize CHF.
诱发性室性早搏（PVCs）在伴有早期和晚期血压下降及过冲时，分别会引起早期交感神经兴奋和后期交感神经抑制。本研究旨在探讨在健康受试者中，自发性PVCs是否也是这种情况。鉴于其在心律失常发生中的病理生理相关性，本研究还旨在确定交感神经反应是否与原发性高血压和充血性心力衰竭中的情况不同。在14名未经治疗的轻度原发性高血压患者（EH；年龄53.8±2.6岁；平均值±标准误）、20名未经治疗的充血性心力衰竭患者（CHF；年龄56.7±2.5岁；纽约心脏协会分级为II或III级）以及16名年龄匹配的Lown分级<II级的健康受试者（对照组）中，我们评估了对孤立单灶性PVCs的血压（Finapres）、心率（心电图）和肌肉交感神经活动（MSNA；通过微神经ography）反应。MSNA以每100次心跳的爆发次数来量化，与对照组（44.6±4.4）相比，EH患者（57.8±3.8，P<0.05）和CHF患者（77.7±4.0，P<0.01）的MSNA显著增加。在对照组中，PVC诱导的血压下降和过冲伴随着交感神经兴奋（144.2±14%），随后是一段交感神经抑制期（平均持续时间，12043±985毫秒）。EH患者的反应与之相似，但CHF患者不同，在CHF患者中，交感神经兴奋的程度尤其是随后交感神经抑制的持续时间显著缩短（平均减少分别为-46.1%和-72.8%）。导致这种减少的最重要因素似乎是压力反射对PVC诱导的血压变化的反应改变。这些数据表明，对照组和EH患者对自发性PVCs的MSNA反应相似，但CHF患者明显受损，推测是由于压力反射改变。这可能是CHF特征性的危及生命的室性心律失常发生的一个重要因素。
