Digitalis and myocardial infarction in man.

Abstract

The use of digitalis after acute myocardial infarction is controversial. The effect of digoxin on computer-quantitated thallium-201 perfusion scintigrams (Tl-201), left ventricular (LV) ejection fraction (EF), and percentage of abnormally contracting LV regions (% ACR) was determined in 23 patients. A correlation was established between creatine kinase MB isoenzyme release and initial radionuclide-gated blood pool wall motion estimates of EF (r = -0.73) and % ACR (r = 0.71). After radionuclide assessments, 14 patients received digoxin 18 +/- 23 hours (mean +/- SD) after the rise in CK-MB from baseline, while the remaining nine patients served as controls. In the control group, the mean EF was 0.33 +/- 0.12 on the first study and 0.30 +/- 0.08 on the second study (p = NS). In the digoxin group, the EF after digoxin administration (mean 0.33 +/- 0.11) was significantly different from the initial EF (mean 0.29 +/- 0.09, p less than 0.03); however, digoxin had no apparent effect on infarct size as assessed by sequential % ACR and Tl-201 perfusion data. These data indicate that digoxin resulted in a minimal but significant improvement in EF that did not occur at the expense of LV perfusion or regional wall motion.

High Doses of Digitalis Increase the Myocardial Production of Proinflammatory Cytokines and Worsen Myocardial Injury in Viral Myocarditis

“…7 This finding has been reported before, though its clinical relevance is unclear. 8 The growing awareness of neurohumoral activation as a contributing factor in the progression of chronic heart failure has redirected attention onto the modulating effects of digoxin on the neurohumoral and autonomic status.…”

Cardiac lysosomes and the mechanism of action of ouabain

“…By contrast, sharp increase in the activity of acid hydrolases caused by toxic dose of the preparation (50 mg/kg) is an unfavorable factor promoting the development of focal necrosis and dystrophy, which was observed in intoxication with cardiac glycosides [17].…”

How to digitalize and to maintain optimal digoxin levels in cogestive heart failure

“…Differences between experimental and clinical studies may be related, at least partially, to the timing of administration of glycosides, acetyl strophantin being given acutely in experimental studies, and glycosides being given an average of 24-48 hours after infarction in clinical studies. Although clinical studies did not show that patients with acute myocardial infarction are more prone to develop toxicity at therapeutic doses, Morrison et al [55] were able to show a beneficial effect in patients with significant left ventricular dysfunction, suggesting that the use of digoxin is both safe and effective in the treatment of congestive heart failure in the setting of an acute myocardial infarction. Some studies suggest that the long-term use of digoxin in post-myocardial infarction may decrease survival, however, these studies were not designed to answer this question [56][57][58].…”