Grines C L, Booth D C, Nissen S E, Gurley J C, Bennett K A, DeMaria A N
Division of Cardiology, College of Medicine, University of Kentucky, Lexington.
J Am Coll Cardiol. 1991 May;17(6):1382-7. doi: 10.1016/s0735-1097(10)80151-2.
Although the mechanism is unknown, clinical trials have suggested that intravenous beta-adrenergic blockade may prevent early cardiac rupture after myocardial infarction. Previous studies have examined effects of beta-blockers on global left ventricular function after myocardial infarction; however, few data exist regarding their immediate effects on regional function or in patients after successful reperfusion. Therefore, 65 patients in whom thrombolysis with or without coronary angioplasty achieved reperfusion at 4.6 +/- 1.7 h from symptom onset were studied. Low osmolarity contrast ventriculograms were obtained immediately before and after administration of 15 mg of intravenous metoprolol (n = 54) or placebo (n = 11). Intravenous metoprolol immediately decreased heart rate (from 92 to 76 beats/min, p less than 0.0001), increased left ventricular diastolic volume (from 150 to 163 ml, p less than 0.001) and systolic volume (from 72 to 77 ml, p less than 0.0005) but did not change systolic and diastolic pressures. Although there was no difference in ejection fraction after metoprolol, centerline chord analysis revealed reduced noninfarct zone motion (from 0.41 to 0.12 SD/chord, p less than 0.05), improved infarct zone motion (from -3.1 to -2.9 SD/chord, p less than 0.01) and smaller circumferential extent of hypokinesia (from 30 to 27 chords, p less than 0.05). Patients with dyskinesia of the infarct zone had the most striking improvement in infarct zone wall motion. Because these changes occurred immediately after beta-blockade, they could not be attributed to myocardial salvage. No significant changes in heart rate, left ventricular volumes or regional wall motion were apparent in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
尽管其机制尚不清楚,但临床试验表明静脉注射β-肾上腺素能阻滞剂可能预防心肌梗死后早期心脏破裂。以往的研究探讨了β受体阻滞剂对心肌梗死后左心室整体功能的影响;然而,关于其对局部功能的即时影响或成功再灌注后患者的相关数据却很少。因此,我们对65例在症状发作后4.6±1.7小时通过溶栓或联合冠状动脉成形术实现再灌注的患者进行了研究。在静脉注射15毫克美托洛尔(n = 54)或安慰剂(n = 11)之前和之后立即进行低渗造影剂心室造影。静脉注射美托洛尔可立即降低心率(从92次/分钟降至76次/分钟,p < 0.0001),增加左心室舒张末期容积(从150毫升增至163毫升,p < 0.001)和收缩末期容积(从72毫升增至77毫升,p < 0.0005),但不改变收缩压和舒张压。尽管美托洛尔治疗后射血分数无差异,但中心线弦分析显示非梗死区运动减弱(从0.41标准差/弦降至0.12标准差/弦,p < 0.05),梗死区运动改善(从-3.1标准差/弦升至-2.9标准差/弦,p < 0.01),运动减弱的圆周范围缩小(从30弦降至27弦,p < 0.05)。梗死区运动障碍的患者梗死区壁运动改善最为显著。由于这些变化在β受体阻滞剂注射后立即出现,因此不能归因于心肌挽救。对照组的心率、左心室容积或局部壁运动无明显变化。(摘要截短至250字)