Petretta M, Bonaduce D, Marciano F, Bianchi V, Valva G, Apicella C, de Luca N, Gisonni P
Institute of Internal Medicine, Cardiology and Heart Surgery, University of Naples "Federico II," Italy.
Hypertension. 1996 Mar;27(3 Pt 1):330-8. doi: 10.1161/01.hyp.27.3.330.
In this study we evaluated in hypertensive patients the effects of drug-induced left ventricular hypertrophy regression on cardiac autonomic control, as assessed by means of heart period variability analysis. Power spectral analysis of 24-hour electrocardiographic monitoring was performed in 30 hypertensive patients with left ventricular hypertrophy at baseline, after 1 year of lisinopril treatment, and after 1 month of drug withdrawal. At the same times, patients underwent 24-hour blood pressure monitoring, echocardiographic study, and plasma renin activity assessment. Lisinopril treatment increased plasma renin activity and reduced 24-hour systolic and diastolic pressures (from 159 +/- 14 to 121 +/- 8 and from 103 +/- 7 to 80 +/- 3 mm Hg, respectively) and left ventricular mass index (from 159 +/- 33 to 134 +/- 26 g/m2); moreover, in 12 of 30 patients, left ventricular mass normalization was achieved. Drug withdrawal was followed by an increase in blood pressure without left ventricular mass modification. In the total study population, only high-frequency power was higher after lisinopril treatment. In the subgroup of patients with left ventricular mass normalization, daytime and nighttime high-frequency powers as well as nighttime total and very-low-frequency powers were higher after 1 year of treatment than at baseline. In the remaining 18 patients, power spectral measures after treatment were slightly lower than at baseline and were even lower after drug withdrawal. Thus, in hypertensive hypertrophic patients, lisinopril treatment improves sympathovagal imbalance when left ventricular mass normalization is achieved. In patients without left ventricular mass normalization, drug withdrawal is followed by a worsening of neural cardiac control.
在本研究中,我们通过心率变异性分析评估了药物诱导的左心室肥厚消退对高血压患者心脏自主神经控制的影响。对30例基线时患有左心室肥厚的高血压患者在接受赖诺普利治疗1年后以及停药1个月后进行了24小时心电图监测的功率谱分析。同时,患者接受了24小时血压监测、超声心动图检查和血浆肾素活性评估。赖诺普利治疗增加了血浆肾素活性,降低了24小时收缩压和舒张压(分别从159±14降至121±8,从103±7降至80±3 mmHg)以及左心室质量指数(从159±33降至134±26 g/m²);此外,30例患者中有12例实现了左心室质量正常化。停药后血压升高,但左心室质量未改变。在整个研究人群中,仅赖诺普利治疗后高频功率较高。在左心室质量正常化的患者亚组中,治疗1年后白天和夜间的高频功率以及夜间的总功率和极低频功率均高于基线水平。在其余18例患者中,治疗后的功率谱测量值略低于基线水平,停药后甚至更低。因此,在高血压肥厚患者中,当实现左心室质量正常化时,赖诺普利治疗可改善交感迷走神经失衡。在未实现左心室质量正常化的患者中,停药后心脏神经控制会恶化。