Suppression Of Ventricular Tachycardia Research Articles

The Role of Ranolazine in the Treatment of Ventricular Tachycardia and Atrial Fibrillation: A Narrative Review of the Clinical Evidence.

Cardiac arrhythmias are among the leading causes of morbidity and mortality worldwide. While antiarrhythmic drugs traditionally represent the first-line management strategy, their use is often limited by profound proarrhythmic effects. Several studies, including randomized control trials (RCTs), have demonstrated the antiarrhythmic efficacy of ranolazine, which is registered as an antianginal agent, while also establishing its safety profile. This review compiles clinical evidence investigating the antiarrhythmic properties of ranolazine, focusing primarily on ventricular tachycardia (VT) and atrial fibrillation (AF), as they are common rhythm abnormalities with serious complications. Data from RCTs indicate that ranolazine reduces VT incidence, although this effect is not universal. Therefore, we attempt to better describe the patient population that gains the most benefit from ranolazine due to VT suppression. Additionally, ranolazine is known to enhance the conversion rate of AF to sinus rhythm when combined with other antiarrhythmic drugs such as amiodarone, highlighting its synergistic effect in the atrium without provoking ventricular dysrhythmias. Despite the heterogeneity in the currently available data, ranolazine appears to be an effective and safe option for the management of various arrhythmias.

A randomized clinical trial of catheter ablation and antiarrhythmic drug therapy for suppression of ventricular tachycardia in ischemic cardiomyopathy: The VANISH2 trial

Recurrent ventricular tachycardia (VT) in patients with prior myocardial infarction is associated with adverse quality of life and clinical outcomes, despite the presence of implanted defibrillators (ICDs). Suppression of recurrent VT can be accomplished with antiarrhythmic drug therapy or catheter ablation. The Ventricular Tachycardia Antiarrhythmics or Ablation In Structural Heart Disease 2 (VANISH2) trial is designed to determine whether ablation is superior to antiarrhythmic drug therapy as first line therapy for patients with ischemic cardiomyopathy and VT.The VANISH2 trial enrolls patients with prior myocardial infarction and VT (with one of: ≥1 ICD shock; ≥3 episodes treated with antitachycardia pacing (ATP) and symptoms; ≥5 episodes treated with ATP regardless of symptoms; ≥3 episodes within 24 hours; or sustained VT treated with electrical cardioversion or pharmacologic conversion). Enrolled patients are classified as either sotalol-eligible, or amiodarone-eligible, and then are randomized to either catheter ablation or to that antiarrhythmic drug therapy, with randomization stratified by drug-eligibility group. Drug therapy, catheter ablation procedures and ICD programming are standardized.All patients will be followed until two years after randomization. The primary endpoint is a composite of mortality at any time, appropriate ICD shock after 14 days, VT storm after 14 days, and treated sustained VT below detection of the ICD after 14 days. The outcomes will be analyzed according to the intention-to-treat principle using survival analysis techniques.The results of the VANISH2 trial are intended to provide data to support clinical decisions on how to suppress VT for patients with prior myocardial infarction.Clinicaltrials.gov registration NCT02830360

Stabilization of RyR2 maintains right ventricular function, reduces the development of ventricular arrhythmias, and improves prognosis in pulmonary hypertension.

Right ventricular (RV) dysfunction and its associated arrhythmias are recognized as important determinants of the prognosis of pulmonary arterial hypertension (PAH). Here, we aimed to investigate whether direct pharmacological intervention in the RV muscle with dantrolene (DAN), a stabilizer of the cardiac ryanodine receptor (RyR2), has a protective effect against RV dysfunction and arrhythmia in a monocrotaline (MCT)-induced PAH rat model. Male 8-week-old Sprague-Dawley rats were injected with MCT for the induction of PAH. Induction of ventricular tachycardia (VT) by catecholamines was also evaluated in association with RyR2-mediated Ca2+ release properties in isolated cardiomyocytes. A pulmonary artery-banding model has also been established to assess the independent effects of chronic pressure overload on RV morphology and function. In the MCT-induced PAH rat model, RV hypertrophy, dilation, and functional decline were observed, with a survival rate of 0% 2 months after MCT induction. In contrast, chronic DAN treatment improved all these RV parameters and increased survival by 80%. Chronic DAN treatment also prevented the dissociation of calmodulin from RyR2, thereby inhibiting Ca2+ sparks and spontaneous Ca2+ transients in MCT-induced hypertrophied RV cardiomyocytes. Epinephrine induced VT in more than 50% of rats with MCT-induced PAH, but complete suppression of VT was achieved by chronic DAN treatment. Stabilization of RyR2 by DAN has potential as a new therapeutic agent against the development of RV dysfunction and fatal arrhythmia associated with PAH.

Endocardial ablation of ventricular tachycardia ablation in arrhythmogenic right ventricular cardiomyopathy aiming epicardial late potential abolition

Abstract Funding Acknowledgements Type of funding sources: None. Background Catheter ablation is frequently needed to treat ventricular tachycardia (VT) in ARVC patients. Ablation aiming non-inducibility (NI) and late potential (LP) abolition has been shown to be effective1. Simultaneous endo-epicardial mapping demonstrate epicardial involvement in most VT2. However epicardial fat and vicinity of coronary artery may prevent effective epicardial ablation. Aims (a) evaluate endocardial-only ablation guided by epicardial late-potential recording (EA-ELP) to achieve LP abolition (LPA) and NI; (b) measure ablation-index(AI) values allowing epicardial LP suppression by endocardial ablation, as a surrogate for transmurality. Methods From 2019 to 2021 the authors (XW, EG) evaluated EA-ELP in ARVC patients patient referred for ablation. Our ablation protocol was previously described3. Endo and epicardial voltage mapping of the right ventricle (RV) were performed in sinus rhythm using 0.5-1.5 mV threshlods for endocardial scar and 0.5-1 mV for the epicardial. All LP were manually tagged. Programmed ventricular stimulation (PVS) was performed till S4 from the RV apex and other sites, all inducible tolerated VT were mapped. Endocardial ablation was performed with an irrigated tip catheter positioned in front of epi-LP recorded by a multi-electrode catheter aiming to eliminate or delay epi-LP as a surrogate for transmurality. For each lesion fulfilling the «transmurality criteria», the AI values were recorded. Remap was performed to validate LPA and NI was tested. Patient follow-up (FU) rely on telemonitoring in ICD-carriers and holter/exercise test for the others. Results 11 patients were enrolled (9M/2F, mean age 45 years), 9 for VT recurrence (3 redo) and 2 for de novo VT. The median ICD therapy before ablation was 5/patient (mean 1.7). The clinical VT originated from the RV outflow tract (RVOT) in 5 patients, peritricuspid (PT) in 2, RV free wall (RFW) in 4. Substrate were more extended in the epicardium compared to the endocardium: epi-LP and scar surfaces were 42.5 cm2/118 cm2 versus 24.5 cm2/25.5 cm2 for the endocardium. In one patient, additional epicardial lesion was necessary to achieve LPA. The mean ablation duration was 3377 s. Remap showed LPA in all patients and PVS was negative in all (not tested in one due to hemodynamic instability). One patient presented retrosternal hematoma after ablation with spontaneous favorable outcome. Endocardial AI values allowing epi-LP abolition were 595 for the inferior wall, 625 in the RVOT, 604 for PT and 639 for RFW. During a mean FU of 12 months (median 16.5 mths), only one patient had VT recurrence. Conclusion Based on this case-series, EA-ELP appeared as a safe and effective method to treat VT in ARVC. EA-ELP ablation allowed VT suppression in 91 % of patients after an mean FU of 12 mths. The RV endocardial AI needed to suppress epi-LP ranged was between 595-639 and could be used as surrogate for transmurality in ARVC.

Stereotactic body radiotherapy for refractory ventricular tachycardia: the overall czech experience

Abstract Funding Acknowledgements Type of funding sources: None. Background Catheter ablation (CA) is a well-established treatment strategy for the management of drug-refractory ventricular tachycardia (VT) in patients with structural heart disease. Stereotactic body radiotherapy (SBRT) was proposed recently as a treatment option for cases of failed CA. Purpose This study reports overall experience with the SBRT from two Czech centers. Methods Since 2014, we enrolled consecutive patients who underwent at least one prior CA for recurrent scar-related VT and had subsequent VT recurrences due to inaccessible substrate. Single-session SBRT for VT was performed without the use of general anesthesia or sedation. A dose of 25 Gy was delivered. Results The study investigated 33 patients (3 women) with a mean age of 66 ± 9 years. Underlying heart disease was ischemic (58%) and nonischemic (39%) cardiomyopathy; one patient had large cardiac fibroma. The mean left ventricular ejection fraction was 31 ± 8%. Seventy-six percent of patients were on amiodarone. Before SBRT, they underwent a median of 2 (IQR: 1-3; range: 1-5) CA that included epicardial access in 42% of patients. Following SBRT with a planned target volume of 42.6 ± 22.8 ml, the immediate effect was not observed in any patient, VT burden gradually decreased over weeks or months. Seventeen (52%) patients died (2 of them suddenly) during the mean follow up of 29 ± 23 months mainly due to the progression of heart failure (Figure 1). One patient died due to bleeding associated with esophagopericardial fistula that developed 9 months after SBRT. Overall, the number of DC shocks after a single procedure decreased significantly from 0.9 ± 1.9 per month in the period of 6 months before SBRT to 0.1 ± 0.3 per month in the period of 6-12 months after SBRT (P=0.008, Figure 2). However, 14 patients (42%) had to undergo additional CA due to VT recurrences at a mean interval of 13 ± 14 months after SBRT. Three patients underwent repeated SBRT (after 3, 29, and 38 months), which was successful in 2 of them. Conclusions SBRT in patients with refractory VT is feasible but the long-term mortality after the procedure is high and reflects mainly the severity of the underlying disease. The treatment effect of SBRT is delayed and additional CA is often necessary for VT suppression. At present, SBRT should be offered as only a bailout procedure for otherwise intractable VT.

A Common Tachyarrhythmia In A Rare Myocarditis

Giant-cell myocarditis (GCM) is a rare type of myocarditis that is characterized as a rapidly progressive and often fatal myocardial disease. It has a diverse clinical presentation which mimics those of other acquired and genetic cardiomyopathies.This case report highlights ventricular tachycardia (VT) as the initial GCM manifestation and demonstrates a unique case with predominantly right ventricular (RV) involvement.A 45-year-old male presented to the hospital with palpitation and pre-syncope. His past medical history included hyperlipidemia and obstructive sleep apnea. He did not have any significant family or social history. Initial workup was significant for an elevated troponin level of 8.49. His initial ECG showed intermittent VT with left bundle branch with left superior axis at 190 beats-per-minute. Chest X-ray showed mild hilar lymphadenopathy. The patient was admitted and intravenous amiodarone was initiated. Coronary angiography revealed non-obstructive coronary disease. With suppression of VT, repeated ECG showed deep T-wave inversion in leads V1-4. Echocardiogram showed mildly reduced ejection fraction of 40% and dilated and hypokinetic RV. Endobronchial ultrasound-guided subcarinal lymph node was performed to rule out sarcoidosis. Implantable cardioverter defibrillator was placed for secondary prevention of sudden cardiac death. Genetic testing for hereditary forms of cardiomyopathies including arrhythmogenic right ventricular cardiomyopathy (ARVC) was performed. Electroanatomic mapping of the RV showed extensive septal scar which guided sites of biopsy. Biopsy confirmed GCM. Beta-blocker and immunosuppression were started. Patient was transferred to a tertiary care center for transplant evaluation but unfortunately passed away after suffering a major stroke.This case demonstrates challenges related to diagnosis of GCM. Its various clinical presentations overlap with those of more common clinical acute myocardial infarction, sarcoidosis and ARVC. Furthermore, this case underlines the importance of early voltage-map-guided biopsy in diagnosis and treatment of GCM. This is also the first case report of biopsy-proven GCM with predominant RV involvement.

Stereotactic radioablation for ventricular tachycardia.

Non-invasive stereotactic radioablation of ventricular tachycardia (VT) substrate has been proposed as anovel treatment modality for patients not eligible for catheter-based ablation or in whom this approach has failed. Initial clinical results are promising with good short-term efficacy in VT suppression and tolerable side effects. This article reviews the current clinical evidence for cardiac radioablation and gives an overview of important preclinical and translational results. Practical guidance is provided, and acardiac radioablation planning and treatment workflow based on expert consensus and the authors' institutional experience is set out.

Cardiac stereotactic ablative radiotherapy for control of refractory ventricular tachycardia: initial UK multicentre experience

BackgroundOptions for patients with ventricular tachycardia (VT) refractory to antiarrhythmic drugs and/or catheter ablation remain limited. Stereotactic radiotherapy has been described as a novel treatment option.MethodsSeven patients with recurrent refractory...

B-PO03-204 DON’T THROW THE BABY OUT WITH THE BATHWATER - VOLTAGE MAPPING STILL MATTERS

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart condition characterized with fibrofatty replacement of myocardium with an increased risk of arrhythmia and sudden cardiac death. Multimodality imaging including cardiac magnetic resonance (CMR) can help deep phenotype cases. Clinical case where voltage mapping identified fibrofatty myocardium undetected by CMR. N/A A 46-year-old female presented with palpitations, ventricular tachycardia (VT) and premature ventricular contractions (PVCs) burden of 17%. The intrinsic sinus ECG was normal She preferred ablation and pre-procedure CMR showed dilated right ventricle without evidence of dyskinesia, inflammation, late gadolinium enhancement, or fatty infiltration. The patient underwent an EP study arriving in sinus rhythm and had dominant clinical PVC with a left bundle inferiorly directed axis, V5 transition and negative in lead I and aVL placing it at the anterior-septal right ventricular outflow tract. Having good pace maps there burst pacing with the ablation catheter induced clinical VT similar to the PVC; radiofrequency ablation slowed and terminated it under 10 seconds. After suppression of VT and PVCs, a detailed voltage map of the RV was obtained demonstrating significant bipolar and unipolar voltage abnormalities on the RV free wall where ablation had not been performed. This scar pattern was suggestive of ARVC Subsequent genetic testing confirmed pathogenic PKP2 mutation. Voltage mapping remains a useful adjunct tool for deep phenotyping and can detect diseased myocardium which may not be visualized with other imaging modalities.

P1115Cardiac SABR for ventricular tachycardia - initial UK experience

Abstract OnBehalf United Kingdom Cardiac SABR consortium Background Stereotactic Ablative Body Radiotherapy (SABR) is a novel non-invasive treatment for Ventricular Tachycardia (VT) refractory to standard catheter ablation. 3 UK hospitals have started compassionate use cardiac SABR programmes, and are working in close collaboration. Purpose To report initial UK experience for treatment of refractory VT with cardiac SABR. Methods All patients had undergone prior unsuccessful invasive ablation with VT recurrence despite anti-arrhythmic drug (AAD) use. High-resolution CT imaging with 3D reconstruction was combined with 12 lead ECGs of VT and prior invasive +/- non-invasive electrophysiology mapping data to define a cardiac target. Treatment margins were modified to account for cardiac/respiratory motion and to minimise off target treatment to other organs as per clinical SABR practice. Single fraction high dose treatment (20-25 Gy) was delivered by CT guided Linear Accelerator. Patients were assessed regularly with clinical review and remote device monitoring. Results 3 patients have been treated so far with aetiologies of prior myocarditis, non-ischaemic dilated cardiomyopathy and ischaemic cardiomyopathy. All patients successfully received planned SABR treatment in <1 hour with no peri-procedural complications. Current follow up is to 4 months. Clinical course was variable – patient 1 had a flare of VT post-SABR requiring temporary escalation of AADs before VT was suppressed, patient 2 had initial suppression of VT but died from decompensated heart failure with further VT after 4 weeks, patient 3 had further VT with a different exit site and underwent repeat invasive ablation and escalated AAD use to achieve VT suppression. Conclusions Cardiac SABR shows promise for VT control, but further experience and trials are needed. Integration of imaging and electrophysiology data to generate accurate targets appears critical. The effect of SABR seems to develop over several weeks after therapy. Patient selection and timing of SABR delivery is important with acknowledgement that competing causes of death exist in patients with refractory VT entering a compassionate use program. Abstract Figure. Example SBRT plan

Stellate Ganglion Blockade for the Treatment of Refractory Ventricular Arrhythmias.

This study sought to describe our institutional experience with establishing a neurocardiology service in an attempt to provide autonomic modulation as a treatment for ventricular arrhythmias (VAs). Treatment-refractory VAs are commonly driven and exacerbated by heightened sympathetic tone. Among patients referred to the neurocardiology service (August 2016 to December 2018), we performed ultrasound-based, bilateral, temporary stellate ganglion blockade (SGB) in 20 consecutive patients. We analyzed outcomes of interest including sustained VA or VA requiring defibrillation in the 24 and 48h before and 24 and 48h afterSGB. The majority of patients were men (n=19, 95%), with a mean age of 58 ± 14 years. At the time of SGB, 10(50%) were on inotropic support and 9 (45%) were on mechanical circulatory support. Besides 1 case of hoarseness, there were no apparent procedural complications. SGB was associated with a reduction in the number of VA episodes from the 24h before (median 5.5 [interquartile range (IQR): 2.0 to 15.8]) to 24h after SGB (median 0 [IQR: 0 to 3.8]) (p<0.001). The number of defibrillation events decreased from 2.5 (IQR: 0 to 10.3) to 0 (IQR: 0 to 2.5) (p=0.002). Similar findings were observed over the 48-h period before and after the SGB. Overall, 9 of 20 (45%) patients had a complete response with no recurrence of ventricular tachycardia (VT) or ventricular fibrillation (VF) for 48h after SGB. Four (20%) patients had no recurrent VT or VF following SGB through discharge. Similar response rates were observed in those with ischemic (median 6 [IQR: 1.8 to 18.8] to 0.5 [IQR: 0 to 5.3] events; p=0.031) and nonischemic (median 3.5 [IQR: 1.8 to 6.8] to 0 [IQR: 0 to 1.3] events; p=0.012) cardiomyopathy. Minimally invasive, ultrasound-guided bilateral SGB appears safe and provides substantial reductioninVA burden with approximately 1 in 2 patients exhibiting complete suppression of VT or VF for 48 h.

Repetitive ventricular tachycardia triggered by a giant benign cardiac lipomyoma

Cardiac lipomyomas are tumors that may produce various signs and symptoms, including life threatening ventricular tachycardia (VT), often requiring surgical resection and/or catheter ablation. Here we report on a 35-year-old female patient with longstanding repetitive VT in the setting of a large cardiac lipomyoma. Diagnostic testing included non-invasive approaches including ECG, echocardiography and CMR. She then underwent electroanatomic mapping, which provided additional information. The patient ultimately underwent partial resection of the tumor. Postoperatively, long term ambulatory ECG showed VT suppression without anti-arrhythmic or catheter ablation for VT.

Propranolol efficiency in prevention of sustained ventricular tachycardia in patients with implanted cardioverter-defibrillator: a case series

Propranolol efficiency in prevention of sustained ventricular tachycardia in patients with implanted cardioverter-defibrillator: a case series

High-density substrate-guided ventricular tachycardia ablation: Role of activation mapping in an attempt to improve procedural effectiveness

Advanced techniques of electroanatomical mapping efficiently guide ventricular tachycardia (VT) ablation strategies; in this context, the adjunctive value of combining activation mapping (AMap) to improve accuracy has not been elucidated. To investigate whether conventional AMap further contributes to the identification of critical sites of VT reentry and whether this translates into a more effective ablation outcome in a cohort of patients undergoing VT ablation. We prospectively enrolled 126 patients (mean age 65.3 ± 10.5 years; left ventricular ejection fraction 33.3% ± 7.2%) with ischemic (n = 89) or idiopathic (n = 37) dilated cardiomyopathy undergoing endocardial (n = 105) or endo-epicardial (n = 21) electroanatomical mapping and ablation. A substrate-guided strategy targeting surrogate markers of reentry was accomplished in all patients, but the feasibility and efficacy of AMap was preliminarily assessed for all induced VTs focusing on early VT suppression obtained during radiofrequency delivery. VT-free survival was assessed by ICD interrogation. AMap successfully guided ablation in 62 of 104 (59.6%) patients with inducible VT(s). At 1 year, 6 of 126 (4.8%) patients died; VT recurred in 28 of 126 (22.2%) patients. No significant difference in VT recurrence rate was observed between patients in whom AMap proved effective versus those in whom substrate-guided ablation was not corroborated by AMap (16 of 62 [25.8%] vs 12 of 64 [18.8%]; log-rank test, P = .3). Our findings support the efficacy of a substrate-guided strategy targeting specific markers of arrhythmogenicity identified during sinus rhythm. AMap proves highly efficient acutely but does not improve overall VT-free survival, suggesting that in patients with advanced cardiac disease, life-threatening arrhythmias can be successfully treated by ablation in sinus rhythm, thus limiting procedural risks.

Sex‐dependent effect of prenatal and early postnatal red palm oil supplementation on cardiac ischemic tolerance of adult rats

Female Wistar rats were fed a standard diet supplemented with 0.25 ml/day of red palm oil (RPO) for 4 wks before mating, during pregnancy and until weaning at the offspring age of 4 wks; the second group was fed a control diet. Body mass of supplemented male and female offspring was higher compared to their respective controls and the faster growth continued after the cessation of RPO supplementation till adulthood. At the age of 14 wks, myocardial antioxidant enzyme levels were assessed and separate groups of offspring were subjected to 20 min of coronary artery occlusion and 3 h of reperfusion. RPO supplementation resulted in a more pronounced down‐regulation of superoxide dismutase 2 and glutathione peroxidase 1 in females than in males. The incidence and severity of ischemic ventricular arrhythmias was much lower in control females than in males. RPO markedly reduced the total number of arrhythmias and arrhythmia score in males to the same level as observed in control females, mainly due to a suppression of ventricular tachycardia. In contrast, RPO had no additive antiarrhythmic effect in females. Myocardial infarct size did not significantly differ between males and females and was not affected by RPO. The results indicate that RPO supplementation during early ontogeny may protect the adult rat heart against malignant ischemic arrhythmias in a sex‐dependent manner.Supported by URF, CPUT, SA and Carotino Malaysia.

Suppression of Ventricular Tachycardia With Dronedarone: A Case Report

Dronedarone is a multichannel blocker with similar electrophysiological properties to amiodarone. Dronedarone has not been studied in humans as an agent to suppress ventricular arrhythmias. This case report describes the dramatic antiarrhythmic effects of dronedarone in a patient with nonischemic cardiomyopathy and recurrent ventricular tachycardia, which was resistant to multiple antiarrhythmic agents and endocardial catheter ablation. Dronedarone was effective in completely suppressing ventricular tachycardia. Further research is needed to establish a potential larger role for dronedarone in controlling ventricular arrhythmias in humans.

Suppression of Ventricular Tachycardia Associated with Cardiac Sarcoidosis by Steroid Therapy

In patients with cardiac sarcoidosis, ventricular tachycardia (VT) is observed in some cases. However, effective therapies for the VT are still unknown.Case: A 50‐year old female with cardiac sarcoidosis underwent DDD pacemaker implantation for a high degree atrioventricular block with symptoms of faintness and shortness of breath. One month after the surgery, she was admitted for frequent episodes of non‐sustained VT. In the electrophysiologic study (EPS), sustained monomorphic VT and ventricular fibrillation were induced; therefore pacemaker was replaced with implantable cardioverter‐defibrillator (ICD). Amiodarone was started orally but it couldn't suppress frequent VT episodes, and frequent ICD shocks were delivered. When the oral steroid therapy was initiated for the cardiac sarcoidosis, it not only suppressed the frequent VT but also improved the atrioventricular nodal dysfunction.In conclusion, steroid therapy might be an option to consider in cardiac sarcoidosis with refractory VT.

Effect of Nifekalant for Acute Conversion of Atrial Flutter: The Possible Termination Mechanism of Typical Atrial Flutter

Nifekalant is a class III antiarrhythmic drug, which is usually used for suppression of ventricular tachycardia (VT) and fibrillation. We studied the efficacy of nifekalant for acute conversion of atrial flutter (AFL) in a prospective, open label study in the intensive care unit (ICU) of cardiovascular medicine. This study consisted of 31 patients. Twenty-six patients (84%) suffered from structural heart diseases. AFL was developed in 15 patients (48%) while on antiarrhythmic therapy with class IA or IC drugs (I-AFL group) for suppressing atrial fibrillation (AF) and in the remaining patients without such drugs (S-AFL group). Patients with prolonged QT interval, hypokalemia were excluded. All patients received one dose of 0.3 mg/kg of nifekalant over 10 minutes under continuous ambulatory monitoring. Four patients with common AFL in each group received nifekalant during electrophysiologic (EP) study. Nifekalant had an overall AFL conversion efficacy of 77.4% within 60 minutes. Eleven patients in S-AFL group (68.8%) and 13 patients in I-AFL group (86.7%) could be converted with mean conversion times of 10.8 +/- 6.2 and 15.0 +/- 8.0 minutes, respectively (n.s.). Conversion rate was significantly higher in patients with a short duration of arrhythmia. The two modes of AFL termination were mainly demonstrated and the preferential mode significantly differed between the two groups. One patient in each group with excessive QT prolongation (6.5%) developed torsade de pointes (TdP), requiring electrical shock in one patient (3.3%). Nifekalant can be used for conversion of AFL with a potent efficacy even in patients with structural heart diseases. However, caution should be required for developing TdP.

Suppression of Ventricular Tachycardia Associated with Cardiac Sarcoidosis by Steroid Therapy

In patients with cardiac sarcoidosis, ventricular tachycardia (VT) is observed in some cases. However, effective therapies for the VT are still unknown. Case: A 50-year old female with cardiac sarcoidosis underwent DDD pacemaker implantation for a high degree atrioventricular block with symptoms of faintness and shortness of breath. One month after the surgery, she was admitted for frequent episodes of non-sustained VT. In the electrophysiologic study (EPS), sustained monomorphic VT and ventricular fibrillation were induced; therefore pacemaker was replaced with implantable cardioverter-defibrillator (ICD). Amiodarone was started orally but it couldn't suppress frequent VT episodes, and frequent ICD shocks were delivered. When the oral steroid therapy was initiated for the cardiac sarcoidosis, it not only suppressed the frequent VT but also improved the atrioventricular nodal dysfunction. In conclusion, steroid therapy might be an option to consider in cardiac sarcoidosis with refractory VT.

Clinical and electrophysiologic effects of calcium channel blockers in patients receiving ibutilide

Background Ibutilide is indicated for the acute termination of atrial fibrillation and atrial flutter. Recent work concludes that ibutilide activates a late inward sodium current that is blocked by nifedipine. Because calcium channel blockers are commonly used in patients with atrial fibrillation, it is important to exclude an antagonistic effect on ibutilide in the clinical setting. Methods We performed a retrospective electrocardiographic (ECG) review of patients enrolled in 3 clinical trials of ibutilide (2 atrial fibrillation conversion protocols and 1 ventricular tachycardia suppression protocol) to determine clinical efficacy and ECG effects of ibutilide in patients receiving and not receiving calcium channel blockers. Calcium channel blockers were administered as clinically indicated. A meta-analysis of the effects of calcium channel blockers on the conversion efficacy of atrial fibrillation and atrial flutter by ibutilide was also performed for studies in the literature. Results One hundred thirty patients were included in the ECG analysis (106 from atrial fibrillation protocols and 24 from the ventricular tachycardia protocol). Sixty-eight of the 130 patients were taking calcium channel blockers at the time of ibutilide administration. There were no differences in the QT or QTc intervals, conversion rate for atrial fibrillation or atrial flutter, or suppression of ventricular tachycardia between patients taking and not taking calcium channel blockers. In the meta-analysis of 4 studies, there was no difference in the conversion rates between patients taking (52%, n = 221) and not taking (45%, n = 402) calcium channel blockers (P =.09). Conclusions In the clinical setting, the concomitant use of calcium channel blockers does not alter the ECG effects or efficacy of ibutilide for the treatment of atrial or ventricular arrhythmias. (Am Heart J 2002;143:176-80.)