Unstable Ventricular Arrhythmias Research Articles

“Rescue” ablation of electrical storm in arrhythmogenic right ventricular cardiomyopathy in pregnancy

BackgroundRadiofrequency ablation (RFCA) became a treatment of choice in patients with recurrent ventricular tachycardia, ventricular fibrillation, and appropriate interventions of implanted cardioverter-defibrillator (ICD), however, electrical storm (ES) ablation in a pregnant woman has not yet been reported.Case presentationWe describe a case of a successful rescue ablation of recurrent ES in a 26-year-old Caucasian woman during her first pregnancy (23rd week). The arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) was diagnosed 3 years earlier and several drugs as well as 2 ablations failed to control recurrences of ventricular tachycardia. RFCA was performed on the day of the third electric storm. The use of electroanatomic mapping allowed very low X-ray exposure, and after applications in the right ventricular outflow tract, arrhythmia disappeared. Three months after ablation, a healthy girl was delivered without any complications. During twelve-month follow-up there was no recurrence of ventricular tachycardia or ICD interventions.ConclusionsThis case documents the first successful RFCA during ES due to recurrent unstable ventricular arrhythmias in a patient with ARVD/C in pregnancy. Current guidelines recommend metoprolol, sotalol and intravenous amiodarone for prevention of recurrent ventricular tachycardia in pregnancy, however, RFCA should be considered as a therapeutic option in selected cases. The use of 3D navigating system and near zero X-ray approach is associated with minimal radiation exposure for mother and fetus as well as low risk of procedural complication.

English

Sudden cardiac death is often precipitated by unstable ventricular arrhythmias. These arrhythmias are particularly amendable to defibrillation. The risk of these arrhythmias is highest immediately following an acute myocardial infarction, especially if there is impaired left ventricular function. Many patients with depressed left ventricular function receive an implantable cardioverter-defibrillator for prophylaxis against these lethal arrhythmias. The current guidelines recommend against implantable cardioverter-defibrillator implantation in the early period following myocardial infarction. This is because, given the time, arrhythmia risk typically decreases. The wearable cardioverter-defibrillator (WCD) can protect these vulnerable patients in the short term when arrhythmia risk is highest. Herein, we present a case of a 69 year old male who suffered a cardiac arrest four days after hospital discharge following an acute myocardial infarction.   Key words: Sudden cardiac death (SCD), defibrillation, implantable cardioverter-defibrillator (ICD), wearable cardioverter-defibrillator (WCD).

Catheter Ablation of Arrhythmias Exclusively Using Electroanatomic Mapping: A Series of Cases

BackgroundCatheter ablation is a treatment that can cure various cardiac arrhythmias. Fluoroscopy is used to locate and direct catheters to areas that cause arrhythmias. However, fluoroscopy has several risks. Electroanatomic mapping (EAM) facilitates three-dimensional imaging without X-rays, which reduces risks associated with fluoroscopy. ObjectiveWe describe a series of patient cases wherein cardiac arrhythmia ablation was exclusively performed using EAM. MethodsPatients who presented with cardiac arrhythmias that were unresponsive to pharmacological therapy were prospectively selected between March 2011 and March 2012 for arrhythmia ablation exclusively through EAM. Patients with indications for a diagnostic electrophysiology study and ablation of atrial fibrillation, left atrial tachyarrhythmias as well as hemodynamically unstable ventricular arrhythmia were excluded. We documented the procedure time, success rate and complications as well as whether fluoroscopy was necessary during the procedure. ResultsIn total, 11 patients were enrolled in the study, including seven female patients (63%). The mean age of the patients was 50 years (SD ±16.5). Indications for the investigated procedures included four cases (35%) of atrial flutter, three cases (27%) of pre-excitation syndrome, two cases (19%) of paroxysmal supraventricular tachycardia and two cases (19%) of ventricular extrasystoles. The mean procedure duration was 86.6 min (SD ± 26 min). Immediate success (at discharge) of the procedure was evident for nine patients (81%). There were no complications during the procedures. ConclusionThis study demonstrates the feasibility of performing an arrhythmia ablation exclusively using EAM with satisfactory results.

Coexisting mutations/polymorphisms of the long QT syndrome genes in patients with repaired Tetralogy of Fallot are associated with the risks of life-threatening events

Coexisting long QT gene mutations/polymorphisms in Tetralogy of Fallot (TOF) patients may aggravate the repolarization abnormality from cardiac repair. We investigated the impact of these genes on the risk of life-threatening events. Genetic variants of the three common long QT genes were identified from patients with repaired TOF. Life-threatening events were defined as sudden cardiac death and hemodynamic unstable ventricular arrhythmia. Biophysical characterization of the alleles of the genetic variants was performed using a whole-cell voltage clamp with expression in Xenopus oocytes. A total of 84 patients (56.0 % male with 1,215 patients-year follow-up) were enrolled. Six rare variants and six non-synonymous single nucleotide polymorphisms (SNPs) were found in 40 (47.6 %) patients. Life-threatening events occurred in five patients; four received implantable cardioverter defibrillator and one died of sudden cardiac death. Life-threatening events occurred more often in those with genetic variants than those without (5/40 vs. 0/44, P = 0.021); particularly, the hERG or SCN5A gene mutations/polymorphisms (2/5 vs. 3/79, P = 0.027 and 5/27 vs. 0/57, P = 0.003, respectively). Among the five patients with life-threatening events, three had compound variants (hERG p.M645R/SCN5A p.R1193Q, hERG p.K897T/SCN5A p.H558R, and KVLQT1 p.G645S/SCN5A p.P1090L), that also increased the risk of events. Their QTc and JTc were all prolonged. Functional study of the novel variant (hERG gene p.M645R) from patients with life-threatening events revealed a dominant negative effect. In conclusion, in repaired TOF patients, coexisting long QT mutations/polymorphisms might have additive effects on the repolarization abnormality from surgery and thereby increase the risks of life-threatening events.

Tai Chi Exercises Benefit Even Oldest Adults

Tai Chi Exercises Benefit Even Oldest Adults

Percutaneous Cardiopulmonary Support for Catheter Ablation of Unstable Ventricular Arrhythmias in High-Risk Patients

In patients with severe cardiomyopathy, recurrent episodes of nontolerated ventricular tachycardia (VT) or electrical storm (ES) frequently cause acute heart failure and cardiac death; the suppression of the arrhythmia is therefore lifesaving, but feasibility of catheter ablation (CA) is precluded by the adverse hemodynamic conditions together with the characteristics of the arrhythmia that interdicts efficacious mapping. The use of the percutaneous cardiopulmonary support (CPS) for circulatory assistance may allow patient's stabilization and enhance efficacy and safety of CA in this emergency setting. 19 patients (19 males; mean age 61 +/- 6 years; chronic ischemic cardiomyopathy, eleven patients; primary dilated cardiomyopathy, six patients; arrhythmogenic right ventricular dysplasia/ cardiomyopathy, two patients) with recurrent nontolerated VT episodes undergoing CPS-assisted CA were retrospectively evaluated. Twelve patients had acute hemodynamic failure refractory to inotropic agents and ventilatory assistance, seven patients had undergone a failing nonconventional CA procedure. 14 patients presented with ES, and in twelve the procedure was undertaken under emergency conditions within 24 h from admission. Patients were ventilated under general anesthesia and assisted by a multidisciplinary team. The CPS system consisted in a Medtronic Bio-Medicus centrifugal pump and in a Maxima Plus oxygenator, a 15-F arterial cannula, and a 17-F venous cannula. Flows between 2 and 3 l/min were activated after induction of 56/62 forms of nontolerated VT, achieving hemodynamic stabilization in all patients. CA was mainly guided by conventional activation mapping and was effective in abolishing 45/56 supported VTs; in 10/19 patients all clinical VTs were suppressed by CA. Mean procedural time was 4 h and 20 min. Complete stabilization was achieved in 13 patients (68%) without VT recurrence during a 7-day in-hospital monitoring. A significant clinical improvement was observed in two patients (11%); one patient (5%) with persistent VT episodes acutely died after heart transplant. At a mean follow-up of 42 months (range 15-60 months), 5/18 patients (28%) were free from VT recurrence, 7/18 (39%) had a clear clinical improvement with reduced implantable cardioverter defibrillator interventions. 5/14 patients (36%) had ES recurrence; among them, three died because of acute heart failure. No serious CPS-related complications were observed. The CPS warrants acceptable hemodynamic stabilization and efficacious mapping in high-risk patients undergoing CA for unstable VT in the emergency setting. Safety and efficacy of this technique translate into significant clinical improvement in the majority of patients. Even if only relatively invasive, CPS should be reserved to patients with ES or intractable arrhythmia causing acute heart failure; moreover, the need for an experienced team of multidisciplinary operators implies that its use is restricted to selected high-competency institutions.

A Method for Guiding Ablation Catheters to Arrhythmogenic Sites Using Body Surface Electrocardiographic Signals

Treatment of hemodynamically unstable ventricular arrhythmias requires rapid and accurate localization of the reentrant circuit. We have previously described an algorithm that uses the single-equivalent moving dipole model to rapidly identify both the location of cardiac sources from body surface electrocardiographic signals and the location of the ablation catheter tip from current pulses delivered at the tip. However, during catheter ablation, in the presence of sources of systematic error, even if the exit site and catheter tip dipole are superposed in real space, their calculated positions may be separated by as much as 5 mm if their orientations are not exactly matched. In this study, we present a method to compensate for the effect of dipole orientation and examine the method's ability to guide a dipole at a catheter tip to an arrhythmogenic dipole corresponding to the exit site. In computer simulations, we show that the new method enables the user to guide the catheter tip to within 1.5 mm of the arrhythmogenic dipole using a realistic number of movements of the ablation catheter. These results suggest that this method has the potential to greatly facilitate RF ablation procedures, especially in the significant patient population with hemodynamically unstable arrhythmias.

Preoperative dobutamine stress echocardiographic findings and subsequent short-term adverse cardiac events after orthotopic liver transplantation

Cardiovascular (CV) complications are the leading cause of non-graft-related death in orthotopic liver transplant (OLT) patients. Pretransplant cardiac evaluation using dobutamine stress echocardiography (DSE) is commonly utilized for risk stratification of OLT candidates. To determine if clinical and echocardiographic variables identify patients with increased CV risk, we performed a retrospective chart review of all 284 patients that underwent OLT at our institution between June 1999 and August 2005. Of these patients, 157 had a DSE prior to their OLT. Serious adverse CV events occurring during surgery and up to 4 months post-transplantation were defined as cardiac-related death, myocardial infarction (MI), new heart failure, or asystole or unstable ventricular arrhythmia requiring acute treatment. Sixteen of 157 patients (10%) had an adverse CV event with 2 deaths. These included ventricular tachycardia (n = 8), asystole (n = 2), MI (n = 5), and new heart failure (n = 1). Nine of the 16 CV events occurred at the time of surgery (including both deaths), 5 occurred postoperatively, and 3 occurred after hospital discharge. Variables that correlated with increased CV events were inability during DSE to achieve >82% of the maximum predicted heart rate (22% versus 6%, P = 0.01), a peak rate pressure product during DSE of <16,333 (17% versus 5%, P = 0.02), and a Model for End-Stage Liver Disease (MELD) score of >24 at the time of OLT. A multivariate model calculated from the DSE maximum achieved heart rate (MAHR) and MELD score (result = 3.78 + 0.07 MELD - 0.05 MAHR) identified a 47% risk for a value > 0 versus a 6% risk for a value < 0 (P < 0.001). In conclusion, the maximum heart rate achieved during DSE together with the MELD score may be a predictor of adverse CV events up to 4 months post-OLT. A large prospective study is needed to more decisively support this conclusion.

Ventricular Tachycardia/Ventricular Fibrillation Ablation in the Setting of Ischemic Heart Disease

Recurrent ventricular tachycardia (VT) in the setting of coronary artery disease is frequently a life-threatening electrophysiologic emergency. Even in patients with an implantable defibrillator, recurrent VT is frequently accompanied by repeated and disabling shock therapy. Catheter ablative therapy offers the ability to provide immediate control of recurrent VT. Long-term elimination of VT should be anticipated in most patients. This article reviews the strategies, tools, techniques, and expected outcome for catheter ablation of stable and unstable ventricular arrhythmias in the setting ischemic heart disease.

Ablation of Nonsustained or Hemodynamically Unstable Ventricular Arrhythmia Originating From the Right Ventricular Outflow Tract Guided by Noncontact Mapping

Conventional activation or pacemapping is effective in guiding ablation of ventricular tachyarrhythmia originating from right ventricular outflow tract (RVOT). However, in selected patients with hemodynamically unstable or nonsustained tachycardia, noncontact mapping may be an effective alternative method to guide ablation in RVOT. Five patients with symptomatic hypotension during ventricular tachycardia (VT) or nonsustained tachyarrhythmia originating from the RVOT had radiofrequency ablation guided by noncontact mapping. All patients had a history of syncope and the tachyarrhythmias were refractory to antiarrhythmic therapy. Four patients had spontaneous sustained VT of a cycle length from 250 to 300 ms and one had symptomatic ventricular ectopic beats. Two patients were diagnosed to have arrhythmogenic right ventricular cardiomyopathy (ARVC). Sustained VT with hypotension was induced in two patients and nonsustained VT in three patients. Isopotential color maps were used to locate the earliest activation site of the tachyarrhythmia in RVOT. Three patients had tachyarrhythmia exit sites at the septal region and two at lateral region of RVOT. Low voltage area and diastolic activity were detected in the two patients with ARVC. Radiofrequency ablation guided by noncontact mapping was performed during sinus rhythm in all patients. The number of ablation attempts ranged from 1 to 14. After follow-up for 12 +/- 5.8 months, there was no recurrence of tachyarrhythmia and syncope in all five patients. Noncontact mapping is a safe and effective alternative method to guide ablation of hemodynamically unstable or nonsustained ventricular arrhythmia originating from RVOT.

Vascular endothelial growth factor and soluble P-selectin in acute and chronic congestive heart failure

Because congestive heart failure (CHF) is characterized clinically by tissue hypoxia, we hypothesized that there would be evidence of neovascularization, possibly resulting from this process. To test this, we measured levels of vascular endothelial growth factor (VEGF), associated with angiogenesis, in the plasma of patients with varying degrees of CHF (presenting acutely and in the chronic phase) and compared levels with those in healthy controls. To test the hypothesis of a link between VEGF and platelet activation and a tendency to hypercoagulability in CHF, 1,2 we also measured plasma levels of fibrinogen and soluble P-selectin, because these markers of coagulation and platelet activation have previously been shown to increase in patients with chronic CHF. 2 Our methods to testing these hypotheses were cross sectional (comparing patients with acute and chronic CHF with healthy controls), interventional (examining markers before and after successful treatment of acute CHF), and using a follow-up approach (at which time we questioned whether or not plasma markers could predict those at risk of mortality). ••• We recruited consecutive patients admitted with acute CHF secondary to impaired left ventricular systolic function, which was documented as an ejection fraction 40%, either by echocardiography, radionuclide imaging, or left ventriculography on admission, or within the previous 6 months. Patients were excluded from the study for the following criteria: concomitant acute coronary syndromes; infection or pyrexial illness; recent (3 months) myocardial infarction or stroke; unstable angina or ventricular arrhythmias; chronic and systemic illnesses including renal failure, hepatic impairment, cancer, and inflammatory connective tissue disease; and use of oral steroids or hormone replacement therapy. Baseline results from patients with acute CHF (i.e., subjects presenting acutely with severe symptomatic disease) were compared with 2 age- and gender-matched control groups; these were outpatients with chronic stable CHF in sinus rhythm (chronic CHF) and healthy control subjects recruited from among healthy hospital staff and from subjects attending the hospital for hernia repairs, varicose vein procedures, or other relatively minor operations. Subjects with CHF were classified according to the New York Heart Association (NYHA) criteria, with class I to II being no or mild symptoms and class III to IV being moderate to severe symptoms. Left ventricular ejection fraction was estimated using transthoracic M-mode echocardiography. All healthy controls had no clinical evidence of vascular, metabolic, neoplastic, diabetic, or in flammatory disease on careful history, examination, and routine laboratory tests. Blood tests were performed in patients with acute decompensated CHF between days 1 and 7 after hospital admission, and again at 3 months after standard treatment for heart failure according to local guidelines. 3 Patients were followed up for clinical end points that consisted of all-cause mortality and hospitalizations for stroke, myocardial infarction, thromboembolism, unstable angina, and revascularization for up to 6 months. Citrated plasma and serum were obtained from

Role of implantable cardioverter defibrillators in dilated cardiomyopathy.

Idiopathic dilated cardiomyopathy (DCM) accounts for about 10,000 deaths per year in western countries. Of these deaths, 8% to 51% occur suddenly, with more than half of the events due to a ventricular arrhythmia. Improvement in diagnostic techniques and therapeutic strategies, together with changes in secular trends, have likely contributed to the reported trend toward improved survival in recent years. Identification of DCM patients at higher risk of sudden death is difficult. Poor left ventricular function is the strongest predictor of all-cause death, whereas a history of sustained unstable ventricular arrhythmia or cardiac arrest identifies patients at high risk of sudden death. Recent data suggest that a history of syncope, regardless of inducibility at programmed electrical stimulation, may be a risk factor of sudden death. Despite the absence of controlled studies, use of implantable cardioverter defibrillator therapy for primary prevention can be considered in patients with unexplained syncope as well as subgroups of DCM patients awaiting transplantation. In patients who survive a cardiac arrest or an unstable ventricular tachycardia, use of implantable cardioverter defibrillator therapy is associated with improved survival during follow-up and should be considered as a first-line therapy.

New advances in class III antiarrhythmic drug therapy.

In the past 2 years, significant advances have been made in class III antiarrhythmic drug therapy. In patients with ventricular arrhythmias and implantable cardioverter defibrillators (ICDs), antiarrhythmic agents are increasingly being used as adjunct therapy to decrease the frequency of ICD discharges. Sotalol was recently shown to be effective in reducing tachyarrhythmias in patients with ICDs. Intravenous amiodarone is being used for the acute treatment of unstable ventricular arrhythmia and is being investigated for the treatment of acute out-of-hospital cardiac arrest. Class III agents are increasingly being used for prophylaxis in patients who have atrial fibrillation or atrial flutter, and data point to an important role for these agents in reducing supraventricular tachyarrhythmias after cardiac surgery. Future studies will need to directly compare these agents with pure anti-adrenergic maneuvers in postoperative patients. In addition to terminating atrial fibrillation and atrial flutter, ibutilide significantly reduces human atrial defibrillation thresholds and increases the percentage of patients who can be cardioverted from atrial fibrillation to sinus rhythm. The US Food and Drug Administration is expected to approve dofetilide for clinical use soon, and it is currently reviewing azimilide (which seems to be devoid of frequency-dependent effects on repolarization) for prophylaxis against atrial fibrillation and atrial flutter. Dronedarone, tedisamal, and trecetilide are now under active study intended to determine their usefulness in patients with cardiac arrhythmias. Experimental studies are ongoing to identify pharmacologic agents that will selectively prolong repolarization in the atria without exerting electrophysiologic effects in the ventricles.

IV Amiodarone for Unstable Ventricular Arrhythmias

Experts in advanced cardiac life support (ACLS) pharmacology summarized the pharmacology of IV amiodarone and reviewed the literature on its use in patients with unstable ventricular arrhythmias. No clinical trial of any antiarrhythmic drug used in cardiac arrest has demonstrated increased survival to hospital discharge. A recent abstract showed …

Cost Effectiveness of Inpatient Initiation of Antiarrhythmic Therapy for Supraventricular Tachycardias

This study assessed the cost effectiveness of inpatient antiarrhythmic therapy initiation for supraventricular tachycardias using a metaanalysis of proarrhythmic risk and a decision analysis that compared inpatient to outpatient therapy initiation. A MEDLINE search of trials of antiarrhythmic therapy for supraventricular tachycardias was performed, and episodes of cardiac arrest, sudden or unexplained death, syncope, and sustained or unstable ventricular arrhythmias were recorded. A weighted average event rate, by sample size, was calculated and applied to a clinical decision model of therapy initiation in which patients were either hospitalized for 72 hours or treated as outpatients. Fifty-seven drug trials involving 2,822 patients met study criteria. Based on a 72-hour weighted average event rate of 0.63% (95% confidence interval, 0.2% to 1.2%), inpatient therapy initiation cost $19,231 per year of life saved for a 60-year-old patient with a normal life expectancy. Hospitalization remained cost effective when event rates and life expectancies were varied to model hypothetical clinical scenarios. For example, cost-effectiveness ratios for a 40-year-old without structural heart disease and a 60-year-old with structural heart disease were $37,510 and $33,310, respectively, per year of life saved. Thus, a 72-hour hospitalization for antiarrhythmic therapy initiation is cost effective for most patients with supraventricular tachycardias.

Mortality Benefit of Implantable Cardioverter-Defibrillator Therapy in Patients With Persistent Malignant Ventricular Arrhythmias Despite Amiodarone Treatment

Implantable cardioverter defibrillators (ICDs) are very effective in preventing sudden cardiac death. However, debate continues as to whether ICD implantation is superior to amiodarone in prolonging survival in patients with life-threatening ventricular arrhythmias. Of 442 consecutive patients treated with amiodarone, we identified 48 patients with symptomatic ventricular arrhythmias who met all of the following inclusion criteria: (1) had inducible sustained ventricular tachycardia at baseline electrophysiologic study, (2) had an oral amiodarone load of at least 10 g over 10 to 14 days, (3) remained inducible with a hemodynamically unstable ventricular arrhythmia at follow-up electrophysiologic study, and (4) were advised to continue amiodarone therapy and undergo ICD implantation. Patients who agreed to undergo ICD implantation (n = 28) had a lower ejection fraction (29 ± 9% vs 40 ± 12% p <0.005) and were younger (61.0 ± 10 vs 69 ± 7 years, p <0.01) than patients who refused device implantation (n = 20). Using a Cox proportional-hazards model, defibrillator therapy was the strongest independent predictor of improved survival in patients with an ejection fraction ≤40% (RR = 0.42; 95% confidence interval 0.22 to 0.79). Thus, patients with depressed ejection fraction and continued inducibility of sustained ventricular tachycardia despite oral amiodarone loading have a poor prognosis. In such patients, ICDs are associated with a 58% reduction in total cardiac mortality. The purpose of the present study was to determine whether implantable cardioverter-defibrillator (ICD) therapy is associated with prolongation of total cardiac survival in patients with symptomatic ventricular arrhythmias refractory to amiodarone treatment. We found that ICD treatment was the strongest independent predictor of improved survival and was associated with a 58% reduction in cardiovascular mortality in patients with an ejection fraction ≤40% (RR 0.42; 95% confidence interval 0.22 to 0.79).

Acute management of ventricular arrhythmias: role of antiarrhythmic agents.

When treating life-threatening ventricular arrhythmias such as symptomatic ventricular tachycardia and ventricular fibrillation (VT/VF), the nature of the arrhythmia must be precisely defined and the approach must be tailored to it. For hemodynamically unstable ventricular arrhythmias, DC cardioversion or high-energy defibrillation remains the approach of choice. Determining the specific role of intravenous drugs in acute conversion of VT/VF and the most appropriate long-term therapy (pharmacologic or nonpharmacologic) to prevent recurrence can be difficult. Pharmacologic conversion of stable VT/VF presents an even greater challenge, as the role of lidocaine considered the first-line agent for many decades, is now being reevaluated. Lidocaine appears to be effective in converting no more than 20% of stable VTs, compared with 70% for intravenous sotalol. The precise efficacies of parenteral procainamide, beta-blockers, and newer class III agents, including intravenous amiodarone, remain to be defined; however, intravenous amiodarone, available recently, can control unstable, recurrent VT/VF that is resistant to lidocaine or procainamide. A standard regimen of concomitant intravenous and oral amiodarone may be given for rapid and sustained control, and allows oral amiodarone to be continued in a significant number of patients.

Mechanism of lethal proarrhythmia observed in the Cardiac Arrhythmia Suppression Trial: role of adrenergic modulation of drug binding.

A variety of recent in vivo studies have sought to clarify the mechanism underlying the proarrhythmic response of flecainide in the Cardiac Arrhythmia Suppression Trial (CAST). Increased inducibility of relatively stable ventricular arrhythmias in subacute and chronic postinfarction models has been universally observed. The arrhythmogenesis has been explained in part by drug induced modulation of anisotropic conduction in persistently ischemic tissue, increased durations of vulnerable windows, enhanced generation of unidirectional block with the introduction of extrastimuli, variability of repolarization within the ventricular wall, and the creation of stable reentrant circuits with narrow central zones of propagation. While these data explain arrhythmogenesis in general, malignant ventricular arrhythmia capable of producing the excess sudden or arrhythmic death mortality in the CAST trial have not been universally observed, nor have the proported beneficial effects of beta-blockade seen in the CAST trial and other studies been explained. Additional studies examining the adrenergic modulation of flecainide binding have shown reversal of flecainide effects in normal tissue, but paradoxical amplification of flecainide induced conduction slowing in depolarized tissue. This variable effect in normal versus abnormal tissue produces significant dispersions of conduction with an expected increased propensity for conduction failure in response to ectopy, increased liminal length for impulse propagation, enhanced vulnerability to premature extrastimuli, and completed reentrant circuits in regions of depressed membrane potentials. This, along with the decrease in action potential duration and accompanying refractoriness in the setting of adrenergic modulation may favor more malignant double wavelet or unstable ventricular arrhythmias.

Emergency intracardiac defibrillation for refractory ventricular fibrillation: Clin Cardiol 1995; 18/2: 109–111

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life-saving capabilities of intracardiac defibrillation.

Emergency intracardiac defibrillation for refractory ventricular fibrillation

Hemodynamically unstable ventricular arrhythmias induced during electrophysiologic testing almost always respond to prompt application of direct current transthoracic shocks. In rare cases, however, ventricular fibrillation may be refractory to conventional treatment. Recently, a technique of intracardiac defibrillation has been successfully used to resuscitate patients with ventricular fibrillation refractory to transthoracic defibrillation. We describe two patients with a history of myocardial infarction and left ventricular dysfunction who were admitted with symptomatic episodes of ventricular tachycardia. Both had inducible sustained monomorphic ventricular tachycardia. During a repeat electrophysiologic study in Patient No. 1 on procainamide and at the initial study in Patient No. 2, right ventricular burst pacing to terminate ventricular tachycardia resulted in ventricular fibrillation refractory to resuscitation efforts, including transthoracic defibrillation with 360 J. Emergency intracardiac defibrillation with 200 and 360 J, respectively, successfully converted both patients to sinus rhythm. Both patients were subsequently discharged from the hospital on amiodarone. These cases illustrate the life-saving capabilities of intracardiac defibrillation.