Sympathetic and baroreflex function in hypertensive or heart failure patients with ventricular arrhythmias
Sympathetic and baroreflex function in hypertensive or heart failure patients with ventricular arrhythmias
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DOI：
10.1097/00004872-200409000-00019
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发表时间：
2004-09-01
影响因子：
4.9
通讯作者：
Mancia, G
中科院分区：
文献类型：
--
作者：
Grassi, G;Seravalle, G;Mancia, G
目的 确定高血压和心力衰竭中室性心律失常的发生是否与交感神经驱动和压力感受反射功能的改变有关。 设计和方法 我们研究了 28 名未经治疗的原发性高血压患者（年龄，53.0 +/- 1.1 岁，平均值的平均标准误），15 名没有单灶性室性早搏 (PVC) 的 Lown I 级患者和 13 名患有单灶性室性早搏 (PVC) 的 Lown I 级患者，以及 30 名心力衰竭患者（年龄，53.0 +/- 1.1 岁，平均标准误）。纽约健康协会 II-III 级中的 53.8 +/- 1.3 岁），17 名无 PVC 的患者和 13 名有 PVC 的患者也属于 Lown I 级。我们对每位患者以及超声心动图变量进行了测量，包括逐次平均血压 (Finapress)、心率 (HR) (EKG)、肌肉交感神经流量 (MSNA)（显微神经造影）、静脉血浆去甲肾上腺素和肾素活性（高压液相色谱法和超声心动图）。分别为放射免疫测定法）。测量在休息时以及动脉压力感受器刺激和失活期间进行，分别通过逐步静脉输注去氧肾上腺素和硝普钠。结果在没有和有 PVC 的高血压患者中，平均血压、HR 和 MSNA 相似。然而，与非心律失常患者相比，伴有 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)。伴有室性早搏的心力衰竭患者的血流动力学和超声心动图变量与无室性早搏的患者重叠。然而，与这些患者相比，他们的 MSNA 值显着增加（75.8 +/- 3.0 与 63.6 +/- 2.8 bs/100 hb，P < 0.05），同时压力反射-HR 和压力反射-MSNA 控制显着受损（-52.5 +/- 5.4 和 -37.5 +/- 3.6%，P < 0.01）。 结论这些数据提供的证据表明，在高血压和心力衰竭中，交感神经和压力反射机制发挥促心律失常的作用。然而，这种作用在心力衰竭中似乎比在高血压中更明显，在高血压中受损的迷走神经功能可能会产生伴随的有利作用。 (C) 2004 年利平科特·威廉姆斯·威尔金斯。
Objective To determine whether in hypertension and in heart failure the occurrence of ventricular arrhythmias is associated with alterations in sympathetic drive and baroreflex function.Design and methods 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.Results 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 exibited 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).Conclusions 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. (C) 2004 Lippincott Williams Wilkins.