The mechanisms for these arrhythmias are multifactorial and include ongoing ischemia, hemodynamic and electrolyte abnormalities, reentry, and enhanced auto- maticity. As many as 10% of hospitalized patients receiv- ing fibrinolytic therapy in the GUSTO-I trial had sustained VT/VF complicating their course.488 An analysis of patients referred for primary PCI in the APEX-AMI (Assessment of Pexelizumab in Acute Myocardial Infarction) trial reported a lower incidence of sustained VT/VF (5.7%); 90% of cases occurred within 48 hours of presentation.489 Compared with patients without VT/VF, 90-day mortality risk was 2-fold higher for patients with early VT/VF (ie, before the comple- tion of primary PCI) and 5-fold higher for patients with late VT/VF (ie, after primary PCI). Several factors were asso- ciated with the occurrence of both early and late VT/VF, including HF, hypotension, tachycardia, shock, and TIMI flow grade. Treatment consists of immediate defibrillation or cardioversion for VF or pulseless sustained VT, respectively, and antiarrhythmic drug therapy in accordance with the 2010 Advanced Cardiac Life Support guidelines for sustained VT with a pulse.490 Prevention of VT/VF is directed to correction of electrolyte and acid/base abnormalities, optimization of myocardial perfusion, eradication of ongoing ischemia, and treatment of associated complications such as HF or shock. Early (within 24 hours of presentation) administration of beta blockers has been associated with a reduction in the incidence and is recommended for all patients without con- traindications (Section 8.1). The prophylactic use of lidocaine is not recommended. Premature ventricular complexes, non- sustained VT not associated with hemodynamic compromise, and accelerated idioventricular rhythms that emerge after reperfusion are not indicative of increased SCD risk and do not require specific therapy in the acute phase of STEMI. 9.5.2. Implantable Cardioverter-Defibrillator Therapy Before Discharge Class I 1. 