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Cardiac thromboembolism attributed to atrial fibrillation (AF) is responsible for up to one-third of ischemic strokes. Stroke may be the first manifestation of previously undetected AF. Given the efficacy of oral anticoagulants in preventing AF-related ischemic strokes, strategies of searching for AF after a stroke using ECG monitoring followed by oral anticoagulation (OAC) treatment have been proposed to prevent recurrent cardioembolic strokes. This white paper by experts from the AF-SCREEN International Collaboration summarizes existing evidence and knowledge gaps on searching for AF after a stroke by using ECG monitoring. New AF can be detected by routine plus intensive ECG monitoring in approximately one-quarter of patients with ischemic stroke. It may be causal, a bystander, or neurogenically induced by the stroke. AF after a stroke is a risk factor for thromboembolism and a strong marker for atrial myopathy. After acute ischemic stroke, patients should undergo 72 hours of electrocardiographic monitoring to detect AF. The diagnosis requires an ECG of sufficient quality for confirmation by a health professional with ECG rhythm expertise. AF detection rate is a function of monitoring duration and quality of analysis, AF episode definition, interval from stroke to monitoring commencement, and patient characteristics including old age, certain ECG alterations, and stroke type. Markers of atrial myopathy (eg, imaging, atrial ectopy, natriuretic peptides) may increase AF yield from monitoring and could be used to guide patient selection for more intensive/prolonged poststroke ECG monitoring. Atrial myopathy without detected AF is not currently sufficient to initiate OAC. The concept of embolic stroke of unknown source is not proven to identify patients who have had a stroke benefitting from empiric OAC treatment. However, some embolic stroke of unknown source subgroups (eg, advanced age, atrial enlargement) might benefit more from non–vitamin K-dependent OAC therapy than aspirin. Fulfilling embolic stroke of unknown source criteria is an indication neither for empiric non–vitamin K-dependent OAC treatment nor for withholding prolonged ECG monitoring for AF. Clinically diagnosed AF after a stroke or a transient ischemic attack is associated with significantly increased risk of recurrent stroke or systemic embolism, in particular, with additional stroke risk factors, and requires OAC rather than antiplatelet therapy. The minimum subclinical AF duration required on ECG monitoring poststroke/transient ischemic attack to recommend OAC therapy is debated.

Background: Atrial arrhythmias are common in patients with implantable cardioverter-defibrillator (ICD). External shocks and internal cardioversion through commanded ICD shock for electrical cardioversion are used for rhythm-control. However, there is a paucity of data on efficacy of external versus internal cardioversion and on the risk of lead and device malfunction. We hypothesized that external cardioversion is noninferior to internal cardioversion for safety, and superior for successful restoration of sinus rhythm. Methods: Consecutive patients with ICD undergoing elective cardioversion for atrial arrhythmias at 13 centers were randomized in 1:1 fashion to either internal or external cardioversion. The primary safety end point was a composite of surrogate events of lead or device malfunction. Conversion of atrial arrhythmia to sinus rhythm was the primary efficacy end point. Myocardial damage was studied by measuring troponin release in both groups. Results: N=230 patients were randomized. Shock efficacy was 93% in the external cardioversion group and 65% in the internal cardioversion group ( P Conclusions: This is the first randomized trial on external vs internal cardioversion in patients with ICDs. External cardioversion was superior for the restoration of sinus rhythm. The unmasking of silent lead malfunction in the internal cardioversion group suggests that an internal shock attempt may be reasonable in selected ICD patients presenting for electrical cardioversion. Clinical Trial Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT03247738.

Introduction: About 5% of all COVID-19 patients require intensive care, mostly because of respiratory failure. Little is known about concomitant multi-organ manifestation under these circumstances. Methods: Retrospective observational study using routine data sets of 13 COVID-19 patients requiring mechanical ventilation in the Regiomed Hospital Coburg, Germany, between March 1 st and June 15 th , 2020. Results: Of 13 patients eligible for this study, all were intubated and ventilated mechanically, with signs of infiltration in chest radiographs. 4 suffered from renal failure and needed dialysis; 3 of these patients died, but none without renal failure. Proteinuria was found in all and microhematuria in all but one patients tested (n=11). All developed metabolic alkalosis (BEmax 9.75±0.99, mean ±SEM), and 6 afterwards polyuria (6.75 ±2.45l per day); both conditions resolved in all surviving patients but 1 spontaneously and were not related to prior renal failure. Liver enzymes were elevated in all patients (γGT 506 ±78U/l), but bilirubin levels only in 4; 2 of these died shortly after. Bacterial superinfection was found in 8 patients, and in all 3 ones finally dying. Rhabdomyolysis affected 12 patients (CKmax 1604±542U/l) and resolved later. All patients had slightly elevated troponin T (0.059 ±0.013ng/ml), and 7 had elevated nt-pro-BNP levels (3566±2359pg/ml), indicating cardiac COVID-19, and elevated d-dimer levels (18.1 ±6.68mg/dl) representing disseminated intravascular coagulation. No thromboembolic was observed. The need of catecholamines was low ( Conclusions: Our data indicate that severe COVID-19 is a multi-organ disease, even though ARDS is the leading problem; renal involvement - together with bacterial superinfection - seems to be a major risk factor for unfavorable disease development. Especially metabolic alkalosis and polyuria without overt renal failure have not been studied yet and require close clinical attention.

Introduction: Mechanisms for persistent atrial fibrillation (AF) are unclear. We reasoned that AF drivers may fluctuate due to competing drivers in stereotypical spatial locations. This may explain why studies focused on small regions may show disordered waves while global mapping shows organized drivers. Hypothesis: That closely-spaced AF drivers may fluctuate more than drivers that are widely separated by mapping AF globally for prolonged durations using 2 independent mapping methods. Methods: In 55 patients with non-paroxysmal AF (24% female; 62.2±9.7 years), ablation at drivers identified by 64 pole baskets (Abbott, CA) terminated AF before pulmonary vein (PV) isolation. We mapped 360±45 AF cycles using (1) an open source phase method and (2) commercial tools, and quantified both fluctuations and locations of mapped drivers. Results: Patients had 4.2 ± 2.0 potential drivers by non-proprietary mapping (fig A), located per fig B. AF termination sites showed rotational/focal patterns (51/55 vs 55/55 patients; p=0.13 methods 1 vs 2) that fluctuated over time. In space, each AF driver was most prevalent in the left atrium, with clustering near left PVs (p2 = 2.11, p=0.12). Conclusions: Potential AF drivers where ablation terminates persistent AF are spatially stable but fluctuate over time. Fluctuations reflected competing sources, trended to be more prevalent in left atrium but were not clearly related to inter-site distance. Studies should examine the functional determinants of AF driver fluctuations.

Approximately 10% of ischemic strokes are associated with atrial fibrillation (AF) first diagnosed at the time of stroke. Detecting asymptomatic AF would provide an opportunity to prevent these strokes by instituting appropriate anticoagulation. The AF-SCREEN international collaboration was formed in September 2015 to promote discussion and research about AF screening as a strategy to reduce stroke and death and to provide advocacy for implementation of country-specific AF screening programs. During 2016, 60 expert members of AF-SCREEN, including physicians, nurses, allied health professionals, health economists, and patient advocates, were invited to prepare sections of a draft document. In August 2016, 51 members met in Rome to discuss the draft document and consider the key points arising from it using a Delphi process. These key points emphasize that screen-detected AF found at a single timepoint or by intermittent ECG recordings over 2 weeks is not a benign condition and, with additional stroke factors, carries sufficient risk of stroke to justify consideration of anticoagulation. With regard to the methods of mass screening, handheld ECG devices have the advantage of providing a verifiable ECG trace that guidelines require for AF diagnosis and would therefore be preferred as screening tools. Certain patient groups, such as those with recent embolic stroke of uncertain source (ESUS), require more intensive monitoring for AF. Settings for screening include various venues in both the community and the clinic, but they must be linked to a pathway for appropriate diagnosis and management for screening to be effective. It is recognized that health resources vary widely between countries and health systems, so the setting for AF screening should be both country- and health system-specific. Based on current knowledge, this white paper provides a strong case for AF screening now while recognizing that large randomized outcomes studies would be helpful to strengthen the evidence base.

In the last two decades, catheter ablation of atrial fibrillation (AF) has evolved into a procedure with both efficacy in reduction of AF burden and safety. This has led to changes in guidelines from ESC, AHA/ACC and HRS 1, 2 now recommending a catheter ablation procedure as a viable first line treatment option for patients suffering from AF with and without heart failure (HF). Current recommendations are based on relief of symptoms and not prevention of mortality and morbidity.

Background/Introduction: The ProAcor Study assessed the effectiveness of a structured patient management program over 12 months in patients who were discharged from hospital after an acute coronary syndrome (ACS) into ambulatory cardiology care (36 hospitals, 56 office-based cardiologists). Methods: The program comprised patient documentation with a specific instrument (BNK cardiac pass with visit scheduling) done jointly by the hospital physician and the office-based cardiologists, the definition of treatment targets and the structured information of patients in order to optimise adherence to therapy. Results: 992 patients with ACS were included (STEMI 44.3%, NSTEMI 39.5%, unstable angina pectoris UA 15.2%). In these groups, acute intervention PTCA was performed in 98.0%, 91.9% and 81.6% of patients, stent implantation in 98.6%, 95.6% and 92.7%, and coronary artery bypass graft in 0.7%, 2.5% and 3.3%, respectively. Mean hospital stay due to ACS was 6 days (median). At 12 months, 18 patients (1.8%) had died (among these, 9 due to cardiac event), while for 51 the status was unknown (5.1%). Based on a conservative approach that considered patients with unknown status as dead, 1-year mortality was 6.9%. Further data on non-fatal cardiac events, medication and quality of life (QoL) were collected from 796 patients (79.4%). Recurrent cardiac events were noted in 119 patients (14.9%), with an about equal distribution across STEMI and NSTEMI patients. On the EQ-5D visual analogue scale (0= worst, 100 best state of health) at 3 months as well as 12 months the median value was 80 points with little differences between subgroups. The EQ-5D index score was 0.91 ± 0.18 points at inclusion (STEMI 0.92, NSTEMI 0.90, UA 0.89) and was unchanged at 12 months. Conclusion: Compared to data based on usual care (e.g. German MONICA registry 13.3%), the 1-year mortality after ACS of only 6.9% in the structured ProAcor patients management program is remarkably low.

Background— The role of pulmonary vein (PV) isolation in ablative treatment of atrial fibrillation (AF) has been debated in conflicting reports. We sought to compare PV conduction in patients who had no AF recurrence (group I), patients who could maintain sinus rhythm on antiarrhythmic medication (group II), and patients who had recurrent AF despite antiarrhythmic medication (group III) after PV antrum isolation (PVAI). Methods and Results— PV conduction was examined in consecutive patients undergoing second PVAI for AF recurrence. We also recruited some patients cured of AF to undergo a repeat, limited electrophysiological study at >3 months after PVAI. All patients underwent PVAI with an intracardiac echocardiography (ICE)–guided approach with complete isolation of all 4 PV antra (PVA). The number of PVs with recurrent conduction and the shortest atrial to PV (A-PV) conduction delay was measured with the use of consistent Lasso positions defined by ICE. Late AF recurrence was defined as AF >2 months after PVAI with the patient off medications. Patients in groups I (n=26), II (n=37), and III (n=44) did not differ at baseline (38% permanent AF; ejection fraction 53±6%). Recurrence of PV–left atrial (LA) conduction was seen in 1.7±0.8 and 2.2±0.8 PVAs for groups II and III but only in 0.2±0.4 for group I ( P =0.02). In patients with recurrent PV-LA conduction, the A-PV delay increased from the first to second procedure by 69±47% for group III, 267±110% for group II, and 473±71% for group I ( P Conclusions— The majority of patients with drug-free cure show no PV-LA conduction recurrence. Substantial A-PV delay is seen in patients able to maintain sinus rhythm on antiarrhythmic medication or cured of AF compared with patients who fail PVAI.

Background— Although implanted cardioverter defibrillators (ICDs) effectively treat sustained ventricular tachyarrhythmias, up to 50% of ICD recipients eventually require concomitant antiarrhythmic drug therapy to prevent symptomatic arrhythmia recurrences and hence reduce the number of device therapies. Methods and Results— A total of 633 ICD recipients were enrolled in a randomized, double-blind, placebo-controlled study to evaluate the effect of daily doses of 75 or 125 mg of azimilide on recurrent symptomatic ventricular tachyarrhythmias and ICD therapies. Total all-cause shocks plus symptomatic ventricular tachycardia (VT) terminated by antitachycardia pacing (ATP) were significantly reduced by azimilide, with relative risk reductions of 57% (hazard ratio [HR]=0.43, 95% CI 0.26 to 0.69, P =0.0006) and 47% (HR=0.53, 95% CI 0.34 to 0.83, P =0.0053) at 75- and 125-mg doses, respectively. The reductions in all-cause shocks with both doses of azimilide did not achieve statistical significance. The incidence of all appropriate ICD therapies (shocks or ATP-terminated VT) was reduced significantly among patients taking 75 mg of azimilide (HR=0.52, 95% CI 0.30 to 0.89, P =0.017) and those taking 125 mg of azimilide (HR=0.38, 95% CI 0.22 to 0.65, P =0.0004). Five patients in the azimilide groups and 1 patient in the placebo group had torsade de pointes; all were successfully treated by the device. One patient taking 75 mg of azimilide had severe but reversible neutropenia. Conclusions— Azimilide significantly reduced the recurrence of VT or ventricular fibrillation terminated by shocks or ATP in ICD patients, thereby reducing the burden of symptomatic ventricular tachyarrhythmia.

Background —The recent availability of implantable cardioverter-defibrillators (ICDs) that record 1024 R-R intervals preceding a ventricular tachyarrhythmia (VTA) provides a unique opportunity to analyze heart rate variability (HRV) before the onset of VTA. Methods and Results —Fifty-eight post–myocardial infarction patients with an implanted ICD for recurrent VTA provided 2 sets of 98 heart rate recordings in sinus rhythm: (1) before a VTA and (2) during control conditions. Three subgroups were considered according to the antiarrhythmic (AA) drug regimen. A state of sympathoexcitation was suggested by the significant reduction in HRV before VTA onset compared with control conditions. β-Blockers and dl -sotalol enhanced HRV in control recordings; nevertheless, HRV declined before VTA independent of AA drugs. A gradual increase in heart rate and decrease in sinus arrhythmia at VTA onset were specific findings of patients who received dl -sotalol. Conclusions —The peculiar heart rate dynamics observed before VTA onset are suggestive of a state of sympathoexcitation that is independent of AA drugs.

Background: Although the use of drug-eluting stents has been shown to limit neointimal hyperplasia, currently available DES may adversely affect re-endothelialization, possibly precipitating late cardiac events. The aim of this study was to evaluate the efficacy and safety of a microbubble delivery of c-myc antisense peptide in preventing restenosis after coronary stenting in de novo stenosis with intravascular ultrasound. Methods: A BMS was implanted in de novo coronary artery lesions (RD ≥ 2.5- ≤4.0mm; TL ≥ 15- ≤ 30mm in length). Serial intravascular ultrasound analysis were performed in 25 lesions. A dose of 16mg RESTEN-MPTM (AVI BioPharma/Global Therapeutics LLC) was intravenously administered after stenting and again 24 hours later. Results: A total of 50 patients were enrolled, 34 in Essen, 13 in Coburg and 3 in Heidelberg. Before stenting, the MLD and length of stenosis was determined by QCA. 18 Patients had a LAD lesion, 21 LCX, 12 RCA. 84% (43/51) of the lesions were either Type B2 or C lesions. At six month follow-up, angiography with a QCA was performed. Generally the neointimal proliferation was minor and open vessel lumen could be demonstrated during follow-up. Of the 30 patients currently studied at six-months in the IVUS sub-study, six patients required TLR. Late lumen loss by QCA was 0.47±0.09mm. Volume stenosis by IVUS was 26 ± 4 %. Generally the neointima proliferation was minor and open vessel lumen could be demonstrated during follow-up. Summary: Microbubble delivery of c-myc antisense seems to be effective in reducing neointimal tissue proliferation without the problem of late stent thrombosis, because the proliferation seems to be attenuated but not fully blocked.

Background: Pulmonary vein antrum isolation (PVAI) is regarded as an effective therapy in patients with atrial fibrillation (AF). Extension and location of ablation lesions often remain unclear during the procedure. We report a new approach on visualization of myocardial injury using magnet resonance imaging (MRI) during PVAI procedure. Methods: Patients who underwent PVAI, received MRI before and at the terminal phase of PVAI. Delayed enhancement (DE-) MRI sequences were applied, and maximum intensity projections (MIP) obtained. Myocardial injury size was then measured on manually segmented 3D images by a computer algorithm using dynamic thresholding. Results: 30 patients received PVAI from January 2008 to May 2008. In a subset of 15 patients, MRI was performed before and during the procedure. Using DE-MRI, the average lesion to healthy myocardium ratio was 7.56±1.27% during PVAI. The figure shows an example of MIP of a DE-MRI scan in 2D (A,B) and 3D segmentation (C,D) in a anterior view pre (A,C), and during PVAI (B,D). Myocardial injury is identifiable as white tissue around PV single ostia (full arrows) and common trunk (dashed arrows). Conclusions: Using MRI is feasible in the course of ablation procedures. In PVAI patients, DE-MRI allowed identification of location and extension of myocardial injury. Therefore, this new MRI approach might improve ablation techniques, and thus long-term success of PVAI.

Preprocedural imaging and its integration into electroanatomical mapping (EAM) is commonly used in atrial fibrillation (AF) ablation. However, intraprocedural imaging based on rotational angiography (DynaCT Cardiac) may be superior in terms of actuality and may lead to an improved work-flow. Feasibility of integrating Dyna CT Cardiac into EAM has not yet been shown. In 23 patients (62±7 years, 16 male) undergoing catheter ablation of paroxysmal (n=10) or persistent (n=13) AF, we intraprocedurally performed rotational angiography enhanced by contrast agent applied to the pulmonary artery with offline segmentation of left atrium (LA) and pulmonary veins (PV). Fig 1 depicts reconstructed LA and PV-anatomy directly importet into CARTOMerge. Distances between the 2 modalities were analyzed. Direct image integration of prereconstructed 3D-anatomy was feasible in all patients. Procedure time was 156 ± 24 minutes including 11 ± 3 minutes for DynaCT Cardiac registration and segmentation. 132 ± 74 mapping points were taken. Mapping points deviated to intraprocedural DynaCT Cardiac 3D-reconstructions by 2.2 ± 0.4 mm (2.3 ± 0.5 mm in patients suffering from paroxysmal atrial fibrillation (AF) vs. 2.1 ± 0.40 mm persistent AF, n.s.). No complications occured. Integration of intraprocedural Dyna CT Cardiac into EAM was feasible and fast. The work-flow seemed to be improved by avoiding additional preprocedural imaging. The novel modality is highly accurate in comparison to EAM.

Coronary Flow Reserve (CFR) is defined as the ratio between flow in a coronary vessel at maximum hyperemia and at rest. It is considered as a marker for the integrity of the coronary mircrocirculation. The measurement is typically performed using dedicated Doppler guidewires and pharmacologic stimulation (CFRdoppler). This measurement is costly, time-consuming and potentially harmful since the Doppler wire has to be advanced into the coronary artery. Today a new angiography based algorithm is available using the first pass kinetic of the injected contrast dye to calculate the CFR. The aim of the present study was, to compare this new algorithm with the conventionally Doppler wire technique. CFR measurements were performed during 27 coronary interventions (10 female, mean age 64 ± 11 years). CFR doppler (Flowire, Volcano corp.) was calculated as the ratio of average peak velocity (APV) during hyperemia (140μg/kg·min −1 ) and at rest. For calculation of angiographic CFR angio , two angiograms were analised, one at base line flow and one at hyperemia state. CFR was calculated by the ratio between the hyperemia representing numbers of the logarithmic Time Density Curve (TDC) linear slope, multiplied with the coronary cross-sections, and the respective baseline representing numbers. An excellent correlation was found between the CFR doppler and the CFR angio values: CFR angio = 1× CFR doppler (r=0.87; p

Objectives: Threedimensional imaging has been widely adopted as a standard component of the AF ablation procedure. We tested the feasibility of the new 3D imaging system (DYNA-CT) using the C-arm to reconstruct the left atrium and the oesophagus and compared it to the established CT-scan imaging modality. Methods and results: We included 14 consecutive patients (7 female, mean age 54 +/− 12) presenting for PVAI in the study. Prior to the ablation procedure ( ). Table 1 demonstrates results of comparison between CT and RTA data. Conclusions: From our initial experience DYNA-CT seems to provide a feasible and reliable left atrial and oesophagus images to help mapping and navigation during the PVAI. Table 1: Anatomical structures demonstrated using the 2 imaging modalities

Sotalol is a beta-adrenergic blocker that also prolongs action potential duration and myocardial refractoriness over the short term (class III effect). Its short-term antiarrhythmic effects were compared with those of metoprolol, which has neither short-term class III nor membrane-stabilizing action, on reentrant ventricular arrhythmias produced by programmed stimulation in 17 conscious dogs 3 to 8 days after myocardial infarction. Ventricular arrhythmias were prevented or significantly slowed by sotalol in 11 of 19 studies (58%) compared with in one of 14 (7%) studies with metoprolol. Sotalol prolonged refractoriness in the infarct zone, measured from an implanted "composite" electrode, by 41 +/- 45% (mean +/- SD, p less than .01), which was significantly greater than the increases it produced in effective refractory period of the normal ventricle (14.0 +/- 5.5%) or QT interval (12.5 +/- 7.8%). Metoprolol had no effect on infarct-zone refractoriness. Sotalol differentially increases refractoriness in potential reentry circuits in ischemic myocardium. Its antiarrhythmic effect in this model is not due to beta-blockade, and is presumably related to prolongation of action potential duration.

We used cesium chloride (CsCl) for electrophysiologic studies in canine hearts in vivo and in vitro to examine the mechanisms underlying ventricular arrhythmias that are related to prolonged repolarization. Cesium is known to depress normal ventricular automaticity and some experimental arrhythmias by blocking delayed outward currents and prolonging action potential duration. In 10 dogs in normal sinus rhythm, 1 to 1.5 mM/kg iv CsCl prolonged the QT (QU) interval and induced ventricular ectopy in all, including multiform ventricular tachycardia. In 12 dogs with atrioventricular block, 1 to 1.5 mM/kg iv CsCl produced marked suppression of idioventricular rates (from 45 +/- 6 to 8 +/- 4 beats/min). These low rates were then associated with bigeminy or bursts of multiform ventricular arrhythmia. Pacing at rates of 60 beats/min or more suppressed these arrhythmias. Low doses of tetrodotoxin (1 microgram/kg) also abolished these bradycardia-dependent arrhythmias without affecting the amplitude of ventricular electrograms. Tissue concentrations of cesium were determined by anatomic absorption spectroscopy in five dogs after injection of 1 mM/kg CsCl. Thirty minutes after the injection, cesium levels in Purkinje fibers were 5.3 +/- 1.0 mM/kg, levels in ventricular muscle were 4.6 +/- 0.9 mM/kg, and levels in atrial muscle were 4.1 +/- 0.8 mM/kg. In eight isolated endocardial preparations from canine ventricles, standard microelectrode techniques were used to study the effects of superfusion with 5 mM cesium. After 30 min, we observed early afterdepolarizations interrupting phase 3 of Purkinje fiber action potentials that already showed prolonged repolarization. Slowing the rate generated single or multiple action potentials arising from partially repolarized levels of membrane potentials (-80 to -65 mV). Pacing rates of 30 to 60 beats/min diminished the afterdepolarizations and suppressed the spontaneous beats. Tetrodotoxin at a concentration of 10(-8) g/ml, which did not affect upstroke velocity, abolished the afterpotentials. We conclude that cesium induced bradycardia-dependent ventricular arrhythmias caused by early afterdepolarizations. These data suggest that an inward current, probably carried by sodium ions, appears to be essential for the occurrence of this phenomenon. The association of delayed repolarization, afterdepolarizations, and triggered activity has similarities to the phenomenon of drug-induced prolongation of the QTU interval associated with multiform ventricular tachycardia in humans, i.e. "torsades de pointes."

Eighteen patients with sustained ventricular tachycardia underwent electrophysiologic studies to establish the therapeutic efficacy of sotalol. In each patient ventricular tachycardia could be reproducibly initiated by programmed stimulation during control studies. Sotalol prevented induction of sustained ventricular tachycardia in 12 of the 18 patients (67%). Prolongation of the QTC interval and of ventricular refractoriness was regularly observed after sotalol but did not reliably predict prophylactic efficacy. Severe adverse effects, including congestive heart failure and sinus node dysfunction, were noted early during sotalol therapy in three patients. Nine patients were placed on long-term oral treatment with sotalol and four patients on another effective agent. In these 13 patients, complete (12 patients) or partial (one patient) long-term prophylaxis against ventricular tachycardia was documented over a mean follow-up period of 16 months (range 8 to 24). The study suggests that sotalol can provide effective prophylaxis against sustained ventricular tachycardia; this prophylactic efficacy is not typical for pure beta-adrenergic antagonism but may at least partly result from experimentally observed prolongation of the ventricular action potential duration.