Intracoronary thrombolysis during acute myocardial infarction in human beings is associated with rapid release of creatine kinase and improvement of the cardiac ejection fraction. To examine the phenomenon of spontaneous coronary-artery recanalization, we studied the release of creatine kinase MB and sequential radionuclide ventriculograms in 52 patients with transmural myocardial infarction. Patients were divided into two groups according to whether the release of creatine kinase MB (time from base-line to peak serum level) was rapid (n = 24) or slow (n = 28). Patients with slow release had no significant change in global or regional ejection fraction from the time of admission to discharge. However, global ejection fraction in patients with rapid release improved from 0.38 +/- 0.09 (mean +/- S.D.) to 0.48 +/- 0.08 (P less than 0.001). The regional ejection fraction of Q-wave regions also improved, from 0.33 +/- 0.11 to 0.43 +/- 0.13 (P less than 0.001). A negative correlation (r = -0.52, P less than 0.001) existed between time to peak enzyme level and degree of improvement in ejection fraction. With increasing left ventricular damage, patients with rapid release had greater increments in creatine kinase MB than comparable patients with slow release (P = 0.03), suggesting enzyme washout. These data are consistent with the idea that spontaneous reperfusion, leading to altered enzyme release and improvement in ventricular function, is not uncommon after acute myocardial infarction.
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.
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