VT Episodes Research Articles

Incidence, Determinants, and Prognostic Implications of True Pleomorphism of Ventricular Tachycardia in Patients With Implantable Cardioverter-Defribillators

Background— The occurrence of monomorphic ventricular tachycardia (M-VT) with >1 QRS morphology during the same episode (pleomorphism [PL]) or in different episodes (multiple morphologies [MM]) has been described through ECG. Implantable cardioverter-defribillator (ICD) electrograms (EGs) provide the opportunity to analyze virtually all spontaneous M-VT episodes. We sought to study the incidence, determinants, and prognostic significance of PL and MM as assessed by ICD-EG in a prospective series of patients with ICDs. Methods and Results— Spontaneous episodes of M-VT were analyzed before ICD intervention. PL was defined as >1 ICD-EG morphology, each having ≥6 consecutive identical beats during the same VT episode, and MM as >1 ICD-EG morphology in different M-VT episodes in the same patient. We analyzed 1881 M-VT episodes from 315 patients followed for 17 months. PL and MM occurred in 6% and 19%, respectively, of the total population (16% and 62% of patients with M-VT). Recurrent M-VT as diagnosis for ICD indication predicted PL and MM. Patients with PL more frequently developed MM (85% versus 15%; P <0.001) compared to patients without PL. Total mortality (5%) was significantly higher in patients with PL (20%), in patients with MM (11.5%), and in women (12%). In multivariate analysis, only PL (odds ratio, 5.33; P =0.009) and female sex (odds ratio, 3.1; P =0.038) predicted mortality. Conclusions— In a prospective series of patients with ICDs, mostly indicated for secondary prevention, both PL and MM of VT, as judged by ICD-EG, were not uncommon and were strongly associated. Female sex and the development of PL VT were the only independent predictors of mortality.

In Secondary Prevention ICD Patients, Does the Initial Presenting VT Cycle Length Predict Subsequent Cycle Length of VT Episodes?

Background: In secondary prevention patients, ICD detection zones are often tailored individually. We aim to determine whether patients initial presenting VT tachycardia cycle length (TCL) prior to ICD implant predicts subsequent VT TCL.Methods: All secondary prevention ICD patients on follow up with available records of appropriate ICD therapy for VT within a 3-year period were studied.Results: 249 VT events in 20 patients were analysed. Mean age 55.8 years, median 5-years follow up. All had sustained VT on 12-lead ECG prior to ICD implant. Mean presenting VT TCL was 313±46 (SD) ms. In majority, post implant VT TCL increased by 20–50 ms compared to at presentation (R=0.52, p=0.02). In the entire group, mean TCL of VTs post implant was 350±43 (SD) ms. Reasons for the increased TCL include medications, ischaemia, scar size changes and different VT circuits.Conclusion: In our population, VT cycle lengths post implant are on average longer, but remain correlated to presenting TCL. Detection cycle lengths 50 ms longer than the TCL of the presenting VT should be programmed if under-detection of subsequent VTs is to be minimised.

198 Ablation of premature ventricular beats in post-ischemic intractable electrical storm

post-ischemic electrical storm (PIES) occurring shortly after the acute phase of myocardial infarction (MI) is a rare but potentially lethal phenomenon. Clinical and therapeutic options are poorly known. 14 pts (12 men, 61 ± 13 years old) underwent RF ablation for intractable PIES. PIES occurred 10 ± 5 days after MI (4 months in one pt). Mean EF was 28 ± 7%. Fast monomorphic VT (10 pts), FV (8 pts) or torsades de pointes (5 pts) recurred in each pt despite maximal anti-arrhythmic therapy (mean 22 ± 13 episodes). MI was inaugural anterior MI in each but 3 pts (subendocardial in 2, inferior in 1), with one vessel disease (left descending artery) in 8 pts (2 or 3 vessels in 6). When performed (4 pts), new PTCA did not control PIES. RF ablation was performed as a last chance solution, targetting ventricular premature beats arising from the left septal Purkinje network (in all patients the arrhythmia was of Purkinje origin, defined by a sharp spike Purkinje-potential preceding ventricular activation during sinus rhythm as well as during arrhythmia). Abolition of Purkinje potentials and of Purkinje premature beats led to resumption of electrical storm in 12/14 pts with 1 procedure (2 in one pt). The two pts with unsuccessful RF ablation died within a few hours from intractable heart failure and recurring arrhythmias. All other pts were implanted with an ICD (two pts had already been implanted before). During a 18 ± 19 months follow-up, 3 pts present with recurring isolated VT episodes found in ICD memories. Seven pts died from cardiac or non cardiac causes (7 ± 10 months). PIES is a rare but potentially lethal event occurring mainly in inaugural large anterior acute MI. RF ablation of initiating Purkinje-premature beats may be an efficient therapeutic solution despite the poor long-term prognosis of such patients.

Clinical Management of Arrhythmogenic Right Ventricular Cardiomyopathy: An Update

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic heart muscle disease characterized by the peculiar right ventricular (RV) involvement. Distinctive pathologic features are myocardial atrophy and fibro-fatty replacement of the RV free wall, and clinical presentation is usually related to ventricular tachycardias with a left bundle branch block pattern or ventricular fibrillation leading to cardiac arrest, mostly in young people and athletes. Later in the disease evolution, progression and extension of RV muscle disease and left ventricular involvement may result in right or biventricular heart failure. In the 1994 an International Task Force proposed standardized diagnostic criteria designed to guarantee an adequate specificity and based on the presence of major and minor criteria encompassing electrocardiographic, arrhythmic, morphofunctional, histopathologic, and genetic factors; more recently, Task Force criteria have been modified to increase their diagnostic sensitivity. Retrospective analysis of clinical and pathologic series including fatal cases identified a series of risk factors such as malignant familial background, youthful age, previous syncope or cardiac arrest, competitive sport activity, severe RV disease with left ventricular involvement, and episodes of complex ventricular arrhythmias or VT. The therapeutic options include beta blockers, antiarrhythmic drugs, catheter ablation, and implantable cardioverter defibrillator (ICD). The ICD is the most effective safe-guard against arrhythmic sudden death. In patients in whom ARVC has progressed to severe RV or biventricular systolic dysfunction with risk of thromboembolic complications, treatment consists of current therapy for heart failure including anticoagulant therapy. In case of refractory congestive heart failure, patients may become candidates for heart transplantation.

Magnesium Sensitive, Adenosine Resistant, Repetitive Monomorphic Ventricular Tachycardia

Repetitive monomorphic ventricular tachycardia (RMVT) is characterized by episodes of ventricular ectopy and nonsustained VT exacerbated by catecholamines. Because this arrhythmia is frequently adenosine sensitive, its mechanism is believed to be cyclic adenosine monophosphate-mediated triggered activity due to delayed afterdepolarizations. We present a case of RMVT associated with significant hypomagnesemia (serum level = 1.1 mg/dL), which did not respond to intravenous (IV) adenosine and terminated repeatedly after IV magnesium. Electrophysiologic study demonstrated an origin from the left sinus of Valsalva, which was successfully ablated. The combination of adenosine resistance and magnesium sensitivity may be consistent with an atypical RMVT mechanism related to inhibition of sodium-potassium adenosine triphosphatase (Na(+)-K(+) ATPase).

Arrhythmogenicity of Low‐Flow Reperfusion Following Acute Local Ischemia in Excised Rat Hearts

Clinical studies show that impaired myocardial reperfusion following thrombolytic therapy for coronary occlusions increases the incidence of ventricular arrhythmias; however the mechanisms are poorly understood. We studied arrhythmias during controlled low‐flow reperfusion (LFRP) in excised Langendorff‐perfused hearts (n=6). The left anterior coronary artery (LAD) was cannulated. An HPLC pump delivered perfusate to the LAD at a rate of 2 mL/min, followed by 20 min of local ischemia (0 mL/min) and then 20 min of LFRP (0.2 mL/min). The electrical response at each flow rate was monitored using an ECG and fluorescence imaging of epicardial potentials. We found that the highest heart rates and lowest heart rate variability occurred during LFRP (p<0.05). LFRP also resulted in the highest incidence of VF (p<0.05). During ischemia heart rate variability was highest and the incidence of VF was much lower than during LFRP (p<0.05). Fluorescence images revealed periodic ectopic beats during ischemia and numerous ectopic beats during LFRP. During LFRP, frequent episodes of monomorphic VT were driven by a single rotor and VF was driven by multiple transient rotors. In summary, LFRP fuels the continuous generation of ectopic beats that precede VT/VF. These findings match with our previous in‐vitro studies where we hypothesized that microreperfusion of ischemic border zones could result in ectopic beats and arrhythmias.

Abstract 5892: Therapy For Device-determined Ventricular Arrhythmias Decrease As Biventricular Pacing Percentage Increases In Heart Failure Patients

Introduction: CRT-D improves cardiac function and quality of life, and decreases HF hospitalization and death for many patients. However, impact on therapy delivered for ventricular arrhythmias is less clear. Methods: Device-determined VT and VF episodes with therapy (n = 1835) from CRT-D patients in two trials (CRT RENEWAL & REFLEX; n = 1698) were analyzed in a post hoc fashion. Patients were divided into lifetime biventricular (BiV) pacing percentage quartiles. Zero-inflated Poisson regression models were used to evaluate impact of pacing on VT/VF incidence and frequency, adjusting for baseline covariates including lifetime ATR mode switch percentage. Results: Patient characteristics: 69 ± 11 years, 73% male, 68% CAD. Dividing patients in quartiles resulted in the following pacing breakdown: 0–92% (n = 445), 93–97% (n = 445), 98–99% (n = 482), and 100% (n = 326). There were no differences in gender, NYHA, or history of diabetes, MI, CAD or hypertension among the groups. Patients paced 0–92% and 93–97% had similar VT/VF therapy incidence (24.72% vs. 24.27%) and frequency (17.05% vs. 16.00%). Patients paced 98–99% had lower VT/VF therapy incidence (15.15%) than patients paced ≤ 97% (p < 0.001) but similar frequency after adjusting for incidence. Patients paced 100% had similar VT/VF therapy incidence (13.80%) and frequency (6.45%) to patients paced 98–99%. The figure shows the time to first therapy for VT/VF. Conclusions: For CRT-D patients in this analysis, incidence and frequency of therapy delivered for VT/VF is significantly decreased when lifetime BiV pacing percentage is above 97%.

Discriminatory Therapy for Very Fast Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

We assessed the efficacy of antitachycardia pacing (ATP) and low-energy (5J) shock for very fast ventricular tachycardia (VFVT), cycle length 200-250 ms, in patients with implantable cardioverter defibrillators (ICDs). One hundred and fifty-two consecutive patients with standard indications for ICD therapy were enrolled. Before discharge from the hospital each patient had an electrophysiological study (EPS) performed through the device, to assess the efficacy of ATP and low-joule shock at terminating VFVT. Initial therapy for VFVT consisted of three bursts of ATP followed by low-energy shock, and high-energy shocks as required. The mean age of enrolled patients was 63 +/- 13 years, and the mean left ventricular ejection fraction (LVEF) was 31 +/- 13%. During the predischarge EPS, a total of 125 VT episodes were induced in 64 patients. In patients with VFVT, the success rate of ATP was 30% (14/46), the acceleration rate was 26% (12/46), and the success rate of low-energy shock was 86% (25/29). In patients with fast ventricular tachycardia (FVT), cycle lengths 251-320 ms, the success rate of ATP was 62% (24/39), the acceleration rate was 18% (7/39), and the success rate of low-energy shock was 94% (17/18). This study has demonstrated for the first time that ATP and low-energy shock are effective, as an alternative to high-energy shock, to revert induced VFVT. Low-energy shock has a very high success rate for VT slower than VFVT. Clinical studies are required prior to consideration for empiric programming.

Abstract 1079: Prevention of Fatal Arrhythmia in a Catecholaminergic Polymorphic Ventricular Tachycardia Mouse Model Carrying Calsequestrin-2 Mutation

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a familial arrhythmia syndrome caused by mutations in the ryanodine receptor (RyR2) or calsequestrin-2 (CASQ2) genes and characterized by exercise or emotional stress-induced sudden death. Beta-adrenergic blockers are only partially effective and other agents have not been widely tested. Recent studies have shown that CPVT is mediated by increased Ca 2+ leak through the RyR2 channel. Our aim was to determine whether agents that inhibit intracellular Ca 2+ leak can effectively prevent CPVT. Methods: The efficacy of intraperitoneal (IP) propranolol (1mcg/g), Mg 2+ (0.002mEq/g), verapamil (8 mcg/g) and diltiazem (8 mcg/g) were tested both in vivo and in vitro using CASQ2 mutant mouse CPVT model. In vivo studies included ambulatory ECG recordings at rest and following epinephrine stress (0.4 mcg/g IP) at baseline and after study drug administration. Experiments for each drug were performed on separate days to avoid confounding effects. In vitro studies included intracellular Ca 2+ transient analysis on isolated cardiomyocytes from mutant mice with and without epinephrine (5.5 μM). Results: All 4 drugs restored sinus rhythm and reduced the frequency of VT episodes induced by epinephrine in CASQ2 mutant mice. Only verapamil completely prevented epinephrine-induced VT in 87% of the mice (p<0.01). Cardiomyocyte studies in basal conditions revealed that Mg 2+ and verapamil inhibited sarcomere contraction and normalized the prolonged Ca 2+ reuptake period in CASQ2 mutants, but did not decrease baseline Ca 2+ peak height. Epinephrine-stressed mutant myocytes had increased diastolic Ca 2+ levels, lower Ca 2+ peak height and spontaneous SR Ca 2+ release events that were partially prevented by verapamil and Mg 2+ . Verapamil was more effective than Mg 2+ in reducing the frequency of spontaneous Ca 2+ releases induced by epinephrine. Conclusions: All 4 agents can inhibit ventricular arrhythmia in CPVT mouse model; however verapamil appears most effective in preventing arrhythmia in vivo and in modifying intracellular abnormal calcium handling. Calcium antagonists might have therapeutic value in CPVT and other RyR2-mediated arrhythmias and should be considered for human clinical studies.

VENTRICULAR TACHYCARDIA

Introduction: Frequent or complex patterns of ventricular ectopic activity,whether occurring during routine activity or induced by exercise, are often a marker for serious heart disease and aharbinger of sudden death. The detection of such arrhythmias is thus an important responsibility of the physician.Objective: To find the prevalence, associated characteristics and prognostic significance of exercise induced nonsustainedVT in a representative population. Material and Methods: Setting: Nishtar Hospital, Multan. Sample size:1000 patients. Duration: Two years. Study design: Descriptive, analytical study. Sampling Technique: Convenientprobability sampling done. Results: Ten subjects, 7 men and 3 women, with exercise induced VT were identified,representing 1.1% of those tested; only 1 was young than 65 years. All episodes of VT were asymptomatic and nonsustained.In 9 of 10 subjects, VT developed at or near peak exercise. The longest run of VT was 6 beats; multiple runsof VT were present in 4 subjects. Two subjects had exercise induced ST segment depression, but subsequent exercisethallium scintigraphic results were negative in each. Compared with a group of age and sex matched control subjects,those with asymptomatic, non-sustained VT displayed no difference in exercise duration, maximal heart rate, or theprevalence of coronary risk factors or exercise induced ischemia as measured by electrocardiography and thalliumscintigrahy. Over a mean follow period of 2 years, no subject has developed symptoms of heart disease or experiencedsyncope or sudden death. Thus, exercise induced VT in apparently healthy subjects occurs almost exclusively in theelderly, is limited to short, asymptomatic runs of 3 to 6 beats usually near peak exercise, and does not portendincreased cardiovascular morbidity or mortality rates over a 2 year period of observation. Conclusion: Exerciseinduced VT in apparently healthy subjects occurs almost exclusively in the elderly, is limited to short, asymptomaticruns of 3 to 6 beats usually near peak exercise, and does not show increased cardiovascular morbidity or mortalityrates over a 2 year period of observation.

Pharmacological separation of early afterdepolarizations from arrhythmogenic substrate in ΔKPQ Scn5a murine hearts modelling human long QT 3 syndrome

AimTo perform an empirical, pharmacological, separation of early afterdepolarizations (EADs) and transmural gradients of repolarization in arrhythmogenesis in a genetically modified mouse heart modelling human long QT syndrome (LQT) 3.MethodsLeft ventricular endocardial and epicardial monophasic action potentials and arrhythmogenic tendency were compared in isolated wild type (WT) and Scn5a+/Δ hearts perfused with 0.1 and 1 μm propranolol and paced from the right ventricular epicardium.ResultsAll spontaneously beating bradycardic Scn5a+/Δ hearts displayed EADs, triggered beats and ventricular tachycardia (VT; n = 7), events never seen in WT hearts (n = 5). Perfusion with 0.1 and 1 μm propranolol suppressed all EADs, triggered beats and episodes of VT. In contrast, triggering of VT persisted following programmed electrical stimulation in 6 of 12 (50%), one of eight (12.5%), but six of eight (75%) Scn5a+/Δ hearts perfused with 0, 0.1 and 1 μm propranolol respectively in parallel with corresponding alterations in repolarization gradients, reflected in action potential duration (ΔAPD90) values. Thus 0.1 μm propranolol reduced epicardial but not endocardial APD90 from 54.7 ± 1.6 to 44.0 ± 2.0 ms, restoring ΔAPD90 from −3.8 ± 1.6 to 3.5 ± 2.5 ms (all n = 5), close to WT values. However, 1 μm propranolol increased epicardial APD90 to 72.5 ± 1.2 ms and decreased endocardial APD90 from 50.9 ± 1.0 to 24.5 ± 0.3 ms, increasing ΔAPD90 to −48.0 ± 1.2 ms.ConclusionThese findings empirically implicate EADs in potentially initiating spontaneous arrhythmogenic phenomena and transmural repolarization gradients in the re-entrant substrate that would sustain such activity when provoked by extrasystolic activity in murine hearts modelling human LQT3 syndrome.

A 6-Month Follow-up of Intermittent Levosimendan Administration Effect on Systolic Function, Specific Activity Questionnaire, and Arrhythmia in Advanced Heart Failure

Background Levosimendan (LS) improves cardiac contractility without increasing myocardial oxygen demand. We administrated LS on a monthly intermittent 24-hour protocol and evaluated the clinical effect after 6 months in a randomized, open, prospective study. Methods and Results Fifty patients (age 45–65 years) with LV systolic dysfunction and New York Heart Association (NYHA) III or IV were randomized in 2 groups. LS group (n = 25) was compared with a control group (n = 25) matched for sex, age, and NYHA class. LS was given monthly on a 24-hour intravenous protocol for 6 months. Patients were evaluated by specific activity questionnaire (SAQ) and echocardiography (ECHO) before and 3 to 5 days after last drug administration, whereas 24-hour Holter recording was performed before and during last drug administration. Patients in LS and control group had same baseline SAQ, ECHO, and Holter parameters. At the end of the study, a larger proportion of patients in the levosimendan group reported improvement in symptoms (dyspnea and fatigue) (65% versus 20% in controls, P < .01). After 6 months, the LS group had a significant increase in LV ejection fraction versus controls (28 ± 7 versus 21 ± 4 %, P = .003), LV shortening fraction (15 ± 3 versus 11 ± 3 %, P = .006) and a decrease in mitral regurgitation (1.5 ± 0.8 versus 2.7 ± 0.6, P = .0001). There was no increase in supraventricular or ventricular beats or supraventricular tachycardia and VT episodes in LS group, compared with controls. Two patients from the LS group died in the 6-month follow-up period, compared with 8 patients in the control group (8% versus 32%, P < .05). Conclusions A 6-month intermittent LS treatment in patients with decompensated advanced heart failure improved symptoms and LV systolic function.

Effects of non‐invasive pressure support ventilation (NI‐PSV) on ventilation and respiratory effort in very low birth weight infants

Nasal continuous positive airway pressure (NCPAP) is used to provide support to non-intubated infants, but it often fails. Pressure support ventilation (PSV) is a mode of synchronized ventilation that can supplement the spontaneous breathing effort, but it is unknown if it is effective in non-intubated very low birth weight (VLBW) infants. To compare the acute physiological effects of non-invasive PSV (NI-PSV) versus NCPAP on tidal volume (V(T)), minute ventilation (V(E)), gas exchange, breathing effort, and chest wall distortion in VLBW infants. Stable preterm infants of birth weight less 1,250 g were studied during consecutive 2 hr periods of NCPAP and NI-PSV in random sequence. VT, V(E), and thoraco-abdominal synchrony were measured using respiratory inductance plethysmography. Breathing effort was measured by esophageal manometry. Gas exchange was measured by pulse oximetry and transcutaneous PCO2. Fifteen infants of birth weight (mean +/- SD) 808 +/- 201 g and 25.9 +/- 1.8 weeks gestational age were studied while on NCPAP 5.3 +/- 0.6 cm H2O and on NI-PSV with 7.9 +/- 1.3 cm H2O above NCPAP of pressure support. There were no differences in VT, V(E), PCO2 or hypoxemia episodes. Peak and minute inspiratory effort were significantly reduced in NI-PSV mode as compared to NCPAP. There was a significant reduction in indices of chest wall asynchrony in NI-PSV mode. When compared to NCPAP, NI-PSV did not increase minute ventilation, but it effectively unloaded the patient's respiratory pump as indicated by a lower inspiratory effort and reduced chest wall distortion.

Modulation of cardiac response to ischemia/reperfusion in hypertensive rats exposed to chronic social stress

Chronic psychosocial stress (S) impairs vascular regulation leading to hypertension (H). However, modulation of cardiac response to ischemia/reperfusion injury (I/R) by S is not fully characterized, in particular, in hypertensive animals. We explored tolerance to I/R in WKY and SHR rats exposed to 8 w of crowding S induced by caging 5 rats/cage (200 cm2/rat), while controls (C) were kept 4 rats/cage (480 cm2/rat). S did not affect left ventricular (LV) weight in any group, however, it amplified increased BP and reduced elevation of cardiac NOS activity in SHR rats. Neither did S modified myocardial function in hearts of both groups under baseline conditions. Ischemic challenge (25_min I/40_min R) revealed markedly impaired recovery of LV developed pressure (LVDP) in C_SHR (15±6% of baseline value vs. 60±1.5% in the control WKY group; P<0.05) and increased susceptibility to lethal arrhythmias (incidence of SVF 25% and duration of VT 84±22 s vs. SVF 0% and VT 30±12 s in C_WKY; P<0.05). S altered contractile recovery in the WKY group (LVDP 32±5%; P<0.05) and exacerbated arrhythmias (incidence of SVF 40%, duration of VT 70±20 s; P<0.05 vs. unstressed WKY). In contrast, SVF was completely suppressed in stressed SHR hearts, in conjunction with shorter episodes of VT (22±5 s) and better recovery of LVDP (47±12%; P<0.05 vs. unstressed SHR). Conclusion: chronic psychosocial stress represents a higher risk of lethal arrhythmias and contractile failure in normotensive rats exposed to an acute ischaemic challenge indicating a potential development of cross effect of adaptation in hypertensive individuals.

Implantable cardioverter defibrillator shock reduction using new antitachycardia pacing therapies

The main purpose of ICDs is to abort sudden death by delivering therapy at the moment of tachycardia. Shocks accomplish this goal but are painful. Alternatively antitachycardia pacing is painless and if deemed safe may be reasonable substitute. Multiple trials show a high efficacy rate by ATP (78-94%) for treating VTs below 200 bpm. ATP has had less efficacy for faster VTs (41-79%) and have higher probability of accelerating tachycardia (5-55%). The PainFREE trials address these issues. The first pilot study PainFREE Rx applied standardized VT detection and ATP regimen to 220 patients with 1100 spontaneous episodes of VT. ATP success for slow VT success was 92% and fast VT > 188 bpm raw success rate was 89%. None of these trials randomize shock versus ATP so comparative safety data was missing. Thus, the PainFREE Rx II trial was designed to make direct safety comparison between shock and ATP therapies for fast VT > 188 bpm. It included 634 patients with either ischemic or nonischemic cardiomyopathy followed for 1 year yielding 1760 episodes of slow VT, fast VT plus VF. The results of the PainFREE Rx II trial showed that a single regimen of ATP, burst pace 8 pulses at 88% VT cycle length could safely terminate 77% of fast VT and 90% of slow VT. Consequently, shocks were reduced by 70% compared to the shock group. Furthermore, ATP was proven safe because there was no increase in sudden death, syncope or even arrhythmia acceleration compared to shock. The quality of life of the ATP group was found to be superior to the shock group validating ATP's intent. Secondary yet important findings also included the fact that by programming the ICD to wait for 18 beats in PainFREE Rx II before treating an episode reduced markedly the number of episodes treated when compared to 12 beat detection as done in PainFREE Rx I. Since syncope occurred in only 1% of episodes, the authors suggested that a longer wait for ICD detection needs to be evaluated.

Long‐Term Follow‐Up of Patients Supplied with Single‐Chamber or Dual‐Chamber Cardioverter Defibrillators

In patients who have an indication for an implantable cardioverter defibrillator (ICD) a dual-chamber device is indicated in the case of concomitant significant sinus node disease or atrioventricular block. It is a matter of debate whether dual-chamber ICD may be beneficial for patients with preserved sinus and atrioventricular nodal function as data from prospective randomized trials are limited. Mid- or long-term follow-up data are unavailable. One hundred patients (age 60+/-12 years, 11 women) with the indication for the implantation of an ICD and without antibradycardia pacing indication were randomly assigned to either receive a dual-chamber ICD (n=52) or a single-chamber ICD (n=48). Patients were followed-up for a mean of 52+/-14 months. Mortality and arrhythmogenic morbidity were assessed. All-cause mortality was 21% for single-chamber and 31% for dual-chamber ICD recipients, respectively (P=0.26). Cardiovascular mortality was 13% for single-chamber ICD recipients versus 21% in the dual-chamber group (P=0.25). Subgroup analysis using 35% of ventricular paced beats as cutoff value in the dual-chamber ICD group revealed a 42% mortality rate for the patients with frequent ventricular pacing compared to 10% of patients with a low rate of ventricular pacing (P=0.05, relative risk 4.21, 95% confidence interval: 0.9-19.8). As for arrhythmogenic morbidity, the difference in the ventricular tachyarrhythmia load was not different in both groups (single chamber: 23+/-74 VT episodes, dual chamber: 54+/-134 VT episodes, P=0.17). In ICD recipients without conventional indication for dual-chamber pacing, dual chamber compared to single-chamber ICD has no advantage concerning mortality and arrhythmogenic morbidity in a long-term follow-up. In these patients the implantation of a single-chamber device is sufficient.

Electrical storm in patients with an implantable defibrillator: incidence, features, and preventive therapy: insights from a randomized trial

The purpose of this study was to assess the incidence, features, and clinical sequelae of 'electrical storm' (ES). This study is a prospectively designed secondary analysis of SHIELD; a randomized trial of azimilide for suppression of ventricular tachycardia/fibrillation (VT/VF) leading to implanted cardioverter defibrillator (ICD) therapies. Systematic and rigorous follow-up and blinded adjudication of ICD therapy allowed identification of all ESs (>/=3 separate VT/VF episodes leading to ICD therapies within 24 h). Of 633 ICD recipients, 148 (23%) experienced at least one ES over 1-year follow-up. No clinical predictors of ES were identified. Frequent VT episodes accounted for 91% of all ESs, with the remaining being VF alone or both VT plus VF. ES led to a 3.1-fold increase in arrhythmia-related hospitalization (95% CI 2.3-4.3; P<0.0001) compared with patients with isolated VT/VF, and to a 10.2-fold increase (95% CI 6.4-16.3; P<0.0001) compared with patients without VT/VF. Compared with placebo, azimilide (75 and 125 mg/day) reduced the risk of recurrent ES by 37% (HR=0.63, 95% CI 0.35-1.11, P=0.11) and 55% (HR=0.45, 95% CI 0.23-0.87, P=0.018), respectively. However, the reduction in time-to-first ES did not reach statistical significance by both doses (75 and 125 mg) of azimilide (HR=0.82, 95% CI 0.56-1.19, P=0.29 and HR=0.69, 95% CI 0.46-1.04, P=0.07), respectively. ES is common and unpredictable in ICD recipients and it is a strong predictor of hospitalization.

Sustained Ventricular Tachycardia Following Alcohol Septal Ablation for Hypertrophic Obstructive Cardiomyopathy

A 49-year-old man with a history of hypertrophic obstructive cardiomyopathy (HOCM) presented in sustained monomorphic ventricular tachycardia (SMVT) 8 days post-alcohol septal ablation. A dual chamber implantable cardioverter defibrillator ICD was implanted and the patient experienced another episode of VT 3 weeks later, which was terminated by an ICD shock. This case demonstrates probable scar-induced reentrant VT post-alcohol septal ablation, a likely rare but hypothesized complication of this procedure.

Prevention of Fatal Arrhythmias in High-Risk Subjects by Fish Oil n-3 Fatty Acid Intake

The long-chain n-3 fatty acids in fish have been demonstrated to have antiarrhythmic properties in experimental models and to prevent sudden cardiac death in a randomized trial of post-myocardial infarction patients. Therefore, we hypothesized that these n-3 fatty acids might prevent potentially fatal ventricular arrhythmias in high-risk patients. Four hundred two patients with implanted cardioverter/defibrillators (ICDs) were randomly assigned to double-blind treatment with either a fish oil or an olive oil daily supplement for 12 months. The primary end point, time to first ICD event for ventricular tachycardia or fibrillation (VT or VF) confirmed by stored electrograms or death from any cause, was analyzed by intention to treat. Secondary analyses were performed for "probable" ventricular arrhythmias, "on-treatment" analyses for all subjects who had taken any of their oil supplements, and "on-treatment" analyses only of those subjects who were on treatment for at least 11 months. Compliance with double-blind treatment was similar in the 2 groups; however, the noncompliance rate was high (35% of all enrollees). In the primary analysis, assignment to treatment with the fish oil supplement showed a trend toward a prolonged time to the first ICD event (VT or VF) or of death from any cause (risk reduction of 28%; P=0.057). When therapies for probable episodes of VT or VF were included, the risk reduction became significant at 31%; P=0.033. For those who stayed on protocol for at least 11 months, the antiarrhythmic benefit of fish oil was improved for those with confirmed events (risk reduction of 38%; P=0.034). Although significance was not achieved for the primary end point, this study provides evidence that for individuals at high risk of fatal ventricular arrhythmias, regular daily ingestion of fish oil fatty acids may significantly reduce potentially fatal ventricular arrhythmias.

Onset of Ventricular Arrhythmias in Ischemic and Non-Ischemic Cardiomyopathies

We consider 17 patients affected by dilated cardiomyopathy (DCM), average ejection fraction (EF) 32% that received a St. Jude Medical Implantable Cardioverter Defibrillators (ICDs) in secondary prevention. The average follow-up is 24 months. We defined two groups: fast-VT (>220 beats per minute), and slow-VT. Results 9 of these patients had 60 VT episodes that onset with 3 different modes: (i) premature ventricular contraction (PVC onset) consisting of 35 EGMs, 7 of which are fast-VT; (ii) PVC preceded by a short-long-short cycle with 15 episodes, none of them was a fast-VT; (iii) paced beats immediately after PVC pause (PM onset) with 10 EGMs, 3 of which are fast-VT. Finally in 4 patients the VT onset with more than 1 mode. Conclusion in secondary prevention DCM patients present a large number appropriate ICD intervention (53%) and rather frequent episodes of fast-VT (12% of episodes). The mode of VT onset varies from patient to patient, this lead to the hypothesis that mechanisms, other than reentry, can determine VT onset in DCM patients.