Duration of chest pain associated with acute myocardial infarction: a predictor of long-term prognosis.

This paper describes 109 patients who had their first myocardial infarction and were then followed up for 3 to 8 years. The following data were collected at the time of the infarction: duration and severity of chest pain, type of infarction and peak SGOT (serum glutamic oxaloacetic transaminase) level. The duration of chest pain has previously been shown to correlate with infarct size. Duration of chest pain, age and peak SGOT level were found to be the most important predictors of survival. None of the other independent variables contributed further to survival when the effects of duration of pain, age and SGOT level were taken into account. However, there was a significant association between pain duration and functional status. These data suggest that the duration of chest pain during first myocardial infarctions is a predictor of long-term prognosis and probably of functional status.

Chest pain duration in myocardial infarction.

Routine clinical and laboratory data were collected from 70 patients with first myocardial infarcts. Compared with the 35 patients whose chest pain duration was less than eight hours, those with chest pain eight hours or longer had higher rises in creatine phosphokinase and SGOT levels, greater summed ST segments (taken from the 12-lead ECG), more transmural infarcts, greater cardiac volumes (measured from subsequent chest roentgenograms), higher temperature rises, and higher WBC counts. These reuslts suggest that pain duration may be an indicator of infarct size.

Chest pain in the early recognition of large infarcts.

Among 90 patients admitted to hospital with a diagnosis of first myocardial infarction consistent significant associations were found between pain duration, increase in concentration of serum glutamic oxaloacetic transminase (SGOT), maximum temperature and type of infarct (transmural or nontransmural). This suggests that infarct size may be associated with pain duration, increase in SGOT concentration and maximum temperature, and that patients with transmural infarcts have larger infarcts than those with nontransmural infarcts. A higher incidence of premonitory pain -- in particular, premonitory rest pain -- was noted in patients with transmural infarcts, who also had a significantly higher leukocyte count than patients with nontransmural infarcts. Pain intensity was also found to be associated directly with increase in SGOT concentration. However, because intergroup differences were not significant consistently, the association between infarct size, premonitory pain, pain intensity and leukocytosis is less certain. If the association between pain duration and infarct size is confirmed, a simple means would be available for the early recognition of the patient with a large infarct and adverse prognosis who would benefit from prompt therapeutic measures to reduce infarct size.

Recurrent electromechanical dissociation due to severe underlying coronary heart disease.

Recurrent electromechanical dissociation, eventually fatal, presented as Stokes-Adams-like syncope in a patient with severe underlying coronary heart disease. Mechanical function was probably suppressed because of myocardial ischemia due to recent occlusion of the proximal right main coronary artery; the left main coronary artery had been occluded previously. Spasm of the proximal right coronary artery may have accounted for his recurrent attacks of pain and syncope. It is suggested that this clinical picture has a grave prognosis, demanding urgent therapeutic measures. While these measures are likely to be more hazardous than usual, the grave prognosis and potential for therapeutic success make them well worth the risk.

Changes in serum creatine phosphokinase during submaximal exercise testing.

The changes in creatine phosphokinase with exercise were studied in 70 subjects who had a submaximal exercise electrocardiogram carried out as part of their routine medical investigation. A significantly greater proportion of the subjects with a positive exercise ECG had a rise in CPK following exercise than did the subjects with a negative exercise ECG. The former had significantly lower initial CPK values, and this difference could be related to the different alteration of CPK with exercise in the two groups, for example by indicating a lower level of physical fitness in the group with positive exercise ECGs. However, the most likely explanation for the greater tendency of subjects with a positive exercise ECG to show a rise in CPK following exercise is greater CPK efflux from their ischemic myocardium.With refinements, measurement of CPK before and after exercise could be useful in helping to evaluate the diagnostic significance of the exercise ECG.