SUMMARY Serum myoglobin concentration and creatine kinase activity were measured serially in 70 consecutive patients presenting within four hours of the onset of symptoms of suspected acute myocardial infarction. Of 36 patients with definite or possible myocardial infarction (WHO criteria), the serum myoglobin concentration was raised (>85 ,g/l) one hour after the onset of symptoms in 25% and at four hours in 890/o. Creatine kinase activity was raised (>140 U/1) one hour after the onset in 25% and at four hours in only 56%. Within 12 hours of the onset of symptoms the myoglobin concentration reached a peak in 83% and the creatine kinase a peak in only 14%. Within 36 hours the myoglobin concentration fell to normal values in 67% while creatine kinase activity fell to normal values in only 3%. Four hours after the onset of symptoms the serum myoglobin concentration distinguished easily those patients with myocardial infarction from those without, whereas when creatine kinase values were used the sensitivity was poor but the specificity high.From the combined results of the two studies and using a single measurement of serum myoglobin concentration at six hours from the onset of symptoms to predict the diagnosis in 114 patients with suspected infarction, the sensitivity was 93% and specificity 890/o.Kiss and Reinhart' first reported abnormal serum PART 1 concentrations of myoglobin 10 to 12 hours after acute Seventy consecutive patients with symptoms suggesmyocardial infarction. Since then, others have ting acute myocardial infarction-that is, typical disconfirmed that most patients with acute myocardial tribution of chest pain with or without electrocardioinfarction have a raised serum myoglobin concentra-graphic changes-and presenting to a mobile and tion shortly after admission to hospital.2-5 Sylven, hospital coronary care unit within four hours of the using data from 40 patients admitted within six hours onset of symptoms were studied. Blood samples were of the onset of symptoms of infarction, estimated that obtained at the time of presentation and at two hourly 20% would have raised serum myoglobin concentra-intervals for 48 hours using an indwelling cannula. tions one hour after the onset of symptoms.6Using an automated colorimetric technique serum Using a mobile coronary care unit we are able to creatine kinase activity was measured in the assess patients at an earlier stage after myocardial refrigerated serum.7 Serum myoglobin concentration infarction. In this study we compared the serum was measured in the frozen serum using a myoglobin concentration with the serum creatine kin-radioimmunoassay (Nuclear Medical Systems).

In this study of 35 patients with a definite or possible myocardial infarction seen within the first 5 h of the onset of symptoms and who could clearly define the onset of symptoms, the serum myoglobin was raised in 20% of those in whom blood was sampled within 1 h of the acute event. In 11 of the 35 (31%) patients the serum myoglobin was normal in the first blood sample. Of the nine patients seen within the first 2 h of the onset of symptoms who had frequent samples taken, the first raised serum myoglobin was recorded from 45 min to 3 h 15 min after the onset of symptoms. The serum levels started to rise 15–20 min before levels greater than 85 ng/mL were reached. In the absence of further chest pain more than one peak in serum myoglobin was recorded in 58% of the patients with acute myocardial infarction. The serum myoglobin level returned to normal within 24 h of the onset of symptoms in 44% of patients and within 36 h in 67%.

SUMMARY Study of 80 consecutive patients undergoing elective diagnostic cardiac catheterisation showed that after the procedure 25 (31%) developed myoglobinaemia. This was attributed to complications of the catheterisation in two. The remaining 23 had received premedication by intramuscular injection. In patients without intramuscular injections myoglobinaemia did not occur after uncomplicated cardiac catheterisation.The study did not support the proposition that cardiac catheterisation results in myocardial damage which can be detected by abnormalities of myoglobin but not by conventional indications of myocardial necrosis.Cardiac catheterisation,' and in particular coronary arteriography,2 have a significant morbidity and mortality; myocardial infarction occurs in a small proportion of patients34 and angina pectoris in a further number.5 Urinary myoglobin has been measured after routine cardiac catheterisation using an indirect haemagglutination method;6 it was detected in 39 (27%) of 146 patients.6 This was attributed to transient and perhaps reversible myocardial injury. All the 146 patients had received premedication by intramuscular injection.Excretion of myoglobin in the urine was first described after extensive skeletal muscle injury.7 It has since been found to be a reliable indicator of myocardial infarction. Eighty consecutive patients undergoing elective cardiac catheterisation were studied. The patients were randomised into two groups, so that half received premedication orally, and half by intramuscular injection. The premedicant drug was determined by the physician undertaking the catheterisation. Most patients received 10 mg diazepam (Valium). Some were given 50 mg pethidine and 25 mg promethazine (Phenergan). One received 25 mg pethidine, 6.25 mg chlorpromazine, and 6*25 mg promethazine. Premedication was given one hour before the catheterisation was started.A venous blood sample was obtained before the administration of the premedication and one, four, eight, and 24 hours after it. Serum creatine kinase was measured in all samples, using an automated method. Serum myoglobin was measured in all samples by radioimmunoassay. Serum aspartate transaminase, lactic dehydrogenase, and blood urea were measured in the first and last samples.Electrocardiograms were recorded before and after the catheterisation. The contrast medium used in all cases was Urografin 370 (meglumine diatrizoate and sodium diatrizoate).

No abstract