The aminoterminal propeptide of type III procollagen provides new information on prognosis after acute myocardial infarction.

The aim of the study was to examine sequential changes in serum levels of the aminoterminal propeptide of type III procollagen (S-PIIINP) after acute myocardial infarction (AMI), and to assess the value of S-PIIINP as a predictor of outcome. The study group comprised 74 patients with AMI, and 24 patients in whom AMI was suspected but disproved. S-PIIINP changed characteristically after AMI, and in patients not receiving thrombolytic therapy or having cardiogenic shock, the changes correlated to peak enzyme values (r = 0.4, p < or = 0.03). S-PIIINP was higher at days 0 to 2 in nonsurviving AMI patients than in survivors (p < 0.05). With use of either the upper quartile for S-PIIINP at day 0 for nonsurviving AMI patients or the mean value of S-PIIINP in a normal population plus 2 SDs as a cutoff, the predictive value of a negative test ranged from 0.79 to 0.87 at days 0 to 2, and the predictive value of a positive test ranged from 0.39 to 0.67. Thus, S-PIIINP on admission and for the following few days after AMI is higher in patients with poor outcome.

[Dilated cardiomyopathy in a user of anabolic steroids]. / Dilateret kardiomyopati hos en bruger af anabole steroider.

A case is described in which a 32-year old male body-builder was admitted with signs of cardiac incompensation after using anabolic steroids (AS) in large amounts for three weeks before admittance. Echo-cardiography showed a dilated left ventricle with decreased systolic function and electrocardiography showed atrial fibrillation. Response to treatment was good and he was discharged to further out-patient treatment. After nine weeks he was admitted with severe cardiac incompensation. There was no response to treatment and he died after three days. At autopsy the heart weighted 527 grams and was diffusely dilated. There were no signs of infarction. Microscopy showed scattered lymphocyte infiltrates consistent with dilated cardiomyopathy, possibly caused by myocarditis. There were no signs of bacterial infection, the patient was a non-alcoholic and no other known cause of myocarditis was shown. We conclude that the patient died from toxic myocarditis with dilated cardiomyopathy caused by AS.