José Luis Terrón Blanco

Predisposing factors and prognostic value of sustained monomorphic ventricular tachycardia in the early phase of acute myocardial infarction.

OBJECTIVES The purpose of the study was to analyze the factors that favor the occurrence of sustained monomorphic ventricular tachycardia in the early phase (< 48 h) of acute myocardial infarction and to establish its prognostic implications. BACKGROUND Sustained monomorphic ventricular tachycardia early in the course of an acute myocardial infarction is an uncommon arrhythmia, and its significance has not been specifically studied. METHODS The clinical characteristics and prognosis of sustained monomorphic ventricular tachycardia were studied in 21 (1.9%) of 1,120 consecutive patients admitted to the coronary care unit with a diagnosis of myocardial infarction. RESULTS Patients with sustained monomorphic ventricular tachycardia had a larger infarct on the basis of peak creatine kinase, MB fraction (CK-MB) isoenzyme activity (435 +/- 253 IU/liter vs. 168 +/- 145 IU/liter, p < 0.001) and higher mortality rate (43% vs. 11%, p < 0.001). By logistic regression analysis, independent predictors of sustained monomorphic ventricular tachycardia were CK-MB (odds ratio [OR] 11.8), Killip class (OR 4.0) and bifascicular bundle branch block (OR 3.1). Moreover, sustained monomorphic ventricular tachycardia was itself an independent predictor of mortality (OR 5.0). Compared with patients with ventricular fibrillation, those with sustained monomorphic ventricular tachycardia had a worse Killip class (Killip class > I: 63% vs. 30%, p < 0.05), higher CK-MB activity (430 +/- 260 IU/liter vs. 242 +/- 176 IU/liter, p < 0.01) and higher arrhythmia recurrence rate (31% vs. 4%, p < 0.01). During the follow-up period, 5 (42%) of 12 survivors in the sustained monomorphic ventricular tachycardia group died of cardiac-related causes. Recurrence of ventricular tachycardia was seen in two patients (17%). CONCLUSIONS Sustained monomorphic ventricular tachycardia during the first 48 h of myocardial infarction is a sign of extensive myocardial damage and an independent predictor of in-hospital mortality.

Lack of effect of glycoprotein IIb/IIIa blockade on myocardial platelet or polymorphonuclear leukocyte accumulation and on infarct size after transient coronary occlusion in pigs

OBJECTIVES We sought to assess the effect of glycoprotein (GP) IIb/IIIa blockade on myocardial platelet and polymorphonuclear leukocyte accumulation and on infarct size after coronary injury and transient coronary occlusion (CO) in pigs. BACKGROUND It has been suggested that platelet GP IIb/IIIa blockade might reduce the severity of microvascular damage after reperfusion. METHODS Sixteen thiopental-anesthetized, open-chest pigs, in whom platelets had been labeled with technetium-99m (99mTc) on the previous day, were submitted to catheter-induced left anterior descending coronary artery (LAD) injury followed by 55 min of CO and 5 h of reperfusion. Five minutes before reflow, the animals were blindly allocated to receive lamifiban (intravenous bolus of 250 microg/kg body weight and continuous infusion of 3 microg/kg per min) or saline. RESULTS Lamifiban had a rapid and potent platelet anti-aggregatory effect, as demonstrated by significant prolongation of the bleeding time and profound (approximately 90%) inhibition of ex vivo platelet aggregation, and completely prevented the development of cyclic flow reductions of the LAD (0 vs. 5 +/- 1, one of them followed by re-occlusion, in control animals, p = 0.005). However, compared with animals receiving placebo, those treated with lamifiban had a similar (p = NS) content of (99m)Tc platelets in the reperfused myocardium (288 +/- 40% vs. 205 +/- 27% of the value in the control region, respectively) and similar myeloperoxidase activity (0.50 +/- 0.17 U/g vs. 0.47 +/- 0.17 U/g, respectively) and infarct size (46.8 +/- 12.0% vs. 49.8 +/- 10.5% of the area at risk, respectively). Arteriolar platelet thromboemboli were very rarely seen on histologic analysis. Lamifiban did not modify platelet P-selectin expression in additional studies. CONCLUSIONS Platelet GP IIb/IIIa blockade has a potent antithrombotic effect at the culprit lesion, but does not significantly reduce the magnitude of microvascular platelet accumulation or myocardial damage after transient CO.