Postinfarction Arrhythmia Management

VF and sustained VT occurring late (>48 h) in the course of an AMI suggest an ominous prognosis. Among 390 patients in a multicenter Dutch study, 49% had recurrent VT or VF over a mean follow-up period of 1.9 yr. Nineteen percent died because of recurrent VT or VF, and the total mortality during this period was 34% (146). Thus, late ventricular arrhythmias during AMI suggest a high risk for arrhythmia recurrence.

As with VT and VF not temporarily related to AMI, the therapeutic approaches are the implantable cardioverter defibrillator (ICD) and antiarrhythmic therapy, primarily with amiodarone. No randomized studies comparing these treatment strategies have been performed in patients recovering from AMI. Nevertheless, extrapolation from the AVID (147), CIDS (148), and CASH (149) trials has led to increased ICD use in patients recovering from AMI. Few data exist to guide clinicians in the management of NSVT in the early post-MI setting. Two recent trials, MADIT (150) and MUSTT (151) showed a significant survival benefit in patients with prior infarct, decreased left ventricular function, NSVT, and inducible VT or VF at EPS when treated with ICDs. AMI patients were excluded from MADIT. Although 17% of the patients in MUSTT were enrolled within 1 mo of AMI, it is not known how many of these patients were enrolled during the AMI admission. Nevertheless, extrapolation from these clinical trials will probably make electrophysiology testing available to AMI patients with late NSVT, with ICD implantation if inducible. The results of the CABG Patch trial (152) suggest that revascularization may also be an important component in preventing sudden cardiac death in coronary patients.

Rigorous, placebo-controlled double-blind studies have been performed in patients with relatively low-grade VEA following AMI. Because asymptomatic VEA is associated with increased mortality following AMI (153,154), the Cardiac Arrhythmia Suppression Trials (CAST) I and II were designed to determine whether expression of asymptomatic VEA would improve survival. Although encainide, flecainide (155), and ethmozine (156) effectively suppressed VPBs, the trials were terminated prematurely because of excess mortality in the encainide and flecainide treatment arms and no possibility of reduced mortality in the ethmozine group. Several smaller studies using other type I drugs have shown either no benefit or an adverse effect (157,158).

Amiodarone, on the other hand, may be of some benefit in post-infarct patients. In CAMIAT, patients with ventricular ectopy 6-45 d post-infarct were randomized to amiodarone or placebo. Amiodarone reduced the likelihood of SCD or resuscitated cardiac arrest, but had no effect on total mortality (159). EMIAT, which enrolled infarct survivors with LVEF <40%, yielded similar results (160). In a meta-analysis of these two trials and other studies of post-infarct and heart-failure patients, amiodarone was associated with a lower mortality than control patients (161). In a randomized, placebo-controlled study involving 1456 post-infarct patients completed in 1980, there was a trend toward lower mortality in patients assigned to racemic sotalol (162). More recently, however, enthusiasm has been dampened by the premature termination of the SWORD trial (163). Post-MI patients randomized to D-sotalol, a pure type III agent, had a higher mortality than patients treated with placebo. Data are beginning to emerge regarding newer class III agents. Preliminary data suggests that dofetilide is mortality-neutral in post-MI patients (DIAMOND-MD) (104), and a similar study utilizing azimilide is in progress (ALIVE) (164).

The results of these trials have been transmitted quickly into clinical practice. The GISSI investigators noted that the use of antiarrhythmic agents in patients after AMI decreased by approx 50% between 1984 and 1994. Throughout this period, amiodarone was the most frequently prescribed agent, although its use diminished significantly during this period (165).

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