The value of the electrocardiogram in assessing infarct size was studied using serial estimates of the MB isomer of creatine kinase (CK MB) in plasma, serial 35 lead praecordial maps in 28 patients with anterior myocardial infarction, and serial 12 lead electrocardiograms in 17 patients with inferior myocardial infarction. In patients with anterior infarcts, sigma ST, sigma R, sigma Q, sigma R/(Q+S), and the number of sites with ST elevation more than 2 mm or with QS waves, were obtained from each map. Correlation between both maximum sigma Q and maximum sigma ST with cumulative CK MB was highly significant. There was also a significant correlation between sigma R and sigma R/(Q+S) with cumulative CK MB. There was no significant correlation between maximum number of sites with ST elevation or with Q or QS waves and cumulative CK MB. Maximum sigma ST and number of sites with ST elevation predicted maximum sigma Q and number of sites with QS or Q waves at a time when infarction was not complete. In patients with inferior infarcts, there was a significant correlation between maximum sigma Q and maximum sigma ST in leads II, III, and a VF, and cumulative CK MB. This study shows that all the waves in the electrocardiogram are useful in assessing infarct size. The fact that maximum sigma ST predicts final sigma Q may be used to assess the efficacy of interventions designed to salvage ischaemic myocardium.
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.
Selection work with the Rhode Island Red breed, involving the extensive collection of records, was first started at Wye College in 1948. Since that time the methods of selection employed have changed substantially in the light of the experience gained and the scheme, as it is operated at present, is shown diagrammatically in Fig. 1.Sixty full-sister groups are recorded from first egg to the end of November. At least three full brothers of each of these sister groups.
The ratio of 6β-hydroxycortisol to 17-hydroxycorticosteroids in the urine of 73 patients with liver disease, and 53 controls has been measured. The mean ratio was significantly greater in the liver disease group (p < 0.001), this elevation being most marked among patients with liver metastases and patients with acute hepatitis. We feel that the use of the ratio as a test of early liver cell dysfunction requires further evaluation, in particular in the early recognition of metastatic liver disease.
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