Schobel H P, Langenfeld M, Gatzka C, Schmieder R E
Medizinische Klinik IV, University of Erlangen-Nurnberg, Germany.
Am Heart J. 1996 Nov;132(5):1004-9. doi: 10.1016/s0002-8703(96)90013-7.
This study was undertaken to compare the effects of alpha-receptor blockade and beta-receptor blockade on left ventricular structure and function in essential hypertension. The increase in left ventricular mass in patients with essential hypertension is at least partly induced by the sympathetic nervous system. We conducted a double-blind, randomized, controlled clinical trial to compare the effects of alpha-blockers and beta-blockers on left ventricular structure and function. Forty-three patients with mild to moderate essential hypertension were randomly allocated to receive antihypertensive therapy with either the alpha-blocker bunazosin (n = 23) or the beta-blocker metoprolol (n = 20). Twenty-four-hour blood pressure measurements and echocardiographic measurements of left ventricular structure and function were performed before therapy, after 6 months of therapy, and 4 weeks after discontinuation of therapy. Bunazosin and metoprolol led to similar reductions in systolic/diastolic blood pressure (-11 +/- 11/-9 +/- 8 mm Hg vs -11 +/- 12/-8 +/- 9 mm Hg, respectively) and left ventricular mass (-25 +/- 42 gm vs -28 +/- 44 gm, respectively) (p = no significant difference, bunazosin vs metoprolol). Neither metoprolol nor bunazosin significantly affected left ventricular systolic function. Diastolic left ventricular filling, however, was increased with beta-blocker medication, as indicated by a decrease in atrial filling fraction (39% +/- 5% to 34% +/- 5%; p < 0.05), but not with the alpha-blocker. The effect of metoprolol resulted from its bradycardiac effect. Four weeks after discontinuation of therapy, blood pressure and left ventricular mass increased to pretreatment levels in both groups similarly. Furthermore, the increase in diastolic filling was lost shortly after withdrawal of metoprolol concomitant with the increase in heart rate. We conclude that alpha-blockers and beta-blockers are equally capable of reducing left ventricular mass in hypertensive patients. beta-Blockers lead to an increase in diastolic left ventricular filling. This effect may be of therapeutic value because diastolic dysfunction may precede systolic dysfunction in hypertensive heart disease.
本研究旨在比较α受体阻滞剂和β受体阻滞剂对原发性高血压患者左心室结构和功能的影响。原发性高血压患者左心室质量增加至少部分是由交感神经系统引起的。我们进行了一项双盲、随机、对照临床试验，以比较α受体阻滞剂和β受体阻滞剂对左心室结构和功能的影响。43例轻度至中度原发性高血压患者被随机分配接受抗高血压治疗，其中23例使用α受体阻滞剂布那唑嗪，20例使用β受体阻滞剂美托洛尔。在治疗前、治疗6个月后以及停药4周后进行24小时血压测量和左心室结构及功能的超声心动图测量。布那唑嗪和美托洛尔导致收缩压/舒张压类似程度的降低（分别为-11±11/-9±8 mmHg和-11±12/-8±9 mmHg）以及左心室质量类似程度的降低（分别为-25±42 g和-28±44 g）（布那唑嗪与美托洛尔相比，p =无显著差异）。美托洛尔和布那唑嗪均未显著影响左心室收缩功能。然而，β受体阻滞剂治疗可增加左心室舒张期充盈，表现为心房充盈分数降低（从39%±5%降至34%±5%；p<0.05），而α受体阻滞剂则无此作用。美托洛尔的这一作用源于其减慢心率的作用。停药4周后，两组患者的血压和左心室质量均类似程度地回升至治疗前水平。此外，停用美托洛尔后不久，随着心率增加，舒张期充盈增加的情况消失。我们得出结论，α受体阻滞剂和β受体阻滞剂在降低高血压患者左心室质量方面同样有效。β受体阻滞剂可导致左心室舒张期充盈增加。这一作用可能具有治疗价值，因为在高血压性心脏病中舒张功能障碍可能先于收缩功能障碍出现。
