Antiarrhythmic Agents (antiarrhythmic + agent)

Distribution by Scientific Domains
Distribution within Medical Sciences


Selected Abstracts


Electrophysiologic Effects of Carvedilol: Is Carvedilol an Antiarrhythmic Agent?

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2005
NABIL EL-SHERIF
The cardiovascular drug carvedilol is characterized by multiple pharmacological actions, which translate into a wide-spectrum therapeutic potential. Its major molecular targets are membrane adrenoceptors, ion channels, and reactive oxygen species. Carvedilol's favorable hemodynamic effects are due to the fact that the drug competitively blocks ,1 -, ,2 -, and ,1 - adrenoceptors. Several additional properties have been documented and may be clinically important, including antioxidant, antiproliferative/antiatherogenic, anti-ischemic, and antihypertrophic effects. The antiarrhythmic action of carvedilol may be related to a combination of its ,-blocking effects with its modulating effects on a variety of ion channels and currents. Several studies suggest that the drug may be useful in reducing cardiac death in high-risk patients with prior myocardial infarction and/or heart failure, as well as for primary and secondary prevention of atrial fibrillation. This article will review experimental data available on the electrophysiologic properties of carvedilol, with a focus on their clinical relevance. [source]


A Common SCN5A Variant Alters the Responsiveness of Human Sodium Channels to Class I Antiarrhythmic Agents

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2007
MOSSAAB SHURAIH M.D.
Background: The potential pathophysiological role of common SCN5A polymorphisms in cardiac arrhythmias has been increasingly recognized. However, little is known about the impact of those polymorphisms on the pharmocological response of hNav1.5 to various antiarrhythmic agents. Methods and Results: The known SCN5A polymorphism, S524Y, was studied in comparison with the wild type (WT) define the SCN5A-Q1077del variant. The ion channel gating kinetics and pharmacology were evaluated using whole-cell patch-clamp methods in HEK-293 cells. Consistent with a previous report, the basal ion channel gating kinetics of S524Y were indistinguishable from the WT. Quinidine (20 ,M) caused similar extent of tonic block reduction of sodium currents at ,120 mV in WT and S524Y. Surprisingly, quinidine (20 ,M) exerted a more use-dependent block by a 10 Hz pulse train in S524Y than in WT at 22C (Ki: WT, 51.3 ,M; S524Y, 20.3 ,M). S524Y significantly delayed recovery from the use-dependent block, compared with the WT (,= 88.6 7.9 s vs 41.9 6.6 s, P < 0.005). Under more physiological conditions using a 2 Hz pulse train at 37C, S524Y similarly enhanced the use-dependent block by quinidine. In addition, S524Y enhanced the use-dependent block by flecainide (12.5 ,M), but not by mexiletine (100 ,M). Conclusion: A common SCN5A polymorphism, S524Y, can enhance a use-dependent block by class Ia and Ic antiarrhythmic agents. Our findings may have clinical implications in pharmacological management of cardiac arrhythmias since this common SCN5A polymorphism might be a contributing factor to the variable antiarrhythmic response. [source]


Usefulness of a New Radiofrequency Thermal Balloon Catheter for Pulmonary Vein Isolation:

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2003
A New Device for Treatment of Atrial Fibrillation
Introduction: A rapidly firing or triggered ectopic focus located within a pulmonary vein (PV) or close to the PV ostium could induce atrial fibrillation (AF). The aim of this study was to evaluate the efficacy and safety of a radiofrequency thermal balloon catheter for isolation of the PV from the left atrium (LA). Methods and Results: Twenty patients with drug-resistant paroxysmal AF were treated by isolating the superior PVs using an RF thermal balloon catheter. Using a transseptal approach, the balloon, which had an inflated diameter 5 to 10 mm larger than that of the PV ostium, was wedged at the LA-PV junction. It was heated by a very-high-frequency current (13.56 MHZ) applied to the coil electrode inside the balloon for 2 to 3 minutes, and the procedure was repeated up to four times. The balloon center temperature was maintained at 60 to 75C by regulating generator output. Successful PV isolation was achieved in 19 of the 20 left superior PVs and in all 20 of the right superior PVs and was associated with a decrease in amplitude of the ostial potentials. Total procedure time was1.8 0.5hours, which included22 7minutes of fluoroscopy time. After a follow-up period of8.1 0.8months, 17 patients were free from AF, with 10 not taking any antiarrhythmic drugs and 7 taking the same antiarrhythmic agent as before ablation. Electron beam computed tomography revealed no complications, such as PV stenosis at ablation sites. Conclusion: The PV and its ostial region can be safely and quickly isolated from the LA by circumferential ablation around the PV ostia using a radiofrequency thermal balloon catheter for treatment of AF. (J Cardiovasc Electrophysiol, Vol. 14, pp. 609-615, June 2003) [source]


Inhibitory effect of erythromycin on potassium currents in rat ventricular myocytes in comparison with disopyramide

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 7 2003
Erika Hanada
ABSTRACT Disopyramide, a class la antiarrhythmic agent, has been reported to induce torsades de pointes (TdP) associated with excessive QT prolongation in electrocardiogram (ECG), especially when concomitantly administered with erythromycin, a macrolide antibiotic agent. In this study, we have evaluated the effects of erythromycin on action potential duration (APD) and potassium currents in rat ventricular myocytes in comparison with disopyramide. We have evaluated the relationship between in-vitro potassium current inhibition and in-vivo QT prolongation observed in a previous study. Action potentials and membrane potassium currents, including delayed rectifier current (IK) and transient outward current (Ito), were recorded using a whole-cell patch clamp method in enzymatically-dissociated ventricular cells. Erythromycin and disopyramide prolonged APD in a concentration-dependent manner. Disopyramide (10,100 ,m) and erythromycin (100 ,m) led to increases in the APD at 90% repolarization level. Disopyramide reduced IK (IC50 = 37.2 + 0.17 ,m) and Ito (IC50 = 20.9 + 0.13 ,m) while erythromycin reduced IK (IC50 = 60.1 + 0.29 ,m) but not Ito. The observed prolongation of APD might be ascribed to the inhibition of potassium currents. Erythromycin produced the prolongation of APD and the inhibition of potassium currents with a lag time after addition of the drugs, which suggested that erythromycin might not reach potassium channels from outside the ventricular cells. The potency of disopyramide was almost equivalent under in-vitro and in-vivo conditions. However, potency of erythromycin in-vitro was far weaker than that in-vivo reported in a previous study, presumably due to a difference in the uptake of erythromycin into ventricular myocytes between in-vivo and in-vitro conditions. Therefore, when drug-induced risks of QT prolongation are to be evaluated, the difference of potencies between in-vitro and in-vivo should be taken into consideration. [source]


A tryptamine analog with high affinity to the heart tissues is a potential antiarrhythmic agent

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 6 2001
Nicholas Bodor
A novel tryptamine analog, 1-methyl-3-[N -(3-indolyl)ethyl]carbamoyl-1,4-dihydropyridine (T-CDS) was synthesized and converted into a stable, solid complex with 2-hydroxypropyl-,-cyclodextrin. An aqueous solution of the complex was given intravenously to dogs and the concentration of T-CDS and its corresponding quaternary (T-Q+) forms were monitored in the blood for 50 min. The effect of the drug on vital heart parameters was monitored throughout the studies. At the end of the experiment the dogs were sacrificed and the concentration of the quaternary pyridinium form (T-Q+) was determined in the different heart tissues, as well as in the kidney, liver, lung, brain, urine and cerebrospinal fluid. The compound was found to be selectively bound to the heart muscles and showed different concentrations in different heart tissues. The T-Q+ concentrations were much higher in the heart after administration of the dihydro form (T-CDS), than after administering T-Q+ directly. The compound was found to be active on certain vital signs of the cardiovascular system and could be an effective and safe antiarrhythmic agent. [source]


Use of intravenous lidocaine to prevent reperfusion injury and subsequent multiple organ dysfunction syndrome

JOURNAL OF VETERINARY EMERGENCY AND CRITICAL CARE, Issue 3 2003
Benjamin H. Cassutto DVM
Abstract Objective: The objective of this article is to review the human and veterinary literature and provide evidence for the potential beneficial effects of intravenous (IV) lidocaine hydrochloride in preventing post-ischemic,reperfusion injury, the systemic inflammatory response syndrome (SIRS), and subsequent multiple organ dysfunction syndrome (MODS). Human data synthesis: Lidocaine is a local anesthetic and antiarrhythmic agent that has been used for years in human and veterinary medicine for the treatment of ventricular dysrhythmias associated with blunt cardiac trauma, myocardial ischemia, and cardiac surgery. More recently, the drug has been touted as a scavenger of reactive oxygen species (ROS), and has been used to prevent reperfusion dysrhythmias after treatment of myocardial infarction, cross-clamping of the aorta, and in trauma medicine. Veterinary data synthesis: Although no clinical experiments with prophylactic intravenous lidocaine exist in veterinary medicine, there is a large body of evidence from experimental animals that support the use of lidocaine as a Na+/Ca2+ channel blocker, superoxide and hydroxyl radical scavenger, inflammatory modulator, and potent inhibitor of granulocyte functions. Lidocaine is being used in some clinical situations in an attempt to prevent the SIRS in veterinary trauma patients.a,b Conclusions: A large body of experimental evidence exists supporting the use of lidocaine as an anti-oxidant and inflammatory modulator useful in preventing reperfusion injury. With the lack of cost-effective and safe treatments for reperfusion injury in veterinary and human trauma medicine, the use of IV lidocaine to prevent the ensuing inflammatory response and MODS makes it an attractive addition to existing treatments. Therefore, it is essential that prospective clinical trials involving lidocaine as a treatment for prevention of reperfusion injury be performed in companion animals to demonstrate its safety and efficacy. [source]


Brugada Pattern Electrocardiogram Associated with Supratherapeutic Phenytoin Levels and the Risk of Sudden Death

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007
BASEL AL ALOUL M.D.
The emergence of Brugada pattern on electrocardiogram in response to class IA or IC antiarrhythmic agents is widely utilized to diagnose concealed Brugada syndrome and recognized as a risk factor for sudden death. Phenytoin, a class IB antiarrhythmic agent, has not been reported to induce Brugada pattern. We report a patient who presented with Brugada electrocardiogram at supratherapeutic phenytoin level. Considering that patients with syncope may falsely be labeled to have seizures and some epilepsy patients are at increased risk of sudden death, all patients with supratherapeutic phenytoin level should be evaluated with an electrocardiogram for emergence of Brugada pattern. [source]


Chronic Amiodarone Effects on Epicardial Conduction and Repolarization in the Isolated Porcine Heart

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2000
DOMINIQUE LACROIX
Amiodarone is a potent antiarrhythmic agent with complex chronic effects, notably on repolarization and conduction, that are not fully understood. Its low arrhythmogenic potential has been related to a lack of increase in repolarizution dispersion. Since its effects are not documented in pigs we conducted a mapping study of activation and repolarization in isolated perfused porcine hearts. Amio20 female pigs (n = 7) received amiodarone 20 mg/kg per day over 4 weeks while Amio 5O female pigs (n = 7) received 50 mg/kg per day over 4 weeks. Concentrations of the drug encompassed values found in clinical studies. Then, activation patterns and activation-to-recovery intervals (ARI) were mapped epicardially from 128 unipolar electrograms in isolated perfused hearts in corroboration of epicardial action potential recordings. Mean ARI was longer in Amio20 experiments compared to the seven control hearts (325 11 ms vs 288 5 m.s at 1,000 ms), whereas ARI dispersion was not different, being comprised between 7 and 11 ms and generating smooth gradients. In Amio5O experiments, mean ARI was further prolonged (390 10 ms at 1,500 ms) with an exaggerated reverse rate dependence concomitant with a depressant effect on the plateau of the action potential. Again, ARI dispersion did not differ from controls. Finally, the drug depressed the maximal rate of depolarization (Vmax) and slowed conduction in a rate dependent and concentration dependent fashion. In conclusion, chronic amiodarone induces Class I and Class HI antiarrhythmic effects in ventricular porcine epicardium that are concentration dependent but does not affect dispersion of repolarization. This may partly explain its low arrhythmogenic potential. [source]


Dofetilide-Induced Long QT and Torsades de Pointes

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007
Mehmet K. Aktas M.D.
Dofetilide, a new class III antiarrhythmic agent, has been approved as an antiarrhythmic agent for the treatment of atrial fibrillation and atrial flutter. Dofetilide selectively inhibits the rapid component of the delayed rectifier potassium current resulting in a prolongation of the effective refractory period. Like other drugs that affect potassium currents, the prolonged QT interval occurring in the patients treated with dofetilide can be complicated by torsades de pointes. We report four cases of dofetilide-induced QT prolongation and torsades de pointes. We discuss the risk factors for the development of dofetilide-induced long QT and torsades de pointes and review the current literature. [source]


Dronedarone: a new option in atrial fibrillation

FUTURE PRESCRIBER, Issue 1 2009
Professor A. John Camm MD
Many antiarrhythmic agents exploiting new mechanisms of action (as well as modified analogues of traditional antiarrhythmic drugs, with different combinations of ion channel- and receptor-blocking effects and less complicated metabolic profiles) are currently being investigated. Dronedarone is an amiodarone derivative that is devoid of iodine atoms and is believed to have a better safety profile than amiodarone. It is the only antiarrhythmic drug for the treatment of atrial fibrillation (AF) that has been shown to improve survival in high-risk patients. This review provides a contemporary insight into the clinical development of dronedarone, its efficacy and safety in preventing recurrent AF, and its potential additional advantage of improving outcome in patients with AF. Copyright 2009 John Wiley & Sons, Ltd. [source]


A Common SCN5A Variant Alters the Responsiveness of Human Sodium Channels to Class I Antiarrhythmic Agents

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2007
MOSSAAB SHURAIH M.D.
Background: The potential pathophysiological role of common SCN5A polymorphisms in cardiac arrhythmias has been increasingly recognized. However, little is known about the impact of those polymorphisms on the pharmocological response of hNav1.5 to various antiarrhythmic agents. Methods and Results: The known SCN5A polymorphism, S524Y, was studied in comparison with the wild type (WT) define the SCN5A-Q1077del variant. The ion channel gating kinetics and pharmacology were evaluated using whole-cell patch-clamp methods in HEK-293 cells. Consistent with a previous report, the basal ion channel gating kinetics of S524Y were indistinguishable from the WT. Quinidine (20 ,M) caused similar extent of tonic block reduction of sodium currents at ,120 mV in WT and S524Y. Surprisingly, quinidine (20 ,M) exerted a more use-dependent block by a 10 Hz pulse train in S524Y than in WT at 22C (Ki: WT, 51.3 ,M; S524Y, 20.3 ,M). S524Y significantly delayed recovery from the use-dependent block, compared with the WT (,= 88.6 7.9 s vs 41.9 6.6 s, P < 0.005). Under more physiological conditions using a 2 Hz pulse train at 37C, S524Y similarly enhanced the use-dependent block by quinidine. In addition, S524Y enhanced the use-dependent block by flecainide (12.5 ,M), but not by mexiletine (100 ,M). Conclusion: A common SCN5A polymorphism, S524Y, can enhance a use-dependent block by class Ia and Ic antiarrhythmic agents. Our findings may have clinical implications in pharmacological management of cardiac arrhythmias since this common SCN5A polymorphism might be a contributing factor to the variable antiarrhythmic response. [source]


Chromanol 293B Inhibits Slowly Activating Delayed Rectifier and Transient Outward Currents in Canine Left Ventricular Myocytes

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2001
Ph.D., ZHUO-QIAN SUN M.D.
Chromanol 293B on Ionic Currents.Introduction: Drugs that selectively inhibit the slowly activating component of the delayed rectifier potassium current (IKs) are being considered as possible antiarrhythmic agents, because they produce more prolongation of action potential duration at fast rates with less transmural dispersion of repolarization compared with blockers of the rapidly activating component (IKr). Although the chromanol derivative chromanol 293B has been shown to be relatively selective in blocking IKs in some species, its selectivity is far from established. Methods and Results: The present study uses whole-cell, patch-clamp technique to examine the selectivity of this compound for inhibition of IKs in comparison with other repolarizing ionic currents, such as IKr, inward rectifier potassium current (IK1), transient outward current (Ito), and L-type calcium current (ICa-L) in canine left ventricular mid-myocardial and endocardial cells. Chromanol 293B blocked IKs with an IC50 of 1.8 ,M and Ito with an IC50 of 38 ,M. Concentrations as high as 30 ,M did not affect IK1, IKr, or ICa-L. Higher concentrations of chromanol 293B (100 ,M) caused a slight, but statistically insignificant, inhibition of IKr. Conclusion: Our results indicate that chromanol 293B is a relatively selective blocker of IKs in canine left ventricular myocytes. [source]


Toxicity in Doberman Pinchers with Ventricular Arrhythmias Treated with Amiodarone (1996,2005)

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2009
M.S. Kraus
Background: Asymptomatic Doberman Pinschers with dilated cardiomyopathy (DCM) often die suddenly owing to ventricular tachycardia that degenerates into ventricular fibrillation. A safe and effective antiarrhythmic drug treatment is needed. This will require a large, well-controlled, prospective study. Hypothesis: Amiodarone toxicity is common in Dobermans with occult DCM and ventricular tachyarrhythmias refractory to antiarrhythmia therapy. Infrequent monitoring of hepatic function is inadequate. Frequent monitoring may be useful to determine dogs in which the dosage should be decreased or the drug withdrawn. Methods: Medical records from the University of Georgia and Cornell University were searched for Doberman Pinschers diagnosed with preclinical DCM that received amiodarone for severe ventricular arrhythmias refractory to other antiarrhythmic agents. Echocardiographic data, Holter recording data, hepatic enzyme serum activity, and serum amiodarone concentrations were recorded. The presence of clinical signs of toxicity was recorded. Serum amiodarone concentrations were obtained in some dogs. Results: Reversible toxicity was identified in 10 of 22 (45%) dogs. Conclusion and Clinical Importance: Adverse effects from amiodarone were common and were, in part, dosage related. Patients should be monitored for signs of toxicity and liver enzyme activity should be measured at least monthly. [source]


Intrahisian Conduction Disease and Junctional Ectopic Tachycardia

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 3 2008
VALENTINO DUCCESCHI M.D.
Junctional ectopic tachycardia (JET) is an uncommon arrhythmia that mainly affects pediatric patients. However, its clinical presentation may rarely occur in adulthood. Owing to its incessant nature, limited responsiveness to antiarrhythmic agents and poor prognosis, catheter ablation of the junctional focus is often required, even though this may be accompanied by the occurrence of complete atrioventricular block. We report the case of a 68-year-old man with episodes of sustained ventricular tachycardia and repetitive JET whose initiation was often anticipated by a sudden intrahisian conduction delay in the immediately preceding sinus beats. [source]


Brugada Pattern Electrocardiogram Associated with Supratherapeutic Phenytoin Levels and the Risk of Sudden Death

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007
BASEL AL ALOUL M.D.
The emergence of Brugada pattern on electrocardiogram in response to class IA or IC antiarrhythmic agents is widely utilized to diagnose concealed Brugada syndrome and recognized as a risk factor for sudden death. Phenytoin, a class IB antiarrhythmic agent, has not been reported to induce Brugada pattern. We report a patient who presented with Brugada electrocardiogram at supratherapeutic phenytoin level. Considering that patients with syncope may falsely be labeled to have seizures and some epilepsy patients are at increased risk of sudden death, all patients with supratherapeutic phenytoin level should be evaluated with an electrocardiogram for emergence of Brugada pattern. [source]


Catheter Ablation of Chronic Atrial Fibrillation with Noncontact Mapping:

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2p1 2003
Are Continuous Linear Lesions Associated with Ablation Success?
SEIDL, K., et al.: Catheter Ablation of Chronic Atrial Fibrillation with Noncontact Mapping: Are Continuous Linear Lesions Associated with Ablation Success?Catheter-based, right and left atrial compartmentalization procedure was evaluated using a noncontact mapping (NCM) system. Its usefulness to identify and close discontinuities in linear lesions in both atria was evaluated. The impact of linear lesion continuity on ablation success of chronic AF was also investigated. Nineteen patients with symptomatic, drug refractory chronic AF were studied. Right atrial ablation with three predefined lines was attempted in all patients. In 18 patients, left atrial ablation was performed with four linear lesions. During a follow-up of 12 3 months, 6 of 19 patients remained in sinus rhythm (SR) without antiarrhythmic agents (AAs). In addition, four patients were maintained in SR with AA. Thirteen of 14 patients with gaps identified during off-line analysis had recurrence of AF. Only one patient with a gap was free of recurrence without AAs. In the remaining five patients without recurrence of AF, no gap was observed during off-line analysis. In all four patients who were free of AF with additional treatment of AAs, two gaps had been identified. In the remaining nine patients with chronic AF recurrence, a mean of 4.9 gaps were identified. Excluding the initial learning period (first five patients) the success rate increased to 43% (6/14 patients) without and to 71% (10/14 patients) with AA. NCM identifies discontinuities in lines of ablation. Successful ablation of chronic AF is associated with continuity of linear lesions and good clinical technique demands a vigilant search for and closure of every gap. (PACE 2003; 26[Pt. I]:534,543) [source]


Antiarrhythmic Induced Electrical Storm in Brugada Syndrome: A Case Report

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007
Sandeep Joshi M.D.
Brugada syndrome (BS) may be "unmasked" by several pharmacological and/or physiological agents in an otherwise normal electrocardiogram. Once diagnosed the possibility of persistent ventricular tachycardia/fibrillation exists. Although this is treated with various antiarrhythmic agents, there remains a cohort of patients who fail to respond to conventional antiarrhythmic therapy therefore, amplifying the electrical storm. We report a case of a BS diagnosed via procainamide challenge, the resultant near fatal electrical storm aggravated by amiodarone and the eventual resolution with isoproterenol. [source]


Update on atrial fibrillation: Part II

CLINICAL CARDIOLOGY, Issue 3 2008
Irina Savelieva MD
Abstract Antiarrhythmic drugs are an essential tool in the management of atrial fibrillation (AF). Although we are already on the threshold of a large expansion in the use of ablation therapies, these will not, however, be appropriate for all patients, and pharmacological therapies will continue to have an important place in the management of atrial fibrillation. The plethora of antiarrhythmic drugs currently available for the treatment of atrial fibrillation is a reflection that none is wholly satisfactory, each having limited efficacy combined with poor safety and tolerability. Improved class III antiarrhythmic drugs, such as dronedarone, new classes of antiarrhythmic agents, such as atrial repolarization delaying agents, and upstream therapies dealing with substrate, represent potential sources of new pharmacological therapies. Copyright 2008 Wiley Periodicals, Inc. [source]


Ventricular tachyarrhythmia associated with cardiac sarcoidosis: Its mechanisms and outcome

CLINICAL CARDIOLOGY, Issue 4 2004
Hiroshi Furushima M.D.
Abstract Background: Cardiac sarcoidosis is increasingly recognized and is associated with poor prognosis. Ventricular tachycardia (VT) associated with cardiac sarcoidosis is the most likely cause of sudden death in most patients, but the mechanism has not been well established. Hypothesis: This study investigated the mechanisms and outcome of VT associated with cardiac sarcoidosis. Methods: The study included eight consecutive patients (five men, three women, aged 54 19 years) who had sustained monomorphic VT associated with cardiac sarcoidosis in our hospital. Results: The average ejection fraction was 43 11%. Twenty-two VTs were observed in these patients, and mean heart rate during VT was 192 29 beats/min (range 144,259). The phenomenon of transient entrainment was documented in 10 of 22 (45%) VTs by ventricular pacing (eight in the active phase). Another five (23%) VTs could not be entrained, but could be initiated by programmed stimulation and terminated by rapid pacing, reproducibly. In 3 of the 22 (14%) VTs, cardioversion was required urgently because of the fast rate, while the remaining 4 (18%) could be induced during electrophysiologic study. Conclusions: In this study, there was a high possibility that the mechanism of 15 (68%) VTs was reentry. Reentrant substrate is formed not only in association with the healing of cardiac granulomas in the inactive phase of cardiac sarcoidosis but also in the active phase. Ventricular tachycardia with cardiac sarcoidosis, even if this mechanism is reentry, has different inducibility between the active and inactive phases in an electrophysiologic study. This makes the therapy for cardiac sarcoidosis (e.g., corticosteroids, antiarrhythmic agents, and catheter ablation) difficult. The implantable cardioverter-defibrillator is an effective treatment for ventricular tachyarrythmia with cardiac sarcoidosis. [source]