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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.

Plasma levels of vasoactive intestinal peptide increase early after acute myocardial infarction (AMI) and are significantly higher during the first 2 weeks of AMI in survivors and younger patients (<60 years) than in those who died and in older (>60 years) patients. Data suggest that vasoactive intestinal peptide is involved in neuroendocrine activation occurring in AMI and could be regarded as a marker of the course of AMI.

Acute myocardial infarction (AMI) is known to be associated with a complex neuroendocrine activation, especially concerning sympathetic and renin-angiotensin systems, cortisol, atrial natriuretic peptide and endothelin. Results of our study show that the vasoactive intestinal peptide (VIP), also, is early involved in the neuroendocrine activation occurring in AMI. Plasma concentration of VIP, significantly increased in AMI patients within 6 hours after the onset of chest pain, soon decreased and remained below than normal along the first week. At the 14th day of the AMI, plasma levels of VIP returned into the normal range. A significant increase of VIP plasma concentration is detectable in the first hours of AMI in survived as compared with died patients. The phenomenon seems to be a suitable process to provide an endogenous support to the ischemic heart and to counteract the negative effects of other neuroendocrine activated factors.

Aim of our study was to investigate the pathophysiological role of vasoactive intestinal peptide (VIP) in the neuroendocrine activation occurring in acute myocardial infarction (AMI). Plasma VIP concentration has been assayed in 30 patients with AMI, 22 males and 8 females, aged 41-82 years, without other important diseases. VIP plasma values, assayed on admission to the Coronary Care Unit, within 4-6 hours after the onset of chest pain, everyday for the first week and on day 14, were significantly higher in survivors and in patients aged < 60 years. VIP plasma concentration was not statistically correlated with CPK and CPK-MB. VIP seems to play a pathophysiological role in the neuroendocrine activation occurring in AMI. Low VIP plasma levels are associated with an unfavorable short-term prognosis. Moreover, it appears that VIP secretion is negatively influenced by aging.