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Background The subcutaneous implantable cardioverter-defibrillator (S-ICD) is developed to overcome lead-related complications and systemic infections, inherent to transvenous ICD (TV-ICD) therapy. The PRAETORIAN trial demonstrated that the S-ICD is non-inferior to the TV-ICD with regard to the combined primary endpoint of inappropriate shocks and complications. This prespecified secondary analysis evaluates all complications in the PRAETORIAN trial. Methods and results The PRAETORIAN trial is an international, multicentre, randomized trial in which 849 patients with an indication for ICD therapy were randomized to receive an S- ICD (N = 426) or TV-ICD (N = 423) and followed for a median of 49 months. Endpoints were device-related complications, lead-related complications, systemic infections, and the need for invasive interventions. Thirty-six device-related complications occurred in 31 patients in the S-ICD group of which bleedings were the most frequent. In the TV-ICD group, 49 complications occurred in 44 patients of which lead dysfunction was most frequent (HR: 0.69; P = 0.11). In both groups, half of all complications were within 30 days after implantation. Lead-related complications and systemic infections occurred significantly less in the S-ICD group compared with the TV-ICD group (P < 0.001, P = 0.03, respectively). Significantly more complications required invasive interventions in the TV-ICD group compared with the S-ICD group (8.3% vs. 4.3%, HR: 0.59; P = 0.047). Conclusion This secondary analysis shows that lead-related complications and systemic infections are more prevalent in the TV-ICD group compared with the S-ICD group. In addition, complications in the TV-ICD group were more severe as they required significantly more invasive interventions. This data contributes to shared decision-making in clinical practice.

ObjectiveThe Rate Control versus Electrical Cardioversion Trial 7–Acute Cardioversion versus Wait and See trial compared early to delayed cardioversion for patients with recent-onset symptomatic atrial fibrillation (AF). This study aims to evaluate the adherence to a 4-week mobile health (mHealth) prescription to detect AF recurrences after an emergency department visit.MethodsAfter the emergency department visit, the 437 included patients, irrespective of randomisation arm (early or delayed cardioversion), were asked to record heart rate and rhythm for 1 min three times daily and in case of symptoms by an electrocardiography-based handheld device for 4 weeks (if available). Adherence was appraised as number of performed measurements per number of recordings asked from the patient and was evaluated for longitudinal adherence consistency. All patients who used the handheld device were included in this subanalysis.Results335 patients (58% males; median age 67 (IQR 11) years) were included. The median overall adherence of all patients was 83.3% (IQR 29.9%). The median number of monitoring days was 27 out of 27 (IQR 5), whereas the median number of full monitoring days was 16 out of 27 (IQR 14). Higher age and a previous paroxysm of AF were identified as multivariable adjusted factors associated with adherence.ConclusionsIn this randomised trial, a 4-week mHealth prescription to monitor for AF recurrences after an emergency department visit for recent-onset AF was feasible with 85.7% of patients consistently using the device with at least one measurement per day. Older patients were more adherent.Trial registration numberNCT02248753.

Background: In the 123-study, we prospectively assessed, in a randomized fashion, the minimal cryoballoon application time necessary to achieve pulmonary vein (PV) isolation (PVI) in patients with paroxysmal atrial fibrillation (AF) with the aim to reduce complications by shortening the application duration. The first results of this study demonstrated that shortened cryoballoon applications (

Objectives This study sought to determine prospectively the rate of conductor externalization (CE), and whether this was associated with electrical failure. Background The Riata family of defibrillator leads was placed under U.S. Food and Drug Administration advisory as of November 28, 2011 because of high rates of CE. Methods A nationwide cohort established in 2012 of 1,029 patients with recalled Riata leads with 147 CE were followed until death, lead discontinuation, or 3 annual screenings with fluoroscopy and device interrogation. Results Follow-up of 882 patients with normal baseline fluoroscopy revealed incident overt CE in 95 leads (11%) after median risk time of 2.9 years, yielding an incidence rate of 4.9 (95% confidence interval [CI]: 3.9 to 5.9) per 100 patient-years. The incidence rate was significantly higher in 8-F Riata leads than in 7-F Riata ST leads (7.0 vs. 3.2 per 100 patient-years; p Conclusions The development of CE is progressive in nature with an incidence rate of new CE of 4.9 per 100 patient-years, with a higher rate for 8-F Riata leads than for 7-F Riata ST leads. Despite the high rate of structural failure, no association between development of CE and electrical failure was observed.

BACKGROUND: Patients with recent-onset atrial fibrillation commonly undergo immediate restoration of sinus rhythm by pharmacologic or electrical cardioversion. However, whether immediate restoration of sinus rhythm is necessary is not known, since atrial fibrillation often terminates spontaneously.METHODS: In a multicenter, randomized, open-label, noninferiority trial, we randomly assigned patients with hemodynamically stable, recent-onset (RESULTS: The presence of sinus rhythm at 4 weeks occurred in 193 of 212 patients (91%) in the delayed-cardioversion group and in 202 of 215 (94%) in the early-cardioversion group (between-group difference, -2.9 percentage points; 95% confidence interval [CI], -8.2 to 2.2; P = 0.005 for noninferiority). In the delayed-cardioversion group, conversion to sinus rhythm within 48 hours occurred spontaneously in 150 of 218 patients (69%) and after delayed cardioversion in 61 patients (28%). In the early-cardioversion group, conversion to sinus rhythm occurred spontaneously before the initiation of cardioversion in 36 of 219 patients (16%) and after cardioversion in 171 patients (78%). Among the patients who completed remote monitoring during 4 weeks of follow-up, a recurrence of atrial fibrillation occurred in 49 of 164 patients (30%) in the delayed-cardioversion group and in 50 of 171 (29%) in the early-cardioversion group. Within 4 weeks after randomization, cardiovascular complications occurred in 10 patients and 8 patients, respectively.CONCLUSIONS: In patients presenting to the emergency department with recent-onset, symptomatic atrial fibrillation, a wait-and-see approach was noninferior to early cardioversion in achieving a return to sinus rhythm at 4 weeks. (Funded by the Netherlands Organization for Health Research and Development and others; RACE 7 ACWAS ClinicalTrials.gov number, NCT02248753.).

Contains fulltext : 209368.pdf (Publisher’s version ) (Open Access) BACKGROUND: The second-generation cryoballoon significantly improves outcome of pulmonary vein isolation (PVI) but may cause more complications than the first generation. Currently, no consensus regarding optimal cryoballoon application time exists. The 123-study aimed to assess the minimal cryoballoon application duration necessary to achieve PVI (primary endpoint) and the effect of application duration on prevention of phrenic nerve injury (PNI). METHODS: Patients

BACKGROUND: Current standard of care for patients with recent-onset atrial fibrillation (AF) in the emergency department aims at urgent restoration of sinus rhythm, although paroxysmal AF is a condition that resolves spontaneously within 24 hours in more than 70% of the cases. A wait-and-see approach with rate-control medication only and when needed cardioversion within 48 hours of onset of symptoms is hypothesized to be noninferior, safe, and cost-effective as compared with current standard of care and to lead to a higher quality of life.DESIGN: The ACWAS trial (NCT02248753) is an investigator-initiated, randomized, controlled, 2-arm noninferiority trial that compares a wait-and-see approach to the standard of care. Consenting adults with recent-onset symptomatic AF in the emergency department without urgent need for cardioversion are eligible for participation. A total of 437 patients will be randomized to either standard care (pharmacologic or electrical cardioversion) or the wait-and-see approach, consisting of symptom reduction through rate control medication until spontaneous conversion is achieved, with the possibility of cardioversion within 48 hours after onset of symptoms. Primary end point is the presence of sinus rhythm on 12-lead electrocardiogram at 4 weeks; main secondary outcomes are adverse events, total medical and societal costs, quality of life, and cost-effectiveness for 1 year.CONCLUSIONS: The ACWAS trial aims at providing evidence for the use of a wait-and-see approach for patients with recent-onset symptomatic AF in the emergency department.

Aims The 5 French Sorin Hepta 4B lead is a bipolar transvenous pacemaker lead with a passive fixation mechanism. From 2003 to 2008, a total of 98 Sorin Hepta 4B right ventricular pacemaker leads were implanted in our hospital. We observed an unexpected high failure rate of this pacemaker lead. The aim of this study is to determine the performance of the Hepta 4B lead. Methods and results A retrospective single-centre survey was conducted on the performance of all implanted Hepta 4B leads in our high-volume tertiary hospital. Information on all implants was stored in a database. Analysis of this database and patients' charts was performed to assess the rate of complications of all implanted Hepta 4B leads. Median time of follow-up was 5.49 (4.15–6.44) years. Of the 98 implanted Hepta 4B leads, 21 (21%) were replaced. A total of 18 (18%) leads showed electrical malfunction, leading to symptoms in five (5%) patients. Electrical malfunction included impedance change, threshold rise, and sensing problems. Conclusion In this single-centre retrospective observation we report an extreme and unexpected failure rate of the Sorin Hepta lead. The most common complication was electrical dysfunction. The reason for this phenomenon has to be analysed, but the co-radial multifilar design, allowing a smaller diameter of the lead, may explain this finding.

Aims Recently, concerns about St Jude's Riata lead family have come to light. We present three cases of patients with Riata internal cardioverter defibrillator (ICD) leads with externalized conductors. Methods and results All patients had the same insulation defect, with externalized conductors, but differed in presentation and symptoms. These cases, which form 3 of 179 (1.68%) of our total Riata lead population, presented four or more years after implantation. This may be an indication that the problem with the Riata lead may well be greater than reported in the recent St Jude Medical device advisory letter. Conclusion The management of the Riata lead problem is discussed as, up until now, management of patients with an implanted Riata lead has been based on detecting electric abnormalities on regular ICD interrogation only.

Introduction A number of predisposing factors have been suggested to be contributing to drug-induced torsade de pointes (TdP) arrhythmias: short–long–short (SLS) sequence, bradycardia, timing of drug administration, anaesthesia, ventricular remodelling, and altered ventricular activation due to ventricular ectopic beats (SLS) or idioventricular rhythm (IVR). Chronic atrio-ventricular (AV)-block (CAVB) dogs are susceptible to dofetilide-induced TdP. Methods and results In 32 anaesthetized animals, the relevance of ventricular remodelling for TdP susceptibility was studied by dofetilide [0.025 mg/kg/5 min intravenously (iv)] during bradycardia in the presence (CAVB, n = 18) or absence [acute atrio-ventricular block (AVB), n = 32] of ventricular remodelling. In sub-protocols, the possible pro-arrhythmic effects of timing of dofetilide administration: prior to ( n = 11), or after creation of AVB ( n = 9) and relevance of SLS pacing ( n = 17) was investigated during IVR. Dofetilide was also given after AVB when the activation of the ventricles was normal: pacing (1000 ms) from the high septum ( n = 7) or abnormal but fixed from the left ventricular apex ( n = 5). Torsade de pointes inducibility was defined as reproducible (≥3 times) occurrence. In acute AV block (AAVB), dofetilide did not induce TdP spontaneously (0 of 32), whereas TdP was seen in 10 out of 18 serially tested dogs in CAVB ( P < 0.001). The other factors: timing of dofetilide (0 of 11 vs. 0 of 9), SLS pacing (0 of 17 vs. 1 of 17), or ventricular activation (0 of 7 vs. 0 of 5) did not increase TdP susceptibility. Beat-to-beat variability of repolarization increased after ventricular remodelling and was highest prior to TdP induction. Conclusion In AAVB dogs, TdP is not spontaneously seen, whereas it is present in CAVB. This implies that ventricular remodelling is a prerequisite for TdP induction in this model.

Objective: Left ventricular hypertrophy has been associated with the prolongation of QT-time, and an increased risk of ventricular arrhythmias. The renin angiotensin system has been implicated in the development of ventricular hypertrophy. At 5 weeks complete AV block (CAVB) in the dog, there is: (1) biventricular hypertrophy associated with a transient activation of components of the renin angiotensin system, (2) increased APD, more pronounced in the left than in the right ventricle leading to spatial dispersion of repolarization, and (3) enhanced susceptibility to drug-induced torsade de pointes arrhythmias. To investigate whether these remodeling processes develop in parallel, time dependency was assessed in absence or presence of the AT1 receptor-blocker Irbesartan. Methods and results: Dogs in sinus rhythm, 2 and 5 weeks CAVB were compared to dogs chronically treated with Irbesartan (30 mg/kg BID). Endocardial monophasic APD of left and right ventricle was measured and susceptibility to torsade de pointes was tested by infusing Dofetilide (0.025 mg/kg/5′). Hypertrophy was determined by relating heart-to-body weight at sacrifice. Left ventricular APD had increased more than right ventricular APD at 2 and 5 weeks CAVB, leading to an increase in spatial dispersion. At that time torsade de pointes were evocable in the majority of the dogs. Hypertrophy had only developed completely at 5 weeks CAVB. Irbesartan had no effect on electrical and structural parameters or on arrhythmogenicity. Conclusions: In the CAVB dog ventricular hypertrophy is not a prerequisite for electrical remodeling or drug-induced torsade de pointes, and the AT1-receptor has no dominant role in the completion of these remodeling processes.

Background— In large mammals and humans, the contribution of I Ks to ventricular repolarization is still incompletely understood. Methods and Results— In vivo and cellular electrophysiological experiments were conducted to study I Ks in canine ventricular repolarization. In conscious dogs, administration of the selective I Ks blocker HMR 1556 (3, 10, or 30 mg/kg PO) caused substantial dose-dependent QT prolongations with broad-based T waves. In isolated ventricular myocytes under baseline conditions, however, I Ks block (chromanols HMR 1556 and 293B) did not significantly prolong action potential duration (APD) at fast or slow steady-state pacing rates. This was because of the limited activation of I Ks in the voltage and time domains of the AP, although at seconds-long depolarizations, the current was substantial. Isoproterenol increased and accelerated I Ks activation to promote APD 95 shortening. This shortening was importantly reversed by HMR 1556 and 293B. Quantitatively similar effects were obtained in ventricular-tissue preparations. Finally, when cellular repolarization was impaired by I Kr block, I Ks block exaggerated repolarization instability with further prolongation of APD. Conclusions— Ventricular repolarization in conscious dogs is importantly dependent on I Ks . I Ks function becomes prominent during β-adrenergic receptor stimulation, when it promotes AP shortening by increased activation, and during I Kr block, when it limits repolarization instability by time-dependent activation. Unstimulated I Ks does not contribute to cellular APD at baseline. These data highlight the importance of the synergism between an intact basal I Ks and the sympathetic nervous system in vivo.

Heterogeneity in cardiac repolarization (ΔAPD) is known to be arrhythmic. In the dog model of chronic complete AV-block and acquired long QT syndrome, an increase in ΔMAPD (defined as left ventricular monophasic action potential duration (MAPD) minus right ventricular MAPD) is often associated with changes in T-wave morphology. The purpose of this study was to correlate known changes in ΔMAPD with the planimetric total area of the T-wave on the surface ECG (J∫T,mV · ms).

We report atrio-ventricular cross talk in a patient with a dual chamber ICD leading to ventricular pacing inhibition. This was observed in an ICD without the ventricular safety pace option, which normally is a sufficient protection against this phenomenon. Cross talk could be prevented effectively by reprogramming ventricular sensitivity to a less sensitive setting.

Background Amiodarone is an effective antiarrhythmic drug rarely associated with torsade de pointes arrhythmias (TdP). The noniodinated compound dronedarone could resemble amiodarone and be devoid of the adverse effects. In the dog with chronic complete atrioventricular (AV) block (CAVB) and acquired long-QT syndrome, the electrophysiological and proarrhythmic properties of the drugs were compared after 4 weeks of oral treatment. Methods and Results Amiodarone (n=7, 40 mg · kg −1 · d −1 ) and dronedarone (n=8, 20 mg/kg BID) were started at 6 weeks of CAVB (baseline). Six dogs served as controls. Surface ECGs and endocardially placed monophasic action potential catheters in the left (LV) and right (RV) ventricles were recorded to assess QTc time, action potential duration (APD), interventricular dispersion (ΔAPD=LV APD minus RV APD), early afterdepolarizations (EADs), ectopic beats, and TdP. Both amiodarone (+21%) and dronedarone (+31%) increased QTc time. Amiodarone showed no increase in ΔAPD in 4 of 7 dogs, whereas dronedarone augmented ΔAPD in 7 of 8 animals. After dronedarone, TdP occurred in 4 of 8 dogs with the highest ΔAPD (105±20 ms). TdP was never seen with amiodarone, not even in the dogs that had ΔAPD values comparable to those with dronedarone. Furthermore, a difference existed in EADs and ectopic activity incidence (dronedarone 3 of 8; amiodarone 0 of 7), which was also seen during an epinephrine challenge. Conclusions In the CAVB dog model, both amiodarone and dronedarone prolong QT time (class III effect). The absence of TdP with amiodarone seems to be related to homogeneous APD lengthening in the majority of dogs and the lack of EADs and/or ventricular ectopic beats in all.

Torsade de Pointes arrhythmias are a feared proarrhythmic effect of (antiarrhythmic) drugs. In dogs with chronic complete AV-block bradycardia-induced volume overload leads to electrical remodeling, which includes increased susceptibility to drug-induced Torsade de Pointes arrhythmias. The IKr channel blocker, dofetilide (Tikosyn, 0.025 mg/kg/5 min), and the less specific ion channel blocker, azimilide (5 mg/kg/5 min), were compared in nine anesthetized dogs at 4 and 6 weeks of AV-block in a randomized cross-over design. Dosages were based on our own dose-dependence studies and on anti-arrhythmic dosages reported in the literature. Monophasic action potential catheters were placed endocardially in both the left and right ventricle to measure action potential duration, visualize early afterdepolarizations, and to assess interventricular dispersion of repolarization (i.e. left ventricular monophasic action potential duration (at 100%) minus right ventricular monophasic action potential duration (at 100%). Cycle length of idioventricular rhythm, QT-time and the occurrence of drug-induced Torsade de Pointes arrhythmias were determined using the surface electrocardiogram (ECG). Before drug administration, the electrophysiological parameters were identical at 4 and 6 weeks. Both azimilide and dofetilide increased monophasic action potential duration, cycle length of idioventricular rhythm, and QT-time. Dissimilar lengthening of left ventricular and right ventricular monophasic action potential duration increased the interventricular dispersion significantly from 55 to 110 ms for both drugs. All dogs had early afterdepolarizations, while, in the majority, ectopic ventricular beats developed (dofetilide 8/9 and azimilide 7/9). Torsade de Pointes arrhythmias incidence was comparable for dofetilide (6/9) and azimilide (5/9). In conclusion, azimilide and dofetilide show similar electrophysiological and proarrhythmic effects in our canine model with a high incidence of Torsade de Pointes arrhythmias.

Background Although atrial fibrillation (AF) is the most commonly encountered arrhythmia, some of the properties make its detection challenging. In daily practice, underdiagnosis can lead to less effective treatment in prevention of stroke. Based on data from studies on treatment of AF, more intensive follow-up strategies, including 7-day Holter recording, 30-day event recording, and even implantable cardiac monitoring devices, are suggested. The study purpose is to evaluate the performance of a continuous single-channel loop recorder with automatic AF detection and transtelephonic electrocardiogram (ECG) transmission capabilities. Methods and Results A consecutive cohort of 153 patients admitted to the stroke unit with a presumptive diagnosis of ischemic cerebrovascular accident was screened for AF. Twenty-four-hour rhythm observation was performed using a single-channel external loop recorder (ELR) configured for automated AF detection. A total of 45 patients with a known history of AF, AF on the admission ECG, or incomplete registrations were excluded. Extensive additional frequency-based settings were used to establish a reference registration. In total, 2923 recordings were transmitted. We evaluated all events, of which 1190 were designated by the device as AF. The sensitivity, specificity, PPV, and NPV for identifying AF using the ELR were, respectively, 93%, 51%, 5%, and 99%. Conclusions In this ELR validation study, the dedicated AF detection algorithm showed to be highly sensitive but not specific for AF. Applicability of an ELR might be limited for efficacious detection of AF, as manual verification is mandatory for a vast amount of recordings.

Para-Hisian pacing at high output simultaneously captures the His bundle or proximal right bundle, as well as the adjacent ventricular myocardium. At lower output, direct His-bundle, or right-bundle, capture is lost which causes an increase in the stimulus to atrium interval. We describe a case with an increment of 68 ms with capture of the His bundle. This seems to be a paradoxical response, which however can be explained by the presence of retrograde dual AV-node physiology. Continuation of this phenomenon could be related to concealed anterograde invasion of the fast pathway thereby maintaining the retrograde activation during para-Hisian pacing on the slow pathway despite paced cycle lengths (His to His intervals) where retrograde fast pathway conduction proved to be possible.

We describe the development of a Brugada ECG together with sinus- and ventricular arrest after intravenous flecainide for atrial fibrillation in a patient in whom eventually a SCN5a mutation was identified. Unrecognized SCN5A mutations could underlie class IC-induced sinus arrest and conduction defects in some patients.

A hybrid atrial fibrillation (AF) ablation procedure (combining an endocardial and epicardial approach under general anesthesia) was performed in a 68-year-old man with symptomatic paroxysmal AF of 4 years duration. The patient also had hypertension and prolapse of the mitral valve. His medication consisted of flecainide, perindopril, and warfarin. Flecainide was stopped 5 days before the procedure. Normal left ventricular (LV) systolic function, an enlarged left atrium (LA) with a volume of 99 mL (normal

Acquired long-QT syndrome in combination with increased beat-to-beat variability of repolarisation duration (BVR) is associated with lethal torsades de pointes arrhythmias (TdP) in dogs with remodelled heart after atrioventricular block (AVB). We evaluated the relative contributions of bradycardia and ventricular remodelling to proarrhythmic BVR with and without pharmacological I(Kr) block in order to identify the individual at risk.Three groups of dogs were used: sinus rhythm dogs (n = 12), dogs with acute AVB (n = 8), and dogs with3 weeks chronic AVB (n = 27). Under anaesthesia, ECG and monophasic action potential duration (MAPD) were measured. Local BVR was quantified as short-term variability from 30 consecutive left ventricular MAPD (STV = summation absolute value(D(n(i)-D(n+1))/[30 x square root of 2])). All dogs received dofetilide iv.The slower ventricular rate acutely after AVB affected neither QTc nor STV (288+/-18 to 293+/-38 ms and 0.7+/-0.1 to 0.7+/-0.1 ms, respectively; P = NS for both), whereas ventricular remodelling increased both (to 376+/-46 and 2.3+/-0.6 ms, respectively; P0.05 for both). Neither dogs in sinus rhythm nor acute AVB showed any TdP, whereas dofetilide induced TdP in 74% of the chronic-AVB dogs. Dofetilide increased the QTc interval in all groups (19-24%; P0.05 for all groups), whereas STV was elevated in chronic-AVB dogs only (to 4.2+/-1.5 ms; P0.05) and further confined to inducible chronic-AVB dogs (5.0+/-0.8 versus 1.9+/-0.4 ms for resistant dogs; P0.05). Variability of the idioventricular rate was increased directly after AVB and did not influence BVR.Under drug-free circumstances, a persistent high BVR in chronic-AVB dogs is remodelling dependent rather than a direct consequence of bradycardia acutely after AVB. Variability of this slower rate does not influence BVR. Dofetilide causes a transient increase in BVR only in proarrhythmic dogs. Thus, BVR may aid the identification of the TdP-susceptible patient.

Increased proarrhythmia in dogs with chronic AV block (AVB) has been explained by ventricular remodeling causing a decrease in repolarization reserve. Beat-to-beat variability of repolarization (BVR) has been suggested to reflect repolarization reserve, in which high variability represents diminished reserve and larger propensity for repolarization-dependent ventricular arrhythmia. A subset of chronic AVB dogs (10%) suffers sudden cardiac death (SCD). With the assumption that repolarization defects constitute a potentially lethal proarrhythmic substrate, we hypothesized that BVR in SCD dogs are larger than in matched control chronic AVB dogs. From a population of 200 chronic AVB dogs, initially two groups were chosen retrospectively: 8 dogs that died suddenly (SCD) and 8 control dogs. Control dogs had a longer lifespan after AVB (10 to 18 weeks) than SCD dogs (5 to 10 weeks). All dogs had undergone electrophysiological testing under anesthesia where ECG, left and right ventricular endocardial monophasic action potentials (MAP) were recorded. BVR was assessed from 30 consecutive beats, illustrated by Poincare plots and was the only parameter discriminating between SCD and control group. All other electrophysiological parameters (RR, QT and MAP durations) were comparable for the two groups. Extending the number of animals and groups confirmed a larger BVR in the SCD group (SCD: 5.1 +/- 2.7; n = 11 versus control: 2.5 +/- 0.4 ms; n = 61; P < 0.05) and showed reverse-use dependence of BVR. In comparison, dogs with acute AVB had low variability (1.3 +/- 0.3 ms; n = 9; P < 0.05 versus chronic AVB). Cardiac electrical remodeling after AVB is associated with an increase in beat-to-beat variability of repolarization. Chronic AVB dogs displaying further elevated variability of repolarization are prone to arrhythmia-related SCD.

Background— Identification of patients at risk for drug-induced torsades de pointes arrhythmia (TdP) is difficult. Increased temporal lability of repolarization has been suggested as being valuable to predict proarrhythmia. The predictive value of different repolarization parameters, including beat-to-beat variability of repolarization (BVR), was compared in this serial investigation in dogs with chronic AV block. Methods and Results— In anesthetized dogs with electrically remodeled hearts, the dose-dependent difference in drug-induced TdP ( d -sotalol, 2 and 4 mg/kg IV over 5 minutes, 25% and 75% TdP, respectively) could not be accounted for by prolongation of QT c (410±37 to 475±60 versus 415±47 to 484±52 ms, respectively). BVR was quantified by Poincaré plots at baseline and immediately before onset of d -sotalol–induced extrasystolic activity. TdP occurrence was associated with an increase in short-term variability (STV) of the left ventricular monophasic action potential duration (3.5±1.5 to 5.5±1.6 versus 3.0±0.7 to 8.6±3.8 ms, respectively), which was reversible when TdP was abolished by I K,ATP activation. The absence of TdP despite QT c prolongation after chronic amiodarone treatment could also be explained by an unchanged STV. In experiments with isolated ventricular myocytes, STV increased after I Kr block and was highest in cells that subsequently showed early afterdepolarizations. Conclusions— Proarrhythmia is not related to differences in prolongation of repolarization but corresponds to BVR, here quantified as STV of the left ventricle. STV could be a new parameter to predict drug-induced TdP in patients.

Heterogeneity in cardiac repolarization (Delta APD) is known to be arrhythmic. In the dog model of chronic complete AV-block and acquired long QT syndrome, an increase in Delta MAPD (defined as left ventricular monophasic action potential duration (MAPD) minus right ventricular MAPD) is often associated with changes in T-wave morphology. The purpose of this study was to correlate known changes in Delta MAPD with the planimetric total area of the T-wave on the surface ECG (integral of J-T, mVx ms).The relationship between Delta MAPD and total area of the T-wave (i.e., JT-area) was assessed in four different protocols with different types of dispersion: (1) class III drugs followed by levcromakalim (n= 7), (2) LAD coronary artery occlusion and reperfusion (n = 6), (3) dronedarone i.v., an amiodarone like agent (n = 5) and (4) steady state pacing at cycle lengths of 1000 ms and 500 ms (n = 5).Class III drugs increased Delta MAPD (55 +/- 40 ms to 120 +/- 50 ms(#), P0.05), which was correlated (r = 0.74, P0.001) with JT-area (50 +/- 40 mV. ms to 95 +/- 35 mV x ms(#)). Ischemia increased both Delta MAPD (30 +/- 25 ms to 90 +/- 40 ms(#)) and JT-area (60 +/- 55 mV x ms to 75 +/- 50 mV x ms(#)). Both levcromakalim and reperfusion reversed these conditions. Dronedarone had no effect on Delta MAPD or on JT-area while a faster frequency reduced both Delta MAPD and JT-area.Changes in dispersion of ventricular repolarization are reflected by alterations in JT-area. This non-invasive parameter may therefore be used to indicate changes in heterogeneity in ventricular repolarization.

When a new (cardiovascular) drug shows signs of QT interval prolongation on the ECG (delay in repolarization time), the regulatory agencies demand screening of its possible proarrhythmic potential before approving it for clinical practice. In this review, identified predisposing factors have been related to specific electrophysiological parameters, allowing quantification of their contribution to Torsade de Pointes arrhythmias. In addition, arrhythmogenic mechanisms involved in the initiation and perpetuation of drug-induced Torsade de Pointes are discussed.

Because of multiple ventricular lead fractures with inappropriate shocks, a 31-year-old male received a completely subcutaneous implantable cardioverter defibrillator (ICD) system with the already existing 'endocardial' ICD functioning as an atrial pacemaker.

A 59-year-old male was admitted to the emergency room with signs of heart failure. The echocardiogram showed an extensive apical infarction with large mobile thrombi in the left ventricle. Doppler examination demonstrated apical rotating flow. Despite adequate anticoagulant therapy, the patient suffered a massive right-sided cerebral infarction leading to right ventricular cerebral compression. The thrombogenic risk of apical rotating flow and the need for anticoagulation are discussed.

Oversensing of external electrical signals can cause inappropriate therapy in cardiac rhythm management devices. In this report, a patient with an implantable cardioverter-defibrillator (ICD) is presented, who received inappropriate shocks due to temporary epicardial pacing after cardiothoracic surgery.

Objectives The purpose of this study was to evaluate the feasibility, safety, and clinical outcomes up to 1 year in patients undergoing combined simultaneous thoracoscopic surgical and transvenous catheter atrial fibrillation (AF) ablation. Background The combination of the transvenous endocardial approach with the thoracoscopic epicardial approach in a single AF ablation procedure overcomes the limitations of both techniques and should result in better outcomes. Methods A cohort of 26 consecutive patients with AF who underwent hybrid thoracoscopic surgical and transvenous catheter ablation were followed, with follow-up of up to 1 year. Results Twenty-six patients (42% with persistent AF) underwent successful hybrid procedures. There were no complications. The mean follow-up period was 470 +/- 154 days. In 23% of the patients, the epicardial lesions were not transmural, and endocardial touch-up was necessary. One-year success, defined according to the Heart Rhythm Society, European Heart Rhythm Association, and European Cardiac Arrhythmia Society consensus statement for the catheter and surgical ablation of AF, was 93% for patients with paroxysmal AF and 90% for patients with persistent AF. Two patients underwent catheter ablation for recurrent AF or left atrial flutter after the hybrid procedure. Conclusions A combined transvenous endocardial and thoracoscopic epicardial ablation procedure for AF is feasible and safe, with a single-procedure success rate of 83% at 1 year. (J Am Coll Cardiol 2012;60:54-61)