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Introduction and Objectives: Our purpose was to investigate the significance of inflammatory acute phase response early after myocardial infarction. We also observed how these indices were influenced by trombolytic therapy., Method: We examined the blood samples of 200 non consecutive patients at the first day of acute myocardial infarction (155 [77%] males; mean age 65 +/- 13 years) to characterize the proteins and proinflamatory reactants profile. Results were correlated with hospital mortality. Thrombolytic therapy was administrated to 117 patients on admission and in these patients the samples were taken after the procedure., Results: Overall mortality was 8%. Serum C-reactive protein (69 vs 41 mg/l), haptoglobine (237 vs 190 mg/dl), gammaglobuline (0.93 vs 0.84 g/dl), alpha-1-globuline (0.28 vs 0.23 g/dl) and alpha-2-globuline (0.7 vs 0.6 g/dl) were significantly higher in patients without trombolytic therapy. Conversely, patients who had received lytic therapy, had higher plasma concentrations of interleukin-1 beta (104 vs 40 pg/dl). The only clinical variable which was associated with mortality was a Killip class > or = 2 on admission (mortality = 21%; odds ratio = 5.2; p = 0.02). Other biochemical variables associated with a higher mortality were a white blood cell count > 10/nl (mortality = 12%; odds ratio = 5.4; p = 0.01), increased activated neutrophils > 80% (mortality = 18%; odds ratio = 5.4; p = 0.004) and C-reactive protein > 20 mg/l (mortality = 11%; odds ratio = 6; p = 0.05). Only patients with activated neutrophils > 80% on admission had a higher probability of dying during hospital stay (Exp[B] = 3.6; B = 1.2; r = 0.29; p = 0.001)., Conclusion: The acute phase reaction in early myocardial infarction is determined by thrombolytic treatment. A high increase of activated neutrophils on patient admission is the only biochemical predictive value for hospital mortality.

Serial signal-averaged electrocardiograms were recorded every 72 hours in 60 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 61.6% (37 patients) during hospitalization. Of these 37 patients, late potentials appeared transiently in 20 (54%), while in 9 patients (24%), once late potentials had appeared, they tended to persist. No specific clinical characteristics were related to the development of late potentials (site of infarction, peak creatine kinasa activity, Killip class, thrombolytic therapy). The presence of late potentials did not identify patients who developed clinically significant ventricular tachyarrhythmias (primary ventricular fibrillation, ventricular tachycardia). The abnormal late potentials were modified by the administration of lidocaine. This lack of correlations suggests that the abnormal signal averaged electrocardiogram and complex ventricular arrhythmias during acute myocardial infarction have different electrophysiological bases. Late potentials could be only a bystander electrophysiological phenomenon without clinical correlation in this clinical phase.