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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 …

Background: Two studies have suggested that seropositivity for Chlamydia pneumoniae (C. pneumoniae) is a risk factor for coronary heart disease (CHD) but the association remains tenuous. Further data is required in other populations to consolidate this observation. Aims: Initially to determine descriptive risk factors for C. pneumoniae seropositivity in a general population sample and subsequently to examine the relation of seropositivity for this organism to CHD for the first time in a British population. Setting: A single general practice health screening clinic and a cardiology clinic involving patients predominantly residing in south London and Surrey. Subjects: 210 consecutive caucasian men (62%) and women (38%) aged 18–79 including 67 men aged 45–65. This latter group acting as controls were then also compared with 103 consecutive males aged 45–65 with angiographically confirmed coronary heart disease. Methods: A questionnaire was administered by a research nurse and serum was analysed for IgG and IgA against C. pneumoniae and other Chlamydiae by a microimmunofluorescence test. Serum was said to be low positive at a specific IgG antibody titre of 16–32, and high positive if 64 or greater. Results: Amongst the general practice health screening clinic population 14 subjects (7%) were excluded due to possible cross-reactivity with other Chlamydia species (predominantly C. trachomatis ). Of the remaining 196 subjects, 13 (6%) had high positive C. pneumoniae IgG titres, 68 (35%) had low titres and 1.25 had no detectable antibody. After adjustment for sex, age, smoking history, social class and family size only one risk factor for high positive titres in this group was identified, which was the number of children currently living in the home (OR 2.29 1.09–4.80, P = 0.03). No factors were significantly related to low titres. 22/100 (22%) cases with coronary heart disease and 3/64 (4.7%) of controls had high positive IgG titres for C. pneumoniae . Similarly 21% of cases and 9.4% of controls had positive C. pneumoniae specific IgA serology. 45% of cases and 44% of controls had low C. pneumoniae IgG titres. The association of CHD with a C. pneumoniae IgG titre of 64 or above was independent of all risk factors (OR 7.4 (1.7–33.1), P Conclusion: Serological evidence of C. pneumoniae infection is common amongst healthy British subjects. Smoking and social class are not important confounding variables in this study. Reinfection from contact with infected children in the home may be important in inducing higher titres in some subjects. These higher titres are more prevalent in subjects with coronary heart disease in the U.K. as reported in Finland and the U.S.A., and provide further evidence that C. pneumoniae may be important in the pathogenesis of this condition in these populations.

The objective of the European Myocardial Infarct Amiodarone Trial (EMIAT) is to assess the efficacy of amiodarone on mortality of patients with depressed left ventricular (LV) function following myocardial infarction (Ml). The rationale for the trial is as follows: patients with poor LV function after acute Ml have a high sudden cardiac death (SCD) mortality; amiodarone is a successful prophylactic therapy against SCD in patients with ventricular arrhythmias; a number of small studies (Canadian Amiodarone Myocardial Infarction Arrhythmia Trial [CAMIAT] pilot study, Basel Antiarrhythmic Study & Infarct Survival [BASIS], and the Polish Amiodarone Trial [PAT]) of prophylactic amiodarone post AMI have shown a beneficial response attributable to amiodarone. Patients are enrolled between 5 and 21 days after acute MI if LV ejection fraction (assessed by multiplegated image acquisition nuclear angiography) is ≤40%. The study group is stratified according to ejection fraction (stratum 1,31–40%; stratum 2, 700 patients are enrolled from >60 centers (13 countries). The total study mortality (10% at 500 days) and the differential mortality of both strata are as anticipated. Side effects have been infrequent and very few patients have been withdrawn from the study. Trial conclusion is forecast for October 1995.

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.

A discrete model has been developed which reproduces the intercellular electrophysiological processes within a block of myocardial tissue. The behaviour of individual elements is introduced in the form of the digitised physiologic and premature action potentials which are comprehended as series of jumps between discrete polarisation levels. For each cellular element, the model introduces the ercitation threshold as the minimum electric flow in the surrounding which can ercite the cell, and the sensitivity towards the electrotonic interactions which can advance or slow down the depolarisation and repolarisation processes of the cell. The ercitation threshold and the electrotonic sensitivity are dependent on the current polarity of the element. The numerical solution of the model is based on discrete planning of asynchronous events. The time increments are dynamically computed according to the chosen precision of the discrete polarity levels. The model enables efficient simulation of the electrophysiological properties in 3-dintensional models of the myocardial tissue. The paper presents a detailed fonnal description of the model.

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.

A computer model of cardiac excitation and recovery processes reproduced chaotic behavior of the simulated tissue to investigate the way that different parameters influence the degree of modeled disorganization. The model included abnormal shapes of action potential curves corresponding to premature excitation, excitation transmission based on transmembrane voltages, and the electronic interactions between neighboring cells. The model was used to examine a one-dimensional cable of simulated cells. The degree of the simulated chaos was examined in the dependence on the shapes of action potential curves, on the threshold of transmembrane voltages initiating an excitation wave, and on the degree of the electrotonic interactions of neighboring cells. The maximum disorganization was achieved when combining the negative influence of all parameters. Changing the shape of the action potential curves had a greater preventive influence on the modeled chaos than variation of the other parameters. >

A computer model reproduced atrio-ventricular (AV) reentrant tachycardia and its termination by overdrive on-circuit pacing. The model simulated activation waves radiating along a one-dimensional circular pathway, the portions of which represent the atrial, AV nodal, His-Purkinje, ventricular, and bypass parts of the tachycardia circuit. The modeled pathway was composed of 289 elements, and the model distinguished only the depolarized and resting states of constituent elements and introduced differential refractoriness and conduction velocity for each element. Cycle length dependence of AV nodal decremental conduction is also introduced. The experiments with the model examined the capability of overdrive on-circuit pacing to terminate the tachycardia. The results of the study suggest that the usual impression of a regular recovery wave and of a regular excitable window moving uniformly along the macro-reentrant circuit is incorrect. >

A discrete model was developed which reproduces the intercellular electrophysiological processes within a block of myocardial tissue. The behavior of individual elements is introduced in the form of the digitized physiologic and premature action potentials which are comprehended as series of jumps between discrete polarization levels. For each cellular element, the model introduces the excitation threshold as the minimum electric flow in the surrounding which can excite the cell, and the sensitivity towards the electronic interactions which can advance or slow down the depolarization and repolarization processes of the cell. The excitation threshold and the electronic sensitivity are dependent on the current polarity of the element. The numerical solution of the model is based on discrete planning of asynchronous events. The time increments are dynamically computed according to the chosen precision of the discrete polarity levels. The model enables efficient simulation of the electrophysiological properties in three-dimensional models of the myocardial tissue. A detailed formal description of the model is given and two series of experiments are presented. >

A computer model is used to reproduce atrioventricular (AV) reentrant tachycardia in order evaluate the possibility of its termination by overdrive 'on-circuit' pacing. The model simulates activation waves radiating along a one-dimensional circular pathway composed of 289 elements. Experiments examined the capability of overdrive on-circuit pacing to terminate the tachycardia and its dependence on various factors. The results suggest the following: (A) the general impression of a regular recovery wave and of a regular excitable window moving uniformly along the macroreentrant circular path is incorrect; (B) the use of overdrive bursts of several stimuli with a short coupling interval has unpredictable effects; and (C) the use of bursts with coupling interval only slightly shorter than the tachycardia cycle length is more safe (with respect to tachycardia reinitiation) and for certain combinations of the coupling interval and cycle length, prolonged bursts do not reinitiate the tachycardia. >

Objective: Atrial fibrillation (AF) is the most common arrhythmia and it is associated with a five-fold risk of stroke. Atrial fibrillation associated ischaemic strokes and embolisms are more disabling and fatal. We aimed to investigate the time to ischemic stroke/embolism after the diagnosis of AF in patients who never used warfarin. Methods: We analyzed the records of 402674 patients over the age 18 who had the diagnosis of non-valvular atrial fibrillation (AF) according to ICD-10 code I48 from a nation-wide claims and utilization management system which processes claims for all health insurance funds in Turkey since 2007. In this study we have used completely anonymized data. Time-to-event analysis were used to measure the time to ischemic stroke/embolism after being diagnosed with AF. Results: A total of 28187 AF patients (7 %) had ischemic stroke or emboli. Time to ischemic stroke and emboli was 61,25 0,05 months from the first diagnosis of AF. Stroke/emboli was observed earlier in the patients with CHA2DS2-VASc score >1⁄4 2; mean 60,72 0,06 months. Stroke/emboli was observed in patients with CHA2DS2-VASc score 0 and 1 in mean 65,39 0,11 months and mean 65,02 0,09 months respectively. Conclusions: Stroke/emboli was observed in a significant portion of AF patients in 5 years, and increased risk score decreased time to ischemic/embolic event. Stroke/emboli is one of the most important adverse events in AF patients and contributes to mortality and observed earlier in patients with higher risk scores. Therefore anticoagulation and strict control is needed. Figure 1. Warfarin Use according to CHA2DS2-VASc Score -OP-243 Results of Anticoagulation in Patients with CHADS2 Score of 0 and CHA2DS2VASC Score of 1; An Investigation Using the National Turkish Atrial Fibriallation (TRAF) Registry. B. Yavuz, N. Ata, E. Oto, K. Aytemir, S. Okutucu, B. Evranos, D.K. Ozturk, R. Koselerli, E. Ertugay, Y.G. Ilhan, A.J. Camm, A. Oto. Kecioren Teaching and Research Hospital; Social Security Institution; Hacettepe University Faculty of Medicine; MITS; St George’s Medical School, London. The American Journal of Cardiology MARCH 13e16, 2014 10 IN AND C Objective: Atrial fibrillation is associated with ischaemic strokes. Stroke risk is not homogenous and is identified by risk stratification schemes created by adding the risk factors.A new risk score, CHA2DS2VASC risk scheme was developed to decrease the intermediate risk group of CHADS2 risk scheme and to decrease the confusion about anticoagulation. But it has also created a new confusion on anticoagulation of very low risk group of patients. Therefore to detect the effect of anticoagulation in CHADS2 score of 0 and CHA2DS2VASC score of 1 patients we compared offwarfarin and onwarfarin patientswhoseCHADS2 score was 0 and CHA2DS2VASC score was 1. Methods: We analyzed the records of 402674 patients over the age 18 who had the diagnosis of non-valvular atrial fibrillation (AF) according to ICD-10 code I48 from a nation-wide claims and utilization management system which processes claims for all health insurance funds in Turkey since 2007. In this study we have used completely anonymized data. Results: Twenty one percent of on warfarin group and 16% of off warfarin group was hospitalized over 5 years follow up. Major hemorrhage was more frequently encountered in on warfarin group than off warfarin group (2,7% and 1,3 respectively). Stroke/TIA/Systemic Embolism/Death composite endpoint was higher in on warfarin group than off warfarin group, (7,8% and 4,6% respectively). Conclusions: This analysis showed that both hospitalization and major hemorrhages were higher in on warfarin group and warfarin did not decrease the joint endpoint of thromboembolism and death in this low risk group. Therefore this result directs us to question the intermediate risk categorization of CHA2DS2VADSc risk scheme.

A microcomputer based development system for on-line analysis of intracardiac electrograms, recognition of arrhythmia and electrical stimulation therapy is described. An amplified and filtered intracardiac signal is digitised using an 8-bit analogue-to-digital converter at sampling rates up to 1 kHz. The resulting digital signal is input to a BBC microcomputer via the parallel user port and is analysed in real time using a BBC-6502 assembly language subroutine. The feature detection algorithm is based on recognising sequences of voltage gradients in the incoming electrical signal. The system has been used mainly to distinguish sinus rhythm complexes from tachycardia complexes and to trigger an external stimulator if tachycardia is sustained. However, it can also differentiate between sinus rhythm and other abnormal rhythms.

The object of the so-called Electrocardiographic Inverse Problem is the algorithmic analysis and diagnosis of the electrocardiogram (ECG). A part of this general problem is the Pacemaker Inverse Problem, which means the analysis of the ECG in order to establish details of heart-pacemaker interaction (HPI) with special reference to the diagnosis of pacemaker failure. The solution to this problem is of practical importance, because it is often impossible to evaluate such records clinically. The ECG patterns of natural cardiac activity and of the events stimulated by the pacemaker may not be distinguishable and many combinations of potential response of the implanted device have to be taken into account. A computer system providing automatic analysis of the HPI, based on ECG data, has been developed and implemented on an IBM PC AT computer. The system uses a complex algorithm which enables the evaluation of all possible combinations of HPI events, and establishes for each of these combinations its correspondence to the specified pacemaker algorithm. The system is written in Turbo Pascal and its source text has more than 11 000 lines.

A total of 167 patients undergoing investigation for suspected coronary artery disease (CAD) were genotyped for restriction fragment length polymorphisms (RFLP) at the apo A-1/C-III locus and the insulin gene locus using cloned human apo A-1 and insulin gene probes. The study group was subdivided into patients with absent or minimal CAD, intermediate CAD and severe obstructive CAD. An Sst-1 polymorphism located in the 3' non-coding region of the apo C-III gene identifies two alleles. One of the alleles (S2) showed a significantly increased frequency in the subjects with severe obstructive CAD (18%) compared with patients with minimal or absent CAD (6%) (P less than 0.025) and normolipidaemic control subjects. This A-1/C-III polymorphism may be a marker for an abnormality in the A-1/C-III genes predisposing to atherosclerosis. In contrast to a previous report, we found no increase in the frequency of the Class 3 insulin alleles in subjects with severe CAD.

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.

Indoramin is a selective post-synaptic alpha blocker. Animal experiments had shown that it has antiarrhythmic effects, but whether this is due to its alpha blocking effect or some other mechanism is not known. Fifteen patients (10 males) underwent electrophysiological investigations before and 15 minutes after intravenous indoramin injection (0.2-0.5 mg kg-1). The plasma level of indoramin was measured and the patients were divided into two groups: group 1 (8 patients) whose plasma level was less than 100 micrograms ml-1 (average 72 micrograms ml-1) and group 2 (7 patients) whose plasma level was more than 100 micrograms ml-1 (average 151 micrograms ml-1). In both groups there was a significant drop in the systolic blood pressure after indoramin (129 +/- 22 to 111 +/- 23 mmHg, P less than 0.001). There was a marked improvement in the sinus node recovery time in group 1 only (253 +/- 92 to 163 +/- 40 ms, P less than 0.01). Similarly there was a decrease in AH interval during fixed rate atrial pacing in group 1 only (128 +/- 33 to 100 +/- 37 ms, P less than 0.05) and a significant decrease in the Wenckebach cycle length after indoramin in group 1 only (372 +/- 85 to 347 +/- 74 ms, P less than 0.05). At the atrial level there were no significant effects in either group but there was a significant increase in the ventricular effective refractory period in group 2 (231 +/- 35 to 264 +/- 64 ms, P less than 0.05) but no change in group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

A computer model of the cardiac conduction process and an integral equation mathematical model have been employed to study the functions of the atrioventricular (AV) node. Special attention has been paid to the dependence of conduction delay on cycle length. The models have been used to evaluate the question as to whether simple cycle length dependences of AV nodal conduction could cause the oscillations of cycle length which are sometimes observed in AV reentry tachycardia. The models consider the AV node as a linear structure in which the depolarisation wavefront radiates in one dimension only. A model representing the node by two parallel linear structures has also been examined. Some results obtained do not conform with those of natural circumstance and clinical experiments, suggesting that the above hypotheses of AV nodal function are too simple and restricted to explain the natural processes.

Summary A 25 year old man had experienced virtually incessant ventricular tachycardia since the age of 16 years, and complained of increasing lethargy and shortness of breath over the past 5 years. Despite medical therapy with numerous conventional antiarrhythmic agents, no single drug or combination of drugs had successfully controlled the tachycardia. Isotope and contrast angiography revealed an enlarged left ventricle with poor function. Electrophysiological studies demonstrated earliest endocardial activation at the left ventricular apex. No electrical procedure terminated tachycardia. Following institution of amiodarone, continuous ECG monitoring revealed periods of sinus rhythm alternating with periods of ventricular bigeminy. Repeat isotope angiography indicated a considerable improvement in L.V. function. There was a corresponding reduction in heart size on the chest radiograph. Clinical improvement was evidenced by disappearance of lethargy and shortness of breath. This report demonstrates that amiodarone, a new antiarrhythmic agent, may suppress long standing incessant ventricular tachycardia resistant to other antiarrhythmic agents. The marked reduction in heart size on amiodarone may suggest that the associated cardiomegaly is secondary to tachycardia.

A computer simulation model of cardiac rhythm disturbances and of the heart/pacemaker interaction has been created and implemented on a NORD-100 minicomputer. The model incorporates important properties including cycle length dependence of the refractory periods of different parts of the heart and of the atrioventricular nodal conduction speed. Computational experiments produce an explicit timetable of polarisation changes, a simulated one-channel electrocardiographic record and a pacemaker marker channel. The simulation program is written infortran and uses discrete event simulation techniques. The heart is modelled using instances of nine simulation process prototypes. The paper presents and discusses several examples in the form of simulated electrocardiographic records and the results show that the model is clinically relevant. Included in the examples are the modelling of rhythm disturbances, pacemaker actions, pacing for tachycardia prophylaxis and atrioventricular nodal conduction disorders.

A computer simulation model of cardiac rhythm and heart-pacemaker interactions has been used to examine the possibility of short atrial-ventricular (AV) delay DDD pacing to prevent junctional reentry tachycardia. The experiments compared the actions of two pacemaker models: a clinically realistic DDD mode operating with quasi-Wenckebach prolongation of the AV delay, and a modification of the DDD mode which is programmed according to atrial and ventricular refractoriness of the heart and the conduction delays of pathological bypass tracts. The pathological phenomena modeled in the experiments simulate different possibilities of tachycardia initiation. The computational results prove that many possible mechanisms of initiation of junctional reentry tachycardia are beyond the prophylactic capabilities of current sophisticated DDD pacemakers. The results also show that the suggested pacing mode improves antitachycardia prophylaxis even when responding to complex pathological episodes of natural cardiac activity. >

Symptomatic myopotential interference was observed in a patient with a respiratory-dependent rate modulated pacemaker (RDP3). During treadmill exercise, prolonged interference suspended the rate responsive function and resulted in reversion to the interference mode with the pacing rate falling back to the basic frequency during the interference. This loss of rate response resulted in severe impairment of exercise tolerance and reduction in cardiac output during exercise. The unit was replaced with a bipolar activity sensing rate modulated pacemaker.

Modern haemodynamic techniques have allowed a greater degree of understanding of the effects of cardiac arrhythmias. The haemodynamic consequences relate to a number of factors which include: the ventricular rate and the regularity of the rhythm, the presence or absence of cardiac disease, the relationship between atrial and ventricular systole, the synchronicity of ventricular contraction, the preservation and level of autonomic tone and disease in other organs1,2.

A computer model simulating both excitation and recovery processes within a block of heart muscle tissue has been developed. It incorporates blocks of tissue consisting of several thousand elements and introduces phenomena which are omitted in other heart models. These include the specific shapes of action potential curve corresponding to excitation of cells which have not been fully recovered. Results of simulation studies are presented in the form of three-lead orthogonal electrocardiograms (ECGs). Another model was used to reproduce the electronic interactions between neighboring cells during recovery phases. It also improves the concept of the modeled excitation and treats the depolarization as an self-initiating process depending only on membrane voltage between coupled cells. Both models have been used in various computational series. The results presented include models of destabilizing the tissue due to fast sequential stimulation models of repolarization changes in ischemia and infarction, and models of 'reflection' mechanisms. >

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.