Markers of necrosis and anoxia in the post-infarct heart failure: Determination of infarct size [MARKERS DI NECROSI E ANOSSIA NELLO SCOMPENSO CARDIACO POSTVALUTAZIONE DELL'ESTENSIONE DELL'AREA INFARTUALE]

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total release (TR) of the two enzymes have been calculated, according to Shell's method modified by Norris. The RT of HBDH have resulted in more prolonged in the decompensated patients (48.1 ± 16.0 vs 37.3 ± 9.1 hrs, t = 2.297; p<0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes: r=0.816, p<0.01 (with failure); r=0.766, p<0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the Tr of the two patient groups. The following conclusions can be drawn: infarct size probably is not the only factor able to induce heart failure during AMI; infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; and the more prolonged release of HBDH during heart failure suggest the hypothesis that lactate accumulation is an important factor influencing the appearance of this complicance.