Kumar B, Hood W B, Joison J, Gilmour D P, Norman J C, Abelmann W H
J Clin Invest. 1970 Feb;49(2):358-64. doi: 10.1172/JCI106244.
Use of digitalis in myocardial infarction is controversial. To determine the efficacy and toxic threshold, serial infusions of 3 mug/kg per min of acetyl-strophanthidin were given to six intact conscious dogs 24 hr before and 1 hr, 2 days, and 7 days after myocardial infarction induced by inflation of a balloon cuff implanted on the left anterior descending coronary artery. Within 1 hr after myocardial infarction, heart rate increased by 28%. Left ventricular end-diastolic pressure increased from 7 to 20 mm Hg, and stroke volume decreased by 25%. At this time acetylstrophanthidin caused no beneficial hemodynamic change, 1 wk later, the heart rate and left ventricular end-diastolic pressure had declined toward normal but remained elevated. At this time, acetylstrophanthidin lowered left ventricular end-diastolic pressure by 25%, and increased the stroke volume and cardiac output by 25% and 21% respectively, without any change in heart rate or aortic pressure. Tolerance to acetylstrophanthidin, defined as appearance of ventricular tachycardia, declined the 1st hr after myocardial infarction by 24% (P<0.05) from the control level of 43 +/-4 mug/kg (SEM), but subsequently returned to control.Thus, immediately after myocardial infarction, tolerance to acetylstrophanthidin was reduced, and left ventricular failure was not ameliorated. 1 wk later in the healing phase of myocardial infarction, tolerance to acetylstrophanthidin returned to normal and left ventricular performance was improved by this drug. The study suggests a limited therapeutic role for digitalis in the treatment of left ventricular failure in the acute phase immediately after myocardial infarction, but beneficial effects may occur in the healing phase 1 wk later.
洋地黄在心肌梗死中的应用存在争议。为确定其疗效和中毒阈值,对6只清醒的健康犬,在通过植入左前降支冠状动脉的球囊袖带充气诱导心肌梗死后24小时、1小时、2天和7天,以每分钟3微克/千克的速率连续输注乙酰洋地黄毒苷。在心肌梗死后1小时内,心率增加28%。左心室舒张末期压力从7毫米汞柱升至20毫米汞柱,每搏输出量减少25%。此时,乙酰洋地黄毒苷未引起有益的血流动力学变化。1周后,心率和左心室舒张末期压力已降至接近正常水平但仍高于正常。此时,乙酰洋地黄毒苷使左心室舒张末期压力降低25%,每搏输出量和心输出量分别增加25%和21%,而心率和主动脉压无任何变化。以室性心动过速的出现定义的对乙酰洋地黄毒苷的耐受性,在心肌梗死后第1小时较对照组水平43±4微克/千克(标准误)下降24%(P<0.05),但随后恢复至对照水平。因此,在心肌梗死后即刻,对乙酰洋地黄毒苷的耐受性降低,左心室衰竭未得到改善。在心肌梗死愈合期的1周后,对乙酰洋地黄毒苷的耐受性恢复正常,且该药改善了左心室功能。该研究提示洋地黄在心肌梗死后急性期治疗左心室衰竭中的治疗作用有限,但在1周后的愈合期可能产生有益效果。