Cardiac troponin I in acute coronary ischemic syndromes. Epidemiological and clinical correlates

The present study was aimed to investigate the variability of cardiac tropo nin I (cTnI) in the first week of acute myocardial infarction (AMI) course with regard to some epidemiological and clinical parameters and in patients with non-AMI acute coronary ischemic disease. Serum cTnI was assayed in 82 patients, 42 affected with AMI and 40 with non-AMI acute coronary ischemic disease, on admission in coronary care unit, within 6 h after the onset of symptoms, and, in AMI group, on 24 and 38 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th d ay. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died. >6 0 years old and with anterolateral necrosis are constantly higher than in s urvivors, <60 years old and with inferoposterior necrosis, respectively. (2 ) The cTnI concentration is already returned in normal range at 7th day of illness course in survivors and in patients with inferoposterior AMI. (3) T he 24-h peak level of cTnI is significantly higher in fibrinolysed than in patients who didn't undergo fibrinolysis. (4) A direct correlation between the cTnI value and the Killip class is present either in the whole group or in any subset of patients and the progressive decrease of the cTnI concent ration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is hi gher in unstable than in stable anginous patients and normal subjects but n ot in stable angina with respect to healthy controls, Conclusions: (1, 2) T he less increase and the early return in normal range of cTnI serum levels which occur in AMI subgroups with a better prognosis could be regarded as f avourable prognostic signs. (3) The persistent higher values of cTnI in fib rinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relas e of cTnI from myocardium represents a reliable biochemical marker followin g the wash-out associated to a successful reperfusion. (4) The persistent i ncrease of cTnI in AMI patients with advanced Killip class suggests that th e high cTnI values are not only a strong index of myocardial necrosis but a lso of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (;) The hypothesis can be reasonably advanced that the higher val ues of cTnI in unstable angina are due to focal areas of myocardial necrosi s undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission. (C) 2001 Elsev ier Science Ireland Ltd. All rights reserved.