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

UNLABELLED: The present study was aimed to investigate the variability of cardiac troponin 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 48 h and 7th day of illness course. cTnI is increased within the first 6 h, remaining above normal until 7th day. However, some distinctive features in the subgroups scheduled for this study are present. (1) The mean values of cTnI in AMI patients who died, >60 years old and with anterolateral necrosis are constantly higher than in survivors, <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) The 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 concentration along the AMI course doesn't occur in Killip>2 group. (5) cTnI is higher in unstable than in stable anginous patients and normal subjects but not in stable angina with respect to healthy controls. CONCLUSIONS: (1, 2) The 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 favourable prognostic signs. (3) The persistent higher values of cTnI in fibrinolysed subjects being associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent relase of cTnI from myocardium represents a reliable biochemical marker following the wash-out associated to a successful reperfusion. (4) The persistent increase of cTnI in AMI patients with advanced Killip class suggests that the high cTnI values are not only a strong index of myocardial necrosis but also of ongoing myocyte injury and hemodynamic impairment predictive of poor outcome. (5) The hypothesis can be reasonably advanced that the higher values of cTnI in unstable angina are due to focal areas of myocardial necrosis undetectable by the conventional serum markers or to a clinically silent AMI occurred in the week or so before in-hospital admission.

[Troponin I in acute ischemic cardiopathy]. / La troponina I nella cardiopatia ischemica acuta.

BACKGROUND: The present study was aimed at investigating cardiac troponin I values in the first week of acute myocardial infarction and in non-infarct acute coronary ischemic syndromes. METHODS: Eighty-two patients, 42 with acute myocardial infarction, 10 with stable angina and 30 with primary unstable angina, were enrolled in the study. Blood was collected within 6 hours of symptom onset and, in the group with acute myocardial infarction, after 24 and 48 hours, and on day 7. RESULTS: Serum troponin I increased within the first 6 hours of myocardial infarction, reached the peak after 24 hours, at 48 hours it decreased, and remained above the normal range until day 7. However, troponin I values 1) were constantly higher in patients who died, in those > 60 years old and in those with antero-lateral necrosis than in survivors, in those < 60 years old and in those with infero-posterior necrosis, respectively; 2) returned to normal range on day 7 in survivors and in patients with infero-posterior acute myocardial infarction; 3) were significantly higher in fibrinolysed patients than in those who did not undergo thrombolysis; 4) were higher in patients classified as Killip class > 2. Serum troponin I values were in the normal range in non-infarct acute coronary ischemic syndromes, but were higher in unstable than in stable angina. CONCLUSIONS: The lesser increase and the early return to the normal range of cardiac troponin I levels in the subgroups of patients with myocardial infarction having a better clinical course could be regarded as a favorable prognostic sign. Since the persistent higher values of cardiac troponin I in fibrinolysed subjects are associated with the angiographic finding of patent coronary arteries, it can be suggested that the large and persistent post-thrombolysis release of cardiac troponin I from the myocardium represents a biochemical marker of a successful reperfusion. The persistent high cardiac troponin I values in patients with advanced Killip class suggest that the neuropeptide is an index of ongoing myocyte injury and hemodynamic impairment as well. The higher values of cardiac troponin I in unstable angina are probably due to focal areas of myocardial necrosis undetectable by conventional enzymatic serum markers.

[Systemic sclerosis after a long-term follow-up]. / Riflessioni sulla sclerosi sistemica dopo un follow-up a lungo termine.

The authors suggest some remarks on the aetiopathogenesis of systemic sclerosis through a critical review of a group of 51 patients affected by this disease for many years. In this paper the authors report their previous studies regarding the correlation of immunological response, both cell-mediated and humoral, hemocoagulative aspects and haemorheological changes. From the results of immunological studies, the authors report a long-term treatment with an immunomodulating drug: thymopentin. Moreover they report a recent work about the connection among stressor event, production of endothelin-1 (ET-1) and serum levels of some stress hormones such as possible pathogenetic factors of Raynaud's phenomenon and of scleroderma. This work ends with a proposal of a pathogenetic scheme that, even if it doesn't exclude an infective pathogenesis, considers stress as a factor able to switch on a series of psycho-neuro-immunoendocrinological reactions that can support, through the activation of lymphocytes, fibroblastic proliferation and finally fibrosis.