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Effects of verapamil in patients with acute myocardial infarction: Hemodynamics and function of normal and ischemic left ventricular myocardium
Authors:Juhani Heikkilä  Markku S. Nieminen
Affiliation:1. Cardiovascular Laboratory, First Department of Medicine, University Central Hospital Helsinki, Finland.;2. the Intensive Care Unit, First Department of Medicine, University Central Hospital Helsinki, Finland.
Abstract:
We evaluated the effects of intravenous verapamil, a calcium antagonist, on hemodynamics and regional left ventricular (LV) performance in patients with acute myocardial infarction (AMI). Twenty patients having uncomplicated infarction or moderate heart failure were randomized to receive either verapamil or placebo and were studied a mean of 12 hours after onset of symptoms. Verapamil, 7.5 mg intravenously, acutely reduced systolic arterial pressure (p < 0.0005), systemic vascular resistance, and LV stroke work (p < 0.005) and rate-pressure product (p < 0.05); the heart rate did not alter. The Frank-Starling relationship by Swan-Ganz catheter did not change for 1 hour. Segmental wall motion amplitudes were recorded from eight standardized segments around the left ventricle by a multidirectional M-mode echocardiographic technique. The systolic wall motion of the uninvolved LV segments and LV cavity size did not change after verapamil. Verapamil improved mechanical performance in the ischemic segments (p < 0.005). Therefore, the overall regional contractile function of the left ventricle improved as well (by 11% to 13%, p < 0.05). This echocardiographic improvement continued after the acute vasodilatory response of intravenous verapamil subsided and was preserved for 1 week, the patients having had oral verapamil, 240 mg daily. Chest pain was relieved in five of the six patients having ongoing slight pain before verapamil injection. No sequential hemodynamic or echocardiographic changes occurred in the placebo-treated patients. Thus, in patients with uncomplicated AMI, verapamil improve contractile function of the acutely ischemic LV segments by hemodynamic unloading and/or by direct myocardial effect, without manifest depression of the uninvolved myocardium.
Keywords:Reprint requests: Juhani Heikkilä   M.D.   Cardiovascular Laboratory   University Central Hospital   SF-00290 Helsinki 29   Finland.
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