Why the study?
Does metoprolol reduce mortality rates in dogs with hypertension and left ventricular hypertrophy subjected to coronary occlusion?
Does metoprolol reduce mortality rates in dogs with hypertension and left ventricular hypertrophy subjected to coronary occlusion?
In a canine model of hypertension and left ventricular hypertrophy, beta-blockade with metoprolol, but not ACE inhibition with enalapril, significantly reduced early mortality from sudden cardiac death during coronary occlusion.
Answers are grounded in this paper and cite their sources.
May favor metoprolol over enalapril against sudden death in LVH models; hypothesis-generating and requires human validation.
Because beta-adrenergic blockade has as one of its many effects altered electrophysiological abnormalities after dogs with left ventricular hypertrophy have been subjected to coronary occlusion, we tested the hypothesis that metoprolol (200-400 mg/day) would reduce mortality rates in dogs with one-kidney, one clip left ventricular hypertrophy while a similar reduction in arterial pressure with enalapril (20-40 mg/day) would not. Dogs with left ventricular hypertrophy were given metoprolol or enalapril for 5-7 days before a 3-hour coronary occlusion. Infarct size and risk area were measured with triphenyltetrazolium chloride stain and barium angiography, respectively. For control (n = 15), left ventricular hypertrophy (n = 17), left ventricular hypertrophy plus metoprolol (n = 12), and left ventricular hypertrophy plus enalapril (n = 15) groups, mean arterial pressure, ratio of infarct size to risk area, and dogs experiencing sudden death were 110 +/- 4, 142 +/- 4, 121 +/- 7, and 120 +/- 3 mm Hg; 44 +/- 5%, 65 +/- 5%, 44 +/- 7%, and 30 +/- 4%; and 27%, 65%, 17%, and 53%, respectively. Thus, the excessive increase in early mortality occurring when dogs with hypertension and left ventricular hypertrophy undergo coronary occlusion is interrupted with beta-blockade, possibly via electrophysiological effects rather than by changes in arterial pressure or infarct size.
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Dellsperger et al. (1990) studied this question.
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