Grassi Guido, Seravalle Gino, Quarti-Trevano Fosca, Dell'Oro Raffaella, Arenare Francesca, Spaziani Domenico, Mancia Giuseppe
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy.
Hypertension. 2009 Feb;53(2):205-9. doi: 10.1161/HYPERTENSIONAHA.108.121467. Epub 2009 Jan 5.
The sympathetic overdrive that characterizes essential hypertension is potentiated when left ventricular hypertrophy or congestive heart failure is detected. No information exists, however, on whether this is the case also for left ventricular diastolic dysfunction. In 17 untreated hypertensive subjects with left ventricular diastolic dysfunction (age: 47.7+/-2.9 years, mean+/-SEM), we measured sympathetic nerve traffic (microneurography), heart rate (ECG), and beat-to-beat arterial blood pressure (Finapres) at rest and during baroreceptor deactivation and stimulation. Data were compared with those collected in 20 age-matched normotensive and 20 hypertensive subjects without a diastolic function impairment. Muscle sympathetic nerve traffic values were markedly and significantly greater in the 2 hypertensive groups than in the normotensive one (55.3+/-1.2 and 71.2+/-1.6 versus 41.7+/-1.0 bursts per 100 heartbeats, respectively; P<0.01 for both). For a similar blood pressure elevation, however, the sympathetic nerve traffic increase was significantly greater in patients with than without left ventricular diastolic dysfunction (+28.9%; P<0.05). In the population as a whole, muscle sympathetic nerve traffic was significantly and inversely related to various echocardiographic indices of diastolic function. Although baroreflex-heart rate control was significantly attenuated in the 2 hypertensive groups, baroreflex-sympathetic modulation was impaired only in those with diastolic dysfunction. These data provide the first evidence that, in hypertension, activation of the sympathetic nervous system may contribute not only at the blood pressure elevation but also at the development of left ventricular diastolic dysfunction. The sympathetic overactivity, which is likely to be related to the baroreflex impairment, may account for the increased cardiovascular risk characterizing diastolic dysfunction.
当检测到左心室肥厚或充血性心力衰竭时，原发性高血压所特有的交感神经过度兴奋会增强。然而，关于左心室舒张功能障碍是否也是这种情况，目前尚无相关信息。在17名未经治疗的患有左心室舒张功能障碍的高血压受试者（年龄：47.7±2.9岁，平均值±标准误）中，我们在静息状态以及压力感受器失活和刺激期间测量了交感神经活动（微神经ography）、心率（心电图）和逐搏动脉血压（Finapres）。将数据与20名年龄匹配的血压正常者以及20名无舒张功能障碍的高血压受试者收集的数据进行比较。两个高血压组的肌肉交感神经活动值明显且显著高于血压正常组（分别为每100次心跳55.3±1.2次和71.2±1.6次爆发，而血压正常组为41.7±1.0次爆发；两者均P<0.01）。然而，对于类似的血压升高，有左心室舒张功能障碍的患者交感神经活动增加明显大于无此障碍的患者（增加28.9%；P<0.05）。在总体人群中，肌肉交感神经活动与舒张功能的各种超声心动图指标显著负相关。虽然两个高血压组的压力反射-心率控制明显减弱，但压力反射-交感神经调节仅在有舒张功能障碍的患者中受损。这些数据首次证明，在高血压中，交感神经系统的激活不仅可能导致血压升高，还可能导致左心室舒张功能障碍的发生。交感神经过度活跃可能与压力反射受损有关，这可能解释了舒张功能障碍所特有的心血管风险增加。
