Aims: Current guidelines do not advocate implantation of cardioverter-defibrillators (ICD) for survivors of ventricular fibrillation (VF) during the first 48 hours of ST-elevation myocardial infarction (STEMI). However, contemporary studies in a real-life setting with long-term follow-up are lacking. We assessed the prognostic impact of early VF in a non-selected population of STEMI patients treated with primary percutaneous coronary intervention (PCI). Methods and results:Consecutive STEMI patients admitted to a Swedish tertiary care hospital during 2007-2009 were identified from the Register of Information and Knowledge about Swedish Heart Intensive Care Admissions (n=1718, age 66±12 years, 70% male). Patients with VF were identified from the register, and medical records were reviewed to determine the time point of VF. Patients surviving VF in the first 48 hours after symptom onset were compared with patients without VF for one-year mortality and a combined endpoint of death, resuscitated VF or appropriate ICD therapy. VF within 48 hours occurred in 7% of STEMI patients (n=121). In patients alive at 48 hours (n=1663), VF patients (n=101) had higher in-hospital mortality (12% vs. 2%, p<0.001). However, in VF patients discharged alive (n=89), mortality was low (1%) and combined endpoint rate (3%) did not differ compared with patients without VF (n=1538; 4% and 4% respectively). Conclusion:In a large non-selected population of STEMI patients treated with primary PCI, VF during the first 48 hours after STEMI is associated with increased in-hospital mortality but does not influence the long-term prognosis for those discharged alive.

Transient QRS widening, commonly associated with a J-wave pattern, appears to predict impending VF in acute ischemia settings and motivates further clinical studies for monitoring immediate risk of VF in MI.

J-wave pattern has been recognized as an arrhythmic risk marker, particularly in myocardial infarction patients. Mechanisms underlying J-wave development in ischemia remain unknown. In myocardial infarction model, we evaluated activation time delay as a prerequisite of J-wave appearance and predictor of ventricular fibrillation. Body surface ECGs and myocardial unipolar electrograms were recorded in 14 anesthetized pigs. 48 intramural leads were positioned across ventricular free walls and interventricular septum. Myocardial ischemia was induced by ligation of the left anterior descending coronary artery and the recordings were done during 40-minute coronary occlusion. The local activation times were determined as instants of dV/dt minimum during QRS complex in unipolar electrograms. During occlusion, ventricular local activation time prolonged in the middle portion of the left ventricular free wall, and basal and middle portions of septum, while J-waves appeared in precordial leads in 11 animals. In logistic regression and ROC curve analyses, activation time delay at a given time-point was associated with J-wave development, and a longer activation time was associated with ventricular fibrillation appearance. In experimental coronary occlusion, activation delay in ischemic myocardium was associated with generation of the J waves in the body surface ECG and predicted ventricular fibrillation.

Antiarrhythmic effects of melatonin have been demonstrated ex vivo and in rodent models, but its action in a clinically relevant large mammalian model remains largely unknown. Objectives of the present study were to evaluate electrophysiological and antiarrhythmic effects of melatonin in a porcine model of acute myocardial infarction. Myocardial ischemia was induced by 40-min coronary occlusion in 25 anesthetized pigs. After ischemia onset, 12 animals received melatonin (4 mg/kg). 48 intramyocardial electrograms were recorded from left ventricular wall and interventricular septum (IVS). In each lead, activation time (AT) and repolarization time (RT) were determined. During ischemia, ATs and dispersion of repolarization (DOR = RTmax − RTmin) increased reaching maximal values by 3–5 and 20–25 min, respectively. Ventricular fibrillation (VF) incidence demonstrated no relations to redox state markers and was associated with increased DOR and delayed ATs (specifically, in an IVS base, an area adjacent to the ischemic zone) (p = 0.031). Melatonin prevented AT increase in the IVS base, (p < 0.001) precluding development of early VF (1–5 min, p = 0.016). VF occurrence in the delayed phase (17–40 min) where DOR was maximal was not modified by melatonin. Thus, melatonin-related enhancement of activation prevented development of early VF in the myocardial infarction model.