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The members of the Task Force on Sudden Death dedicate this paper to the memory of our former friend and colleague, Professor Ronald W. F. Campbell. Ronnie spent his life working in the field of sudden cardiac death; he contributed much and helped many. But his own life fell victim to this very problem, sadly illustrating its unexpected nature. With Ronnie’s memory in mind the Task Force has worked diligently to describe the extent of our expanding knowledge in this field, hoping that our small contribution might help to appease his sad and sudden death.

Atrial fibrillation, a commonly encountered arrhythmia, has in recent years, been the subject of increased interest and intensive clinical research. There is also increasing awareness that atrial fibrillation is a major cause of embolic events which in 75% of cases are complicated by cerebrovascular accidents[1,2]. Atrial fibrillation is often associated with heart disease but a significant proportion of patients (about 30%) have no detectable heart disease[3]. Symptoms, occasionally disabling, haemo-dynamic impairment and a decrease in life expectancy are among the untoward effects of atrial fibrillation, resulting in an important morbidity, mortality and an increased cost for the health care provider[4]. The Working Group of Arrhythmias of the European Society of Cardiology created a Study Group on Atrial Fibrillation in order to establish recommen-dations for the better management of this arrhythmia and to promote multicentre studies. The purpose of this paper is to briefly outline the state of our knowledge on the clinical presentation, the causes, the mechanisms and therapeutic approaches currently available and to propose recommendations for management. Although atrial flutter can coexist with atrial fibrillation, it is considered a different arrhythmia and will not be covered in the present paper.

We read with interest the 2012 focused update of the ESC Guidelines for the management of atrial fibrillation (AF), and more specifically the recommendations formulated for catheter ablation (CA).1 A class I-level of evidence (LoE) A recommendation is attributed to CA for paroxysmal AF in symptomatic drug-refractory patients. In randomized controlled trials (RCTs), AF recurs off-antiarrhythmic drug (AAD) in one-third of patients, 1 year after a single CA.2,3 We have documented that AF recurs in up to 50% after 2 years, which is in line with other observational studies.4,5 The procedure has a …

Visible T wave changes of the 1st sinus beat following a ventricular premature beat (VPB) are sometimes observed in the electrocardiograms (ECG) of both healthy subjects and cardiac patients. We hypothesized that ventricular repolarization of the post-VPB beat can be modulated even without visible T wave changes. We analyzed 12-lead ECGs acquired in 7 healthy subjects, with at least 1 VPB/ECG with no visible changes of the 1st post-VPB beat. The spatial T loop of each sinus beat was reconstructed in derived XYZ leads and was characterized by 5 parameters. The 1st post-VPB beat was compared with the 2nd and 3rd pre-VPB beats. In 6 subjects, 1 to 3 T-loop parameters were significantly modified with an average change from -18.9% to 30.1% signifying increased repolarization heterogeneity. In conclusion, heterogeneity of the post-VPB sinus beat can be increased in the absence of visible T wave changes.

Background: Evidence from earlier studies indicates that intake of very long-chain n-3 polyunsaturated fatty acids (n-3 PUFA, also named omega-3 fatty acids) as present in fish oil reduces the risk of sudden death. Sudden death forms a major part of mortality from cardiovascular disease and is in most cases a direct consequence of cardiac arrhythmia. n-3 PUFA may exert their protective effect through reducing the susceptibility for cardiac arrhythmia. Objective: To investigate the effect of n-3 PUFA on the incidence of recurrent ventricular arrhythmia. This paper presents the rationale, design and methods of the Study on Omega-3 Fatty acids and ventricular Arrhythmia (SOFA) and discusses problems encountered in conducting a multicentre clinical trial on food. Design: A randomised, parallel, placebo-controlled, double blind intervention study, which obeys the guidelines for Good Clinical Practice. Setting: Multiple cardiology centres in Europe. Subjects: A total of 500 patients with an implantable cardioverter defibrillator (ICD). An ICD detects, treats and stores cardiac arrhythmic events in its memory chip. Interventions: Patients receive either 2 g/day of fish oil, containing approximately 450 mg eicosapentaenoic acid and 350 mg docosahexaenoic acid, or placebo for 12 months. Primary outcome: Spontaneous ventricular tachyarrhythmias as recorded by the ICD or all-cause mortality. Conclusion: SOFA is designed to answer the question whether intake of n-3 PUFA from fish-a regular food ingredient-can reduce the incidence of life-threatening cardiac arrhythmia. If this proves to be true, increasing the intake of n-3 PUFA could be an easy, effective and safe measure to prevent fatal arrhythmia in the general population.

Two patients with dystrophia myotonica showed high-grade atrio-ventricular block. Both underwent electrophysiological studies which revealed sinus and A-V nodal disease with normal intraventricular conduction in 1 case and His-Purkinje conduction disease in the other. Dystrophia myotonica may, therfore, involve all parts of the cardiac conduction system and may affect the generation of cardiac impulses. Pacemaker implantation may be necessary especially if drugs such as procainamide, which in addition to controlling myotonic symptoms may aggravate conduction disorders, are to be used.

The SWORD trial was designed to enroll 6400 patients to test the hypothesis that d-Sotalol would reduce total mortality in high risk survivors of a myocardial infarction (MI). Patients (pts) ≥ 18 years of age with an LVEF ≤ 40% and a recent (6–42 days) MI or a remote (g42 days) MI with overt heart failure (NYHA class II or III) were randomized to placebo or d-Sotalol (100 mg bid, or 200 mg bid if tolerated) for a follow up ≥ 18 mos. The trial was stopped on 11/1/95 after enrolling 3119 pts (mean follow up = 156 days) because the boundary for harm was crossed (z = -2.8), 42 (2,7%) pts died on placebo; 71 (4.6%) died on d-Sotalol (p = 0.005). All baseline comparisons between placebo and d-Sotalol showned no significant difference; mean LVEF was 30,8%; 29.2% pts had a recent MI; 70.8% of pts had a remote MI. Download : Download high-res image (84KB) Download : Download full-size image Conclusion Prophylactic therapy with oral d-Sotalol in a post MI population with LV dysfunction resulted in a significantly increased mortality.