A decision tree for the early diagnosis of acute myocardial infarction in nontraumatic chest pain patients at hospital admission

STUDY OBJECTIVE: To find an accurate algorithm for the diagnosis of acute myocardial infarction in nontraumatic chest pain patients on presentation to the emergency department. DESIGN: In a prospective clinical study, we compared the diagnostic performances of clinical symptoms, presenting ECG, creatinine kinase, creatine kinase MB activity and mass concentration, myoglobin, and cardiac troponin T test results of hospital admission blood samples. By classification and regression trees, a decision tree for the diagnosis of acute myocardial infarction was developed. SETTING: Emergency room of a Department of Internal Medicine (University Hospital). PATIENTS: One hundred fourteen nontraumatic chest pain patients (median delay from onset of chest pain to hospital admission, 3 h; range, 0.33 to 22): 26 Q-wave and 19 non-Q-wave myocardial infarctions, 49 patients with unstable angina pectoris, and 20 patients with chest pain caused by other diseases. MEASUREMENTS AND RESULTS: Of each parameter taken by itself, the ECG was tendentiously most informative (areas under receiver operating characteristic plots: 0.87 +/- 0.04 [ECG], 0.80 +/- 0.08 [myoglobin], 0.80 +/- 0.04 [creatine kinase MB mass], 0.77 +/- 0.04 [creatine kinase activity], 0.69 +/- 0.06 [clinical symptoms] 0.67 +/- 0.06 [creatine kinase MB activity], 0.67 +/- 0.05 [troponin T]). In patients presenting 3 h or less after the onset of chest pain, ECG signs of acute transmural myocardial ischemia were the best discriminator between patients with and without myocardial infarction. In patients presenting more than 3 h, however, creatine kinase MB mass concentrations (discriminator value, 6.7 micrograms/L) were superior to the ECG, clinical symptoms, and all other biochemical markers tested. This algorithm for diagnosing acute myocardial infarction was superior to each parameter by itself and was characterized by 0.91 sensitivity, a 0.90 specificity, a 0.90 positive and negative predictive value, and a 0.90 efficiency. CONCLUSIONS: We found an algorithm that could accurately separate the myocardial infarction patients from the others on admission to the emergency department. Therefore, this classifier could be a valuable diagnostic aid for rapid confirmation of a suspected myocardial infarction.     

Shed blood autotransfusion influences ischemia-sensitive laboratory parameters after coronary operations

The diagnostic significance of ischemia-sensitive laboratory parameters in respect to possible interference with shed blood autotransfusion was assessed in a prospective study with 100 patients undergoing elective coronary artery bypass grafting. Serum levels of creatine kinase, creatine kinase MB activity, creatine kinase MB mass concentration, 2-hydroxybutyrate dehydrogenase, lactate dehydrogenase-1, troponin-T, myoglobin, and glutamicoxaloacetic transaminase were repeatedly assessed up to the sixth postoperative day. Thirty-seven patients were excluded from the study due to postoperative development of myocardial infarction (n = 4), transient ischemic events (n = 25), and left bundle-branch blocks (n = 8). In the remaining group of 63, 37 patients were retransfused with 580 +/- 370 mL shed blood up to the twelfth postoperative hour, and 26 patients did not receive autotransfusion due to minimal mediastinal blood loss. The results of our study show that the ischemia-sensitive laboratory parameters were significantly influenced by shed blood autotransfusion: 8 hours postoperatively, creatine kinase (272%), creatine kinase MB fraction (151%), 2-hydroxybutyrate dehydrogenase (130%), lactate dehydrogenase-1 (133%), troponin-T (200%), myoglobin (159%) and glutamic-oxaloacetic transaminase levels (153%) were significantly elevated (p < 0.05) in patients with postoperative autotransfusion, although there were no electrocardiographic signs of myocardial ischemia in this group of patients. Our study shows that postoperative autotransfusion of mediastinal shed blood may interfere with the diagnosis of perioperative myocardial ischemia by laboratory parameters in coronary bypass patients.     

Comparison of serum myoglobin and creatine kinase MB isoenzyme in early diagnosis of acute myocardial infarction

We compared the clinical usefulness of serum myoglobin and creatine kinase MB (CK MB) isoenzyme determinations in the early diagnosis of acute myocardial infarction in 109 consecutive patients admitted to a coronary care unit. Of these, 37 patients were diagnosed as having definite infarction, three possible infarction, and 69 no infarction, using World Heath Organisation criteria. Blood samples were taken on admission and two to four hours later, Both CK MB and myoglobin were raised in the initial serum samples in 24 of the 37 patients with definite infarction. In an additional seven patients both CK MB and myoglobin were negative in the first specimen though both were detected in the second sample. In five patients CK MB preceded the appearance of myoglobin while in the remaining patient myoglobin appeared before CK MB. We conclude that the detection of serum myoglobin does not offer any clinical advantage over CK MG as an early indicator of myocardial infarction.     

Serum enzymes and isoenzymes after surgery

Serum creatine kinase, aspartate transaminase, and hydroxybutyrate dehydrogenase activities were abnormal in 76, 50, and 28% respectively of 50 patients studied within 26 hours of surgery. No patient showed clinical evidence of myocardial infarction. Creatine kinase MB isoenzyme elevation, and lactate dehydrogenase LD1 activity greater than LD2 (LD) greater than LD2) were infrequent (6 and 10% respectively). No patient showed the combination of transient MB isoenzyme elevation and LD1 greater than LD2, although their rare association without infarction after surgery is to be anticipated.     

Plasma MB creatine kinase activity and other conventional enzymes. Comparison in patients with chest pain and tachyarrhythmias

We studied 67 patients with tachycardia and chest pain admitted with suspected myocardial infarction; 29 had myocardial infarction (20 transmural, nine subendocardial) with elevated MB creatine kinase (CK) activity, as well as elevated total CK and lactate dehydrogenase (LDH) levels. However, hydroxybutyric dehydrogenase and SGOT activity remained normal in three and four patients, respectively. Despite abnormal ECGs in 84% and typical chest pain in 54%, 38 patients had normal MB CK activity. However, 15 of them had elevated MM CK levels, presumably due to release from skeletal muscle. In total, 29 patients had elevated activity of MM, CK, LDH, or SGOT, but 72% of these patients had cardiac failure, hypotension, or skeletal muscle trauma due to cardioversion. Eleven patients with normal MB CK had elevated hydroxybutyric dehydrogenase activity. Despite elevated activity of other enzymes, MB CK remained normal. Thus, elevated plasma MB CK activity appears to remain a good diagnostic marker of myocardial necrosis in patients with tachyarrhythmias.     

Accumulation of amphotericin B in human macrophages enhances activity against Aspergillus fumigatus conidia: quantification of conidial kill at the single-cell level

Several cardiac serum markers such as cardiac myosin light chain, creatine kinase MB, and cardiac troponins have been shown to be elevated in patients with acute myocardial infarction. These markers are well utilized as clinical indicators for diagnosis and prognosis of myocardial necrosis. Recent studies have strongly indicated that cardiac structural protein troponin T and I are predictive of future cardiac events in patients with acute coronary syndromes including unstable angina pectoris. Immunoassays have also been developed to measure serum levels of cardiac troponins in recent years. These biochemical markers may be useful as a guide for intervention in the near future.     

Elevation of plasma MB creatine kinase and the development of new Q waves in association with pericarditis

A 64-year-old woman with an acute exacerbation of chronic relapsing pericarditis had initial clinical and ECG features that were consistent with an acute anterior myocardial infarction. Transient Q waves were observed in the precordial leads, and she also exhibited elevated plasma MB creatine kinase (MB CK) activity. However, the overall clinical and laboratory data, including angiographic and radionuclide studies, suggest that the myocardial damage was secondary to pericarditis per se, rather than ischemic myocardial infarction. This case emphasizes that Q waves and elevated MB CK activity can be seen in association with pericarditis, and this must be differentiated from myocardial infarction secondary to coronary artery disease.     

Myoglobin concentration in serum as an early marker of reperfusion in patients with acute myocardial infarction after thrombolytic therapy

Detection of coronary artery reperfusion in patients after thrombolytic therapy because of acute myocardial infarction includes, except angiography, disappearance of anginal pain, regression of electrocardiographic and echocardiographic myocardial ischaemia symptoms, increased activity of creatine kinase (CPK) and its isoenzyme CK-MB. The aim of the study was to check whether changes in myoglobin serum concentration could be an early marker of coronary artery reperfusion after thrombolysis in patients with acute myocardial infarction. The studies comprised 50 patients treated by thrombolysis due to threatening myocardial infarction, including 29 men and 21 women aged 43-84 years. The patients were divided into 2 groups: the first (i)-patients without symptoms of coronary artery reperfusion and the second (ii)-those with symptoms of coronary artery reperfusion. It was assumed that the basis for successful reperfusion would be the reduction of total elevations of the ST segment 70% or more in electrocardiographic recording performed 3 hours after the start of thrombolytic treatment. Reperfusion was considered completely unsuccessful when reduction of total elevations was less than 30%. In patients with reperfusion after thrombolysis the concentrations of myoglobin were much higher and the activity of CPK and CK-MB significantly more intensive in comparison with patients without reperfusion symptoms in electrocardiographic assay. The evaluation of myoglobin concentration, CPK and CK-MB activity in the 3rd hour after the start of thrombolytic treatment in relation to maximum values is characterised by high sensitivity and specificity in the prediction of reperfusion onset Maximum myoglobin concentration in serum appears significantly earlier than maximum CPK and CK-MB activity and this marker is characterised by higher sensitivity and specificity in the evaluation of coronary artery reperfusion than the activity of CPK and CK-MB.     

QT dispersion may be a useful adjunct for detection of myocardial infarction in the chest pain center

BACKGROUND: QT dispersion has been proposed as a noninvasive measurement of the degree of inhomogeneity in myocardial repolarization. Increased QT dispersion has been reported after myocardial infarction. We hypothesized that increased QT dispersion may be a useful adjunct for risk stratification in patients being evaluated in a chest pain center. METHODS AND RESULTS: Patients were admitted to the chest pain center for evaluation of chest pain. Exclusion criteria included (1) systolic blood pressure <90 mm Hg, (2) ischemia or infarction on the initial electrocardiograph (ECG), (3) elevated creatine kinase or MB fraction, and (4) chest pain associated with cocaine use. Serial creatine kinase and MB levels and ECGs were obtained at 0, 6, and 9 hours. Patients were monitored for (1) creatine kinase and MB rise, (2) ECG changes for infarction, (3) ST-segment changes, and (4) rest angina. A negative evaluation at the chest pain center led to an exercise stress test. Patients with a positive exercise stress test were admitted for further evaluation and patients with a negative exercise stress test result were discharged home. Patients were divided into 3 groups. Group 1 consisted of patients who were found to have an acute myocardial infarction (AMI), group 2 consisted of patients with prior history of coronary artery disease but no evidence of AMI, and group 3 consisted of patients without prior coronary artery disease or AMI. QT dispersion was measured on the initial ECG in all patients. A total of 586 patients were evaluated. Group 1 consisted of 13 patients with mean QT dispersion of 44.6+/-18.5 ms, group 2 consisted of 267 patients with a mean QT dispersion of 10.0+/-13.8 ms, and group 3 consisted of 303 patients with a mean QT dispersion of 10.5+/-10.0 ms. Analysis of variance showed a significantly higher QT dispersion in patients who had AMI compared with other patients with chest pain (P< .001). CONCLUSIONS: QT dispersion can be a useful diagnostic adjunct for detection of AMI in patients with chest pain with a normal ECG and normal cardiac enzymes.     

Interference of CK-BB isoenzyme in the determination of CK-MB using the immunoinhibition method in patients with pulmonary diseases

An increase in serum creatine kinase-MB (CK-MB) isoenzyme is regarded as a specific indicator of acute myocardial infarction. We analyzed retrospectively the clinical data of 94 patients whose serum creatine kinase MB (CK-MB) was measured with immunoinhibition kit which measures all residual CK activity following inactivation of M-subunit. There were 21 patients with chronic obstructive lung disease (COLD), 17 patients with pneumonia, 17 patients with pulmonary tuberculosis (TBC), 16 patients with non-small cell lung cancer (NSCLC), 10 patients with small cell lung cancer (SCLC), 8 patients with malignancies of other origin (NPL), and 5 patients with chronic heart diseases. The results revealed that serum concentrations of CK-MB in SCLC, NSCLC and TBC were significantly greater than those in other groups (P < 0.1). Clinical examination showed no evidence of myocardial infarction, injury, or tumor involvement of the heart. We assumed that those results are due to interference of the CK-BB isoenzyme in the immunoinhibition method. So we suggest that in clinical practice, markedly elevated levels of CK-MB measured with immunoinhibition kit, after the exclusion of the myocardial injury, may point toward the existence of a malignancy or TBC of the lungs.     

Colorimetric determination of creatine phosphokinase isoenzymes: detection in tissues and serum, and usefulness as an aid to diagnosis of myocardial infarction

1. A colorimetric procedure for creatine phosphokinase (E.C.2.7.3.2.) isoenzymes suitable for routine laboratory use its described. The method utilizes a commercial product for visualization of CK isoenzymes in both serum and tissues. 2. The technic has been applied as an aid to the diagnosis of acute myocardial infarction. An intermediate migrating isoenzyme band (CK-MB) was detected in sera of 19 patients with clinical evidence of myocardial infarction and two patients with myocardial ischemia. The CK(MB) was absent in three patients presenting with symptoms suspect of, but not clinically confirmed as having myocardial infarction.     

Concentration time courses of troponin and myosin subunits after acute myocardial infarction

BACKGROUND: As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage. METHODS: This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment. RESULTS: Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion. CONCLUSION: Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.     

False increased CK-MB value after cryoablation of the prostate without myocardial infarct

The authors report on a profound increase in creatine kinase isoenzyme MB (CK-MB) activity in three patients following uneventful cryoablation of the prostate under general anaesthesia: Just after the arrival at the recovery room CK-MB levels were 321 U/l, 245 U/l and 433 U/l, respectively. Other clinical investigations as well as additional laboratory tests ruled out myocardial infarction in all three patients. Electrophoresis of the CK-isoenzymes revealed an increase in CK-BB activity and an increase in atypical CK-BB as a cause of these findings. The presence of these isoenzymes leading to interferences with the antibody commonly used in CK-MB assays could explain the determination of a false positive CK-MB elevation in the three patients. Moreover, it is shown that this method of CK-MB activity determination may result in CK-MB levels higher than 100% of the whole CK activity. In addition, it is discussed that in patients suffering from prostatic carcinoma or other malignoma, "non-CK-M elevations" may occur. Therefore, the authors conclude that after cryoablation of the prostate additional tests like troponin T test and 12 channel ECG are required to rule out suspected myocardial infarction.     

Normal frontal perfusion in patients with frozen gait

With the aim to compare the diagnostic efficacy as regards acute myocardial infarction of two rapid dry-strip tests, one with both creatine kinase MB (CK-MB) and myoglobin (C + M) and the other with troponin T, and to test the reliability of bedside diagnosis by the coronary care unit (CCU) nurse, 151 patients with acute chest pain admitted to the CCU were investigated. There was no difference in diagnostic performance between rapid tests and quantitative determinations. With <6-hour duration of symptoms, the sensitivity was better for C + M than for troponin T (72% vs 33%, p < 0.05). With symptoms lasting >12 hours on arrival, troponin T performed better, with 100% sensitivity and a negative predictive value of 100% in the 6-hour retest. For exclusion of damage, the two tests have similar and reliable diagnostic capacities 12 hours after the onset of symptoms. The bedside diagnosis or exclusion of acute myocardial infarction was carried out rapidly (within 20 minutes) and reliably by the CCU nurses.     

Clinical evaluation of an immunoinhibition procedure for creatine kinase-MB

We have clinically evaluated the Dade "Cardiozyme" immunoinhibition procedure for determination of creatine kinase isoenzyme MB (CK-MG) in 71 patients who were suspected of having had an acute myocardial infarction. Electrophoresis for CK-MB was also carried out. On the basis of diagnostic sensitivity and specificity for myocardial infarction, we found the Dade procedure for CK-MB to be somewhat inferior to electrophoresis. In 11 patients for whom the time of infarction was known, we observed normal CK-MB results for two of them by both immunoinhibition and electrophoresis during the first 24 h, but subsequently could detect abnormal CK-MB results by both methods. Thus in some patients such data are not helpful for making a diagnosis in the first 24 h. The Dade procedure is easy to perform, but lacks sensitivity in the region of low CK-MB activity, requires a very stable spectrophotometer, is imprecise, and produces negative numerical results in patients without myocardial infarction.     

Troponin T and creatinine kinase isoenzyme MB mass in the diagnosis of myocardial infarction

The aim of this study was to compare troponin T (TnT) and creatine kinase isoenzyme MB mass (CK-MBm) with conventional enzymes, ie CK, CK-MB activity and lactate dehydrogenase isoenzyme 1, in the diagnosis of myocardial infarction (MI). 624 patients (351 men and 273 women, median age 69 years) were admitted to hospital with suspicion of an acute coronary heart disease event. TnT was elevated (> 0.10 microg/L) in 100%, CK-MBm (> 5.0 microg/L) in 99%, and both markers in 99% of the 89 patients with the diagnosis of a definite MI according to modified FINMONICA criteria. In the 60 patients with the diagnosis of a probable MI, TnT was elevated in 65%, CK-MBm in 67% and both markers in 60%. In the patients with unstable coronary artery disease (unstable angina or prolonged chest pain attack) and conventional enzymes within normal limits, TnT was elevated in 14%, CK-MBm in 17% and both markers in 9%. The use of TnT and CK-MBm did not lead to a major change in the diagnostics of definite MI. However, TnT and CK-MBm did not confirm the diagnosis of probable MI in one-third of the events. These new markers revealed a myocardial injury in about 15% of those patients who had unstable coronary artery disease and conventional enzymes within normal limits.     

Biochemical markers in acute myocardial infarct

Exact and early diagnosis of acute myocardial infarction is essential for the subsequent routine management of this frequent cardiovascular disease. At present, the clinical biochemistry possesses a set of more or less cardiospecific protein markers for early detection of myocardial ischemic damage. After the admission of patient to the hospital, serial estimations of rather non-specific enzyme activities (creatine kinase, its MB-izoenzyme, lactate dehydrogenase, hydroxybutyrate dehydrogenase) are currently used for the detection of acute myocardial infarction and for the further monitoring of the patient and managing his therapy. In the past decade, many cardiospecific biochemical markers were discovered and gradually introduced into the routine clinical practice. The most perspective markers are some molecules of contractile proteins of heart myofibrils (troponins, myosin chains) as well as "rediscovered" myoglobin. The aim of this review article is to inform about the commonly used, as well as about the new biochemical markers, to discuss some problems of diagnostic strategy in the early and exact detection of ischemic myocardial damage and to attract attention to the difficulties. However its disadvantage resides in its presence in both myocardium and skeletal muscles which arise when the diagnosis of acute myocardial infarction is prematurely excluded from consideration and such patients are discharged too soon from hospital. (Fig. 1, Tab. 1, Ref. 72.)     

Serum levels of cardiac troponin I and troponin T in estimating myocardial infarct size soon after reperfusion

BACKGROUND: Cardiac troponin I (TnI) and troponin T (TnT) are highly specific myocardial markers. OBJECTIVE: To determine whether their serum levels can be used to estimate myocardial infarct size soon after reperfusion. METHODS: We measured the serum levels of TnI, TnT, and creatine kinase every 3 h, and the serum cardiac myosin light chain I (MLCI) every 24 h, in 42 patients with acute myocardial infarction in whom reperfusion therapy had successfully been performed. We calculated the severity of regional hypokinesis by analyzing the follow-up ventriculograms with the centerline method. RESULTS: The time from reperfusion to the peak level for TnI was 6.1 +/- 3.5 h, significantly shorter than those for creatine kinase (7.5 +/- 4.1 h) and MLCI (55 +/- 28 h). The time to peak level for TnT (6.8 +/- 4.0 h) differed significantly from that for MLCI but not from that for creatine kinase. There was a significant correlation between the peak levels of TnI and TnT (r = 0.86). The peak TnI and TnT levels were correlated well to the peak creatine kinase level (r = 0.67 and 0.69, respectively), total creatine kinase release (r = 0.66 and 0.66), and the peak MLCI level (r = 0.71 and 0.80). We observed excellent correlations between the peak levels of TnI and TnT, and regional hypokinesis (r = -0.84 and -0.85, respectively). These were comparable to the correlations between regional hypokinesis and the peak creatine kinase level (r = 0.75), total creatine kinase release (r = -0.72), and the peak MLCI level (r = -0.76). CONCLUSIONS: These results suggest that the peak serum levels of TnI and TnT in patients with successful reperfusion are accurate and early indices of infarct size.     

Non-invasive methods for evaluating reperfusion in acute myocardial infarct: enzymes and MIBI-SPECT cardiac gammagraphy

INTRODUCTION: Several studies point out the importance of what is called rescue angioplasty or fibrinolysis when thrombolysis has been ineffective in acute myocardial infarction. Therefore, it is necessary to make use of new non-invasive methods to asses reperfusion and to safely establish that such a treatment has not been effective. PATIENTS AND METHOD: We present a work which is based on the assessment of patients with acute myocardial infarction treated with or without fibrinolysis. After determining cardiac enzymatic profiles of creatine kinase and MB isoform (time course, peak, appearance rate constant time-activity: K1). With cardiac imaging gammagraphies 99mTc-isonitrile-single-photon emission computed tomography pre and post treatment after to calculating myocardium at risk, salvage and relationship. RESULTS: In patients treated with fibrinolysis, the salvage myocardium was higher (8.3% vs 3.0%; p < 0.05). Considering that an improvement in perfusion defect (salvaged myocardium/myocardium at risk) higher than 30% can be viewed as an effective reperfusion, we can see that the percentage in the group treated with fibrinolysis being 45.8%, and the percentage in the group under conventional treatment being just 6.7%. Patients with acute myocardial infarction treated with fibrinolysis show much shorter start of rise-peak time and pain-peak time, all this with very significant differences for the creatine kinase (p < 0.0001) as well as for the MB (p < 0.001). Patients with reperfusion show a rapid increase in activity enzymatic, as demonstrated by the pain-peak time variable and the appearance rate constant time-activity (K1), with very significant differences in the latter (p < 0.0001). In relation with gammagraphy, values of K1 higher or equal to 0.19 for the creatine kinase and 0.14 for the MB isoform, achieved a sensibility of 83% and 91%, and a specificity of 85% and 80% respectively, to asses reperfusion. CONCLUSION: We think that cardiac imaging gammagraphy with isonitriles as well as as determination of the appearance rate enzymatic constant time-activity, can be useful in monitoring treatment with fibrinolysis in infarction patients. New studies are needed to assess these same aspects, with a lesser number of enzymatic determinations.     

Inability of methylprednisolone sodium succinate to decrease infarct size or preserve enzyme activity measured 24 hours after coronary occlusion in the dog

Methylprednisolone sodium succinate (50 mg/kg) was given 30 minutes before or after the start of a 90 minute occlusion of the left circumflex coronary artery (LCX) in one group of dogs. In a second group, methylprednisolone sodium succinate was given 15 minutes after permanent occlusion of the left anterior descending artery (LAD). Infarct size was determined by dehydrogenase staining after 24 or 96 hours. Heart slices were incubated with nitro-blue tetrazolium and nonstaining infarcted tissue was dissected and weighed. Myocardial depletion of creatine phosphokinase activity (CPK) and lactate dehydrogenase activity (LDH) were determined 24 hours after temporary LCX occlusion. When measured after 24 hours, methylprednisolone sodium succinate treatment did not reduce infarct size or decrease enzyme loss. After temporary LCX occlusion infarct size was 30.4 +/- 3.6% of left ventricular weight in control dogs and 30.0 +/- 2.3% in treated dogs. No significant difference in infarct size was observed in hearts examined 24 or 96 hours after myocardial infarction. After permanent LAD occlusion, infarct size in control dogs was 39.2 +/- 1.6% of left ventricular weight and 33.7 +/- 3.5% in treated dogs. CPK activity in the LCX area decreased by 26.5 +/- 7% in controls and by 28.1% +/- 7% in treated dogs. Treated dogs sustained a significantly greater fall in arterial blood pressure after LCX occlusion than did controls. During LCX occlusion and upon reperfusion, methylprednisolone sodium succinate treated dogs exhibited a significantly greater number of premature ventricular beats. Since infarct size and enzyme depletion were not reduced when measured after 24 hours, methylprednisolone sodium succinate treatment does not appear to have enhanced myocardial cell viability.