Variability of electrocardiographic and enzyme evolution of myocardial infarction in man.

Abstract

We have studied the time course of development of ST segment elevation, R wave loss, and Q wave development in 41 patients using 35 lead praecordial mapping or 12 lead electrocardiograms in those with anterior and inferior infarcts, respectively. The first recording was at a mean time of six hours after the onset of pain; subsequent records were taken every eight hours for 24 hours, every 12 hours for the second day, and every day thereafter. Serial CK MB estimates were obtained at every four hours for the first 72 hours. There was good agreement in the time course between the electrocardiogram and enzyme evolution. Forty-one per cent of patients showed rapid infarction with R wave and Q wave evolution complete within 12 hours of pain and accompanied by a short duration of enzyme release (mean = 19.30 hours). Fifty-nine per cent of patients showed more prolonged infarction with longer R wave and Q wave evolution and enzyme release (mean = 30 hours). Four patients also showed delayed reinfarction. ST segment elevation was maximal at six hours in the whole group and was significantly lower thereafter. Patients with rapid infarction showed high initial ST segment elevation which decreased promptly compared with those with prolonged infarction, who showed moderate but more persistent ST segment elevation. This study shows the variability in the time course of the electrocardiogram and enzyme evolution after myocardial infarction in man.

Effect of Early Metoprolol Injection Followed by Oral Dosage on CK-MB Release, and Myocardial Function in Suspected Acute Myocardial Infarction

“…Enzyme release was smaller in the metoproloi group unrelated to the site and type of infarction. The benefit of late-entry patients may be due to more subtotal occlu sions in late-entry patients [17] and due to continuation of cell death for 24 h or longer based on serial ECG R wave measurements and CK-MB release [18], Yet, our result on enzyme release is not consistent with the whole MIAMI material. In the latter a smaller enzyme release was found only in patients randomized early, but not in those randomized later than 7 h after the onset of symptoms [19].…”

Early Intravenous Beta-Blockade in Acute Myocardial Infarction

“…Most of the damage occurs during the first 6-12 h. About 50% of ECG signs of necrosis is com plete within 6 h, 75% within 12 h and nearly all by 18-24 h after the onset of pain [14], The frequency of pain and arrhythmias are highest during the first few hours; their fre quency then decreases rapidly [15]. Conse- Fig.…”

Early intravenous beta‐blockade in myocardial infarction.

“…Praecordial mapping showed that after six hours only about half of the total R wave loss had occurred, and we speculated whether up to this time the size of the infarct could be modified by treatment, (Figure 1 in Yusuf et al, 1981). The natural history of untreated infarction was not consistent: some (type A) produced a rapid CKMB release, but in an equal number (type B), the total release was slower and peaked at times up to 32 hours.…”