Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Konttinen, Aarne; Somer, Hannu

doi:10.1136/bmj.1.5850.386

Cited by 102 publications

(23 citation statements)

References 16 publications

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“…Despite differing isoenzyme assay techniques, the sensitivity and specificity of an elevated serum CK-MB in the diagnosis of myocardial infarction is well in excess of 90% (Konttinen et al, 1973;Roberts et al, 1975). This high specificity has been attributed to the finding that cardiac muscle is the only normal human tissue containing sufficient amounts of CK-MB to account for appreciable elevations of CK-MB activity in the serum (Roberts et al, 1975).…”

Section: Introductionmentioning

confidence: 97%

Elevated CK‐MB and CK‐BB in serum and tumor homogenate of a patient with lung cancer

Lee

Bach

Horton

et al. 1985

Clinical Cardiology

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Summary: Elevated serum levels of creatine kinase (CK) were found in a patient with small-(oat) cell carcinoma of the lung. Fractionation of the enzyme showed markedly elevated CK-MB and CK-BB isoenzymes. Clinical and subsequent pathological examination showed no evidence of infarction, inflammation, or tumor involvement of the heart; however, analysis of tumor tissue for CK showed predominance of CK-MB and CK-BB isoenzymes, thus implicating tumor as the source of the circulating levels of CK-MB and CK-BB. Our case is the first to document CK-MB from neoplastic tissue homogenates, and illustrates that markedly elevated circulating levels of CK-MB, or increased levels of CK-MB in combination with CK-BB may point away from a myocardial source, and toward the existence of a malignancy.

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Section: Introductionmentioning

confidence: 97%

Elevated CK‐MB and CK‐BB in serum and tumor homogenate of a patient with lung cancer

Lee

Bach

Horton

et al. 1985

Clinical Cardiology

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“…, 1978), as the necrosis of the myocardium results in the release into the serum of relatively more L D H l than LDH2, reversing the normal ratio. Elevated levels of creatine kinase-MB in the presence of normal serum total creatine kinase in patients with acute coronary insufficiency have been reported Konttinen and Somer, 1973; Marmor et a/. , 1978,1979).…”

Section: Discussionmentioning

confidence: 99%

“Flipped” lactic dehydrogenase pattern in acute coronary insufficiency

Weinberger

Rotenberg

Sagie

et al. 1986

Clinical Cardiology

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Summary: Serum lactic dehydrogenase (LDH) isoenzymes were measured 24, 48, and 72 hours after admission in 85 patients with acute coronary insufficiency (ACI) and 10 patients with stable angina pectoris who served as controls. The above patients did not develop myocardial infarction according to the criteria of development of new Q waves or elevation of cardiac enzymes. In 15 patients with ACI a "flipped" LDH pattern (LDH, > LDH2) was found in the presence of normal total LDH activity and normal creatine kinase-MB. The values of LDH 1 :2 ratio ranged between 1.02 and I . 13 (normal values 0.45-0.75). In the 10 control patients, normal levels of total LDH and normal LDH enzyme distribution and creatine kinase-MB were found. A possible explanation for the flipped LDH pattern in the ACI patients (indicating some myocardial damage) could be myocytolysis and coagulation necrosis found on postmortem examinations. The conclusion of our study is that LDH isoenzymes should be measured in patients with ACI to determine the LDH 1.2 ratio. The finding of B "flipped" LDH pattern demonstrating myocardial damage, lacking in stable angina, may also be helpful in patients who developed the clinical picture of ACI more than 24 hours before arrival at the hospital, since by that time the creatine kinase-MB may have already returned to nonnal. An additional advantage of measuring LDH isoenzymes in these patients may be that patients with "Hipped" LDH pattern may need a longer rest and earlier coronary angiographic evaluation.

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“…After the initial hospital discharge, reinfarction was documented electrocardiographically and enzymatically in 11 patients. However, 15 patients died at home, and we could not determine whether the deaths were associated with infarction. The time of occurrence of the 11 late episodes of documented reinfarction were evenly distributed throughout the followup.…”

Section: Temporal Pattern Of Reinfarctionmentioning

confidence: 92%

Recurrent myocardial infarction: clinical predictors and prognostic implications.

Marmor¹,

Geltman²,

Schechtman³

et al. 1982

Circulation

126

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SUMMARY Based on a prospective study in 200 consecutive patients with myocardial infarction, we reported previously that early recurrent myocardial infarction is more frequent after nontransmural than transmural infarction. Multiple logistic regression analysis using 14 clinical variables identified, in addition to type of infarction (nontransmural), three other risk factors for early recurrent infarction: obesity, female gender and recurrent chest pain. Early recurrent infarction was documented by reelevation in plasma MB CK activity. The present study was performed to assess the accuracy of these variables as prospective predictors of early recurrent infarction. Studies were performed in a new population of 150 patients admitted consecutively with acute myocardial infarction (test set). The regression coefficients derived by multiple logistic analysis from the training set population were applied by comparable analysis to the test set population and the presence or absence of recurrent infarction was predicted correctly for 80% of the patients. Patients were followed prospectively for 9 months (range 3-18 months) and life-table analysis was performed to assess the impact of recurrent infarction on short and long term survival. During the first 21 days after infarction, mortality was 23% for patients with transmural and 10% for nontransmural infarction (p < 0.01). However, among patients with nontransmural infarction, hospital mortality was 23% among those with early recurrent infarction and 8% for those without recurrence (n < 0.05). At the conclusion of follow-up, mortality was 34% among patients with nontransmural infarction and recurrence, compared with 23% among patients with nontransmural infarction and no recurrence. Thus, early recurrent infarction has a distinct deleterious effect on survival, and a subset of patients more likely to experience recurrent infarction can be prospectively identified.EARLY recurrent myocardial infarction, or extension of infarction, has been recognized clinically for many years as manifested by severe prolonged recurrent chest pain and new ST-T-wave abnormalities on the ECG.' Results of earlier studies suggested an incidence of early recurrent infarction of up to 86% ,2 but recent studies using objective specific enzymatic criteria have reported an incidence of 17-25%).6 In a previous report of 200 consecutive patients with acute myocardial infarction, early recurrent infarction detected by reelevation of plasma MB creatine kinase (MB CK) was observed in 17% of patients with documented myocardial infarction.7 8Analyses were performed to determine whether certain clinical characteristics of the population might identify a subset of patients at high risk for subsequent recurrent infarction. Those who experienced an initial nontransmural myocardial infarction comprised one subset of patients at high risk. high risk of developing early recurrent infarction. Obesity was defined as at least 25% in excess of ideal body weight for the person's height and recurrent pain was defined ...

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Specificity of Serum Creatine Kinase Isoenzymes in Diagnosis of Acute Myocardial Infarction

Cited by 102 publications

References 16 publications

Elevated CK‐MB and CK‐BB in serum and tumor homogenate of a patient with lung cancer

Elevated CK‐MB and CK‐BB in serum and tumor homogenate of a patient with lung cancer

“Flipped” lactic dehydrogenase pattern in acute coronary insufficiency

Recurrent myocardial infarction: clinical predictors and prognostic implications.

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