Grassi Guido, Seravalle Gino, Dell'Oro Raffaella, Facchini Annalisa, Ilardo Valeria, Mancia Giuseppe
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano Bicocca, Italy.
J Hypertens. 2004 Sep;22(9):1747-53. doi: 10.1097/00004872-200409000-00019.
To determine whether in hypertension and in heart failure the occurrence of ventricular arrhythmias is associated with alterations in sympathetic drive and baroreflex function.
We studied 28 untreated essential hypertensives (age, 53.0 +/- 1.1 years, mean +/- standard error of the mean), 15 without and 13 with monofocal premature ventricular contractions (PVCs) in Lown class I, and 30 heart failure patients (age, 53.8 +/- 1.3 years) in New York Health Association class II-III, 17 without and 13 with PVCs also in Lown class I. In each patient we measured, along with echocardiographic variables, the beat-to-beat mean blood pressure (Finapress), heart rate (HR) (EKG), muscle sympathetic nerve traffic (MSNA) (microneurography), venous plasma norepinephrine and renin activity (high-pressure liquid chromatography and radioimmunoassay, respectively). Measurements were performed at rest and during arterial baroreceptor stimulation and deactivation via stepwise intravenous infusion of phenylephrine and nitroprusside, respectively.
The mean blood pressure, HR and MSNA were similar in hypertensive patients without and with PVCs. However, compared with non-arrhythmic patients, hypertensives with PVCs displayed a baroreflex-HR and baroreflex-MSNA modulation reduced by 27.7 +/- 4.2 and 17.9 +/- 2.8%, respectively (P < 0.05). Heart failure patients with PVCs showed haemodynamic and echocardiographic variables superimposable to those without PVCs. Compared with these patients, however, they exhibited a significant increase in MSNA values (75.8 +/- 3.0 versus 63.6 +/- 2.8 bs/100 hb, P < 0.05), coupled with a significant impairment in baroreflex-HR and baroreflex-MSNA control (-52.5 +/- 5.4 and -37.5 +/- 3.6%, P < 0.01).
These data provide evidence that in both hypertension and heart failure, sympathetic and baroreflex mechanisms exert a pro-arrhythmogenic role. This role, however, appears to be more pronounced in heart failure than in hypertension, in which the impaired vagal function may exert a concomitant favouring effect.
确定在高血压和心力衰竭患者中，室性心律失常的发生是否与交感神经驱动和压力反射功能改变有关。
我们研究了28例未经治疗的原发性高血压患者（年龄53.0±1.1岁，均值±均值标准误），其中15例无单灶性室性早搏（PVC），13例为Lown I级单灶性PVC；以及30例纽约心脏协会II - III级心力衰竭患者（年龄53.8±1.3岁），其中17例无PVC，13例为Lown I级PVC。在每位患者中，除了测量超声心动图变量外，还测量逐搏平均血压（Finapress）、心率（HR）（心电图）、肌肉交感神经活动（MSNA）（微神经ography）、静脉血浆去甲肾上腺素和肾素活性（分别采用高压液相色谱法和放射免疫分析法）。测量在静息状态下进行，以及分别通过静脉逐步输注去氧肾上腺素和硝普钠进行动脉压力感受器刺激和失活时进行。
无PVC和有PVC的高血压患者的平均血压、HR和MSNA相似。然而，与无心律失常的患者相比，有PVC的高血压患者的压力反射 - HR和压力反射 - MSNA调节分别降低了27.7±4.2%和17.9±2.8%（P < 0.05）。有PVC的心力衰竭患者的血流动力学和超声心动图变量与无PVC的患者相当。然而，与这些患者相比，他们的MSNA值显著增加（75.8±3.0对63.6±2.8次/100次心跳，P < 0.05），同时压力反射 - HR和压力反射 - MSNA控制显著受损（分别为 - 52.5±5.4%和 - 37.5±3.6%，P < 0.01）。
这些数据表明，在高血压和心力衰竭中，交感神经和压力反射机制均发挥促心律失常作用。然而，这种作用在心力衰竭中似乎比在高血压中更为明显，在高血压中迷走神经功能受损可能会产生协同促进作用。
