Effect of supplemented intake of omega-3 fatty acids on arrhythmias in patients with ICD: fish oil therapy may reduce ventricular arrhythmia.

PURPOSE: The aim of this study was to evaluate the effects of fish oils, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), on ventricular tachyarrhythmic episodes (VTEs) in implantable cardioverter defibrillator (ICD) recipients with ischemic cardiomyopathy. METHODS: One hundred five ICD recipients with ischemic cardiomyopathy received 3.6 g of EPA and DHA and placebo for 6 months, each at a random order, with a 4-month washout period between treatments. Eighty-seven patients completed the 16-month study protocol. The primary end point was any VTE (including sustained and non-sustained ventricular tachycardias at a rate of >150 bpm) as recorded by the ICDs. Secondary end points included device therapy (anti-tachycardia pacing (ATP) or shocks). RESULTS: During treatment with fish oils, there was a significant increase in EPA and DHA concentrations in red blood cells (RBCs) and subcutaneous fat tissue. Among 87 patients who completed the study protocol, the mean number of VTEs was significantly lower during treatment with fish oil (1.7) vs. placebo (5.6; p = 0.035). Appropriate device therapy for VTE occurred in 18 (21%) patients. Fish oil therapy was associated with a trend toward fewer VTEs terminated with ATP (2.8 ± 13.7 vs. 0.5 ± 2.1, respectively; p = 0.077). VTE terminated by ICD shocks, however, was rare, and rates were similar between both groups (0.11 ± 0.6 vs. 0.10 ± 0.4, p = not significant, respectively). CONCLUSIONS: Our data suggest that fish oil therapy may be associated with a reduction in the frequency of VTE in ICD recipients with ischemic cardiomyopathy.

Long-term outcome of patients who received implantable cardioverter defibrillators for stable ventricular tachycardia.

INTRODUCTION: Evidence is inconclusive concerning the role of implantable cardioverter defibrillators (ICDs) to treat patients with hemodynamically stable ventricular tachycardia (VT). The goal of this study was to estimate future risk of unstable ventricular arrhythmias in patients who received ICDs for stable VT. METHODS AND RESULTS: We reviewed complete ICD follow-up data from 82 patients (age 66.1 +/- 11.3 years; left ventricular ejection fraction 32.3%+/- 11.2%; mean +/- SD) who received ICDs for stable VT. During the follow-up period of 23.6 +/- 21.5 months (mean +/- SD), 15 patients (18%) died, and 10 (12%) developed unstable ventricular arrhythmia, 8 of whom had the unstable arrhythmia as the first arrhythmia after ICD placement. Estimated 2- and 4-year survival in the whole group was 80% and 74%, respectively. Estimated 2- and 4-year probability of any VT and unstable VT was 67% and 77% and 11% and 25%, respectively. There were no differences in age, ejection fraction, sex, underlying heart disease, cycle length, symptoms, baseline electrophysiologic study results, or QRS characteristics of qualifying VT between patients who developed unstable ventricular arrhythmia and patients who did not. Twenty-nine patients (35%) had at least one inappropriate shock, and 11 (13%) underwent further surgery for ICD-related complications. CONCLUSION: Patients who present with hemodynamically stable VT are at risk for subsequent unstable VT. ICD treatment offers potential salvage of patients with stable VT who subsequently develop unstable VT/ventricular fibrillation, although complications and inappropriate shocks are considerable. No predictors could be found for high and low risk for unstable arrhythmias. These findings support ICD treatment for stable VT survivors.

Modulation of ventricular fibrillation in isolated perfused heart by dofetilide.

The authors studied the involvement of IKr potassium current in ventricular fibrillation during perfusion. Electrophysiologic parameters were measured before and after dofetilide administration (2.5, 7.5, and 12.5 x 10-7 M, n = 8) in isolated perfused feline hearts. During pacing, these parameters included epicardial conduction time, refractoriness, and the fastest rate for 1:1 pacing/response capture. During 8 minutes of electrically induced tachyarrhythmias, they included heart rate and normalized entropy reflecting the degree of organization. In all groups, arrhythmia rate was slower in the right ventricle than in the left ventricle. Dofetilide decreased the arrhythmia rate more than it increased organization, reduced its maintenance, or increased difficulty in initiation. Refractoriness was prolonged in a reverse use-dependent way which was less than 1:1 pacing/response capture. Unexpectedly, a moderate prolongation of conduction time was observed. Inverse correlation was found between the arrhythmia rate and changes in refractoriness and conduction time and between the degree of organization and refractoriness (both ventricles) and conduction time (right ventricle). Dofetilide, which intensively blocks IKr current and unexpectedly suppressed conduction, has different quantitative effects on fibrillation features. These changes in fibrillation suggest that these effects are mainly associated with refractoriness prolongation and do not seem to be attenuated by conduction suppression.

ST-segment deviation following implantable cardioverter defibrillator shocks: incidence, timing, and clinical significance.

ST-segment analysis is frequently used during surgical procedures, while ST deviation is considered a sign of myocardial injury. ST deviations were reported following transthoracic and epicardial electrical shocks. The prevalence, timing, and clinical significance of ST-segment deviation following endocardial ICD shocks are discussed in this article. Twenty-eight patients undergoing 125 shock episodes during ICD implantation or testing were included. A 12-lead ECG was recorded at baseline, continuously during the first 3-10 seconds, 1 minute after test shocks, 3-10 seconds and 1 and 5 minutes after each shock given to terminate VF. ST deviation was diagnosed when the ST-segment was displaced > or = 1 mm in at least one lead compared to baseline. ST-segment deviations were observed after 49 (39%) of all shock episodes in 17 (61%) of patients. ST elevation was observed after 30 (24%) of all shock episodes, and ST depression after 31 (25%). Following 13 shock episodes in seven patients, ST-elevation and depression were observed. ST depressions occurred more frequently after shocks given to terminate VF than after lower energy test shocks (28% vs 18% respectively, P = 0.045). However, there was no significant difference in the prevalence of ST elevations between the lower or higher energy shocks. No adverse clinical events were observed in patients with or without postshock ST-segment deviation. ST-segment deviation following endocardial ICD shocks is a frequent phenomenon, occurring acutely and resolving during the first few minutes postshock. It mayhave no prognostic implications.

Effects of adrenaline on electrophysiological parameters during short exposure to global ischemia. A ventricular fibrillation study in isolated heart.

BACKGROUND: The mechanisms by which adrenaline may enhance defibrillation success rate, is poorly understood. OBJECTIVES: To study electrophysiological effects of adrenaline during short exposure to global ischemia. METHODS: In isolated perfused feline hearts, coronary perfusion was eliminated repeatedly for 1 min with 10 min reperfusion intervals. Treatment included: (1) continuous perfusion alone-control, (2) global ischemia alone, (3) adrenaline (10(-7) M) during perfusion, (4) adrenaline (10(-7) M) during global ischemia (n = 10), in separate hearts, (5) control and higher adrenaline concentration (1 x 10(-6) M), (6) during perfusion, (7) during global ischemia (n = 9). Measurements during pacing included: (1) diastolic threshold of excitability; (2) refractoriness; (3) epicardial conduction time; and (4) all tissue resistivity to indirectly detect changes in passive properties of conduction. Measurements during 1 min (or 90 sec) of electrically induced ventricular fibrillation included-all tissue resistivity and, based on maximal entropy spectral analysis and normalized entropy, rate of arrhythmia and degree of arrhythmia organization. RESULTS: Adrenaline (10(-7) M) during global ischemia vs control caused spontaneous arrhythmia termination, increased threshold significantly but reduced conduction time. Higher adrenaline concentration (1 x 10(-6) M) during global ischemia improved the passive properties of conduction and arrhythmia organization and reduced arrhythmia rate. Global ischemia alone increased conduction time but had a deleterious effect on passive properties. Adrenaline (10(-7) M) during perfusion improved conduction, but did so less than during global ischemia. Higher adrenaline concentration during perfusion (10(-6) M) improved arrhythmia organization and caused spontaneous arrhythmia termination but again less than during global ischemia. CONCLUSIONS: During short periods of global ischemia adrenaline improved the passive properties of conduction and arrhythmia organization, reduced arrhythmia rate and increased its spontaneous termination. Such changes may be operative in improving defibrillation success.