Ingwall J S, Kramer M F, Fifer M A, Lorell B H, Shemin R, Grossman W, Allen P D
N Engl J Med. 1985 Oct 24;313(17):1050-4. doi: 10.1056/NEJM198510243131704.
We measured creatine kinase activity, isozyme composition, and total creatine content in biopsy samples of left ventricular myocardium from 34 adults in four groups: subjects with normal left ventricles, patients with left ventricular hypertrophy due to aortic stenosis, patients with coronary artery disease without left ventricular hypertrophy, and patients with coronary artery disease and left ventricular hypertrophy due to aortic stenosis. As compared with specimens of normal left ventricles, those from all patients with left ventricular hypertrophy had lower creatine kinase activity, higher MB creatine kinase isozyme content and activity, and lower creatine content. Specimens from the patients without left ventricular hypertrophy had normal creatine kinase activity, increased MB creatine kinase isozyme content and activity, and decreased total creatine content. The normal ventricles showed almost no MB isozyme content or activity. These data suggest that changes in the creatine kinase system occur in both pressure-overload hypertrophy and coronary artery disease. Patients with myocardial infarction who have mild or no preexisting fixed coronary artery disease or pressure-overload hypertrophy would not be expected to have elevation of serum MB creatine kinase.
我们测定了四组34名成年人左心室心肌活检样本中的肌酸激酶活性、同工酶组成和总肌酸含量:左心室正常的受试者、因主动脉狭窄导致左心室肥厚的患者、无左心室肥厚的冠心病患者以及因主动脉狭窄导致左心室肥厚的冠心病患者。与正常左心室标本相比,所有左心室肥厚患者的标本肌酸激酶活性较低,MB肌酸激酶同工酶含量和活性较高,肌酸含量较低。无左心室肥厚患者的标本肌酸激酶活性正常,MB肌酸激酶同工酶含量和活性增加,总肌酸含量降低。正常心室几乎没有MB同工酶含量或活性。这些数据表明,肌酸激酶系统的变化发生在压力负荷性肥厚和冠心病中。预计既往有轻度或无固定性冠状动脉疾病或压力负荷性肥厚的心肌梗死患者血清MB肌酸激酶不会升高。