Abstract
Early studies suggested that digitalis exacerbated ischemia (ST segment data); however, there are no studies assessing the effect of this agent on anatomic infarct size with the use of a risk zone technique. Therefore, the aim of this study was to assess quantitatively whether digitalis extends necrosis in a model of coronary artery occlusion. Anesthetized dogs were subjected to 6-hour occlusion and, 30 minutes after occlusion, were randomized to digoxin (250 μg bolus/5 min intravenously, n = 9) or saline (n = 9) groups. At 6 hours, in vivo area at risk was determined by monastral blue dye injection and area of necrosis was assessed by tetrazolium staining. Heart rate and blood pressure were not different between groups before treatment or at 6 hours after occlusion. Left ventricular dPdt was similar in both groups before occlusion (2350 ± 293 mm Hg/sec digoxin vs 1839 ± 122 mm Hg/sec saline, p = NS), but after 6 hours of coronary occlusion, had increased in the digoxin group to 2583 ± 340 mm Hg/sec while it decreased in the saline group to 1517 ± 128 mm Hg/sec (p < 0.05 between groups at 6 hours), suggesting that digoxin increased contractility. Area at risk was 17.7 ± 1.3% of the left ventricle in the digoxin group and 20.9 ± 2.0% of the left ventricle in the saline group (p = NS). Area of necrosis, expressed as a percentage of area at risk, was 90.0 ± 3.5% in the digoxon group vs 88.6 ± 2.1% in the saline group (p = NS). Therefore, during acute myocardial infarction, digitalis confers a moderate increase in contractility without extending necrotic damage.
Published Version
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