Spontaneous Sustained Monomorphic Ventricular Tachycardia Research Articles

Scar characteristics for prediction of ventricular arrhythmia in ischemic cardiomyopathy.

Better risk-stratification tools are needed to identify the best candidates for implantable cardioverter defibrillator implantation. Infarct characterization by cardiac magnetic resonance (CMR) has become an evolving potential tool for risk stratification. We assessed the ability of scar characteristics by CMR in patients with postinfarction left ventricular (LV) dysfunction to predict sustained monomorphic ventricular tachycardia (SMVT). Forty-eight patients with postinfarction LV dysfunction underwent CMR study. Twenty-four patients had history of SMVT and the other 24 were control group and underwent electrophysiological study to assess SMVT inducibilty. Various scar characteristics were assessed in the spontaneous SMVT group and were compared with the inducible and noninducible SMVT groups. Only six patients in the control group had inducible SMVT. In univariable analysis, total scar (absolute and as percent of LV), scar core (absolute and as percent of LV), peri-infarct zone (absolute and as percent of LV), mean infarct transmurality, and number of segments with late gadolinium enhancement (LGE) were statistically significant predictors of spontaneous SMVT experience and SMVT inducibility. In multivariable analysis, total infarct as percent of LV mass was the only significant independent predictor of spontaneous SMVT experience (odds ratio [OR] 1.33 per% change, 95% confidence interval [CI] 1.12-1.6, P = 0.001) and SMVT inducibility (OR 1.3 per% change, 95% CI 1.1-1.6, P = 0.004). Characterization of myocardial infarct by LGE-CMR, specifically total infarct size, is better predictor of spontaneous SMVT experience and SMVT inducibility than LV ejection fraction.

Fundamental Differences in Electrophysiologic and Electroanatomic Substrate Between Ischemic Cardiomyopathy Patients With and Without Clinical Ventricular Tachycardia

The aim of this study was to compare the electrophysiologic substrate in ischemic cardiomyopathy (ICM) patients with and without sustained monomorphic ventricular tachycardia (SMVT). Despite the universal presence of potentially arrhythmogenic left ventricular (LV) scarring, it is not clear why the majority of ICM patients never develop SMVT. Detailed electroanatomic mapping of the LV endocardium was performed in 17 stable control ICM patients (16 males) without clinical SMVT. They were compared with 17 ICM patients (15 males) with spontaneous SMVT. Standard definitions of low-voltage zones and fractionated, isolated, and very late potentials were used. There were no significant baseline differences between the groups in terms of LV diameter, ejection fraction (27% vs. 28%), infarct territory, or time from infarction. However, control patients had smaller total low-voltage area < or =1.5 mv (30% of surface area vs. 55%, p < 0.001); smaller very low-voltage area <0.5 mv (7.3% vs. 29%, p < 0.001); higher mean voltage of low-voltage zones; fewer fractionated, isolated, and very late potentials with lower density of these scar-related electrograms per unit low-voltage area; and less SMVT inducibility. Potential conducting channels within dense scar and adjacent to the mitral annulus were more frequent in SMVT patients. Compared with ICM patients with SMVT, an otherwise similar control group demonstrated markedly smaller endocardial low-voltage zones, lower scar-related electrogram density, and fewer conducting channels with faster conduction velocity. These findings may explain why some ICM patients develop SMVT and others do not.

Amiodarone Is Poorly Effective for the Acute Termination of Ventricular Tachycardia

It is hypothesized that intravenous (IV) amiodarone is poorly effective for the acute termination of sustained monomorphic ventricular tachycardia because of the relatively slow onset of its Vaughn-Williams class III effect to prolong myocardial depolarization and the refractory period. This study is designed to determine the effectiveness and safety of IV amiodarone for the termination of sustained monomorphic ventricular tachycardia. A retrospective case series was collected at 4 urban university-affiliated hospitals from September 1996 to April 2005 after institutional review board approval with waiver of informed consent. Emergency department (ED) patients treated with IV amiodarone for ventricular tachycardia were identified by ED treatment and hospital pharmacy billing records, International Classification of Diseases, Ninth Revision discharge codes, and ECG characteristics. All consecutive patients who received at least 150 mg amiodarone in 15 minutes or less for spontaneous sustained monomorphic ventricular tachycardia were eligible for inclusion. Sustained monomorphic ventricular tachycardia was defined as a tachycardia with uninterrupted duration or rapid recurrence despite automatic internal cardiac defibrillator therapy for at least 5 minutes before amiodarone treatment, monomorphic morphology, rate greater than 120 beats/min, QRS duration greater than 120 ms, and subsequently determined to be ventricular tachycardia by ECG criteria (eg, atrioventricular dissociation), implanted device interrogation, or formal electrophysiology study. Measured outcomes included sustained termination of ventricular tachycardia within 20 minutes of initiation of amiodarone infusion and any documented adverse effects. Rates of successful termination and adverse effects and their 95% confidence intervals (CIs) were calculated. The presence or average values of potentially confounding predictors in patients with and without ventricular tachycardia termination after amiodarone were also calculated and compared. Thirty-three patients were identified and included. Five patients received electrical therapy within 20 minutes of initiation of amiodarone infusion, and the response to amiodarone was unknown. Twenty-seven of the remaining 28 patients received 150 mg amiodarone, and the rate of successful ventricular tachycardia termination was 8 of 28, 29% (95% CI 13 to 49). Two of 33 patients, 6% (95% CI 1 to 20), required direct current cardioversion for presyncope or hypotension temporally associated with amiodarone treatment. IV amiodarone, as currently administered, is relatively safe but ineffective for the acute termination of sustained ventricular tachycardia.

Sustained Monomorphic Ventricular Tachycardia: Immediate Evaluation and Management, Long-Term Management

Immediate evaluation and management Patients with sustained monomorphic ventricular tachycardia (SMVT) demonstrate a wide range of clinical presentations, from essentially asymptomatic to critically ill. The rate of the tachycardia is the major determinant of the degree of hemodynamic compromise, although the extent of structural heart disease is also important. The acuity of the immediate management is dictated by the severity of the symptoms. Immediate synchronous cardioversion is indicated for the hypotensive, unconscious patient; acute cardioversion is also used after adequate sedation is obtained in conscious but symptomatic patients. Lidocaine infusion has been advocated for patients with well tolerated SMVT, mostly based on analogy to its usefulness in preventing VF in acute myocardial infarction. Several recent studies have that lidocaine is infrequently successful in terminating SMVT. Only 10 of 121 episodes of induced and 0 of 27 spontaneous SMVT terminated with lidocaine infusion in a study by Nasir et al.1 In a small randomized study,2 sotalol (100 mg IV over 5 minutes) converted 69% of SMVT episodes compared to 18% with lidocaine. In unusual cases, recognized by characteristic electrocardiographic manifestations and the absence of structural heart disease (Fig. 1), episodes of SMVT can be treated with medications typically reserved for treating supraventricular arrhythmias, such as adenosine, calcium antagonists and beta-blockers. The need for diagnostic certainty before using agents that could produce hypotension during SMVT cannot be overstated. After termination of the presenting episode, the acute management centers on the prevention of SMVT recurrence. In the majority of cases (digitalis intoxication is one exception) SMVT is the consequence of a permanent electrical substrate. Although it is prudent to investigate and correct contributing factors such as electrolyte abnormalities and acute ischemia, these factors can serve as triggers but not as the proximate cause of the arrhythmia. Lidocaine is often administered continuously after an episode of SMVT, and is may be helpful in selected patients following acute infarction or cardiac surgery. In light of the signi~cant potential for side effects and particularly because most patients with SMVT have infrequent recurrences, antiarrhythmic drugs should not be given re_exively after a single SMVT episode. The unusual patient with multiple acute recurrent episodes of SMVT is often critically ill and very dif~cult to control. Several recent multicenter studies con~rmed previous case reports of the ef~cacy of intravenous amiodarone in the treatment of recurrent, poorly tolerated SMVT.3–5 A dose ranging study by Levine and coworkers3 enrolled 273 patients who had previously failed treatment with lidocaine, procainamide and bretylium. In this extremely high risk group, the initial infusion of intravenous amiodarone (500–2100 mg/24 hours) prevented SMVT recurrence in 40.3%. In the remainder, supplemental doses of amiodarone or addition of another agent often resulted in arrhythmia control. The most frequently encountered acute side effects were hypotension (15%) and bradycardia (5%). Despite this encouraging success, the 24 hour and 90 day allcause mortality in this cohort was 19 and 52%, respectively; the cause of death in just under 50% of patients was refractory VT/VF. In patients with frequently recurring or incessant well tolerated SMVT, particularly if acute attempts at antiarrhythmic drug therapy fails, catheter ablation in the acute setting can be helpful.6 In patients with refractory, poorly tolerated SMVT emergent subendocardial resection has been performed with some degree of success. The second component of the acute management of patients with SMVT involves assessment of the nature and extent of underlying structural heart disease (Table 1). The purpose of this determination is twofold. First, patients with SMVT in the absence of structural heart disease need to be promptly identi~ed as their prognosis, therapeutic options and response to therapy is much different than patients

Spontaneous sustained ventricular tachycardia in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial

Objectives. We compared the QRS waveforms of the initial and subsequent complexes of spontaneous sustained monomorphic ventricular tachycardia and the rhythm induced at electrophysiologic study to test the theory that premature ventricular complexes “trigger” spontaneous ventricular tachycardia and that a stable substrate exists such that the spontaneous arrhythmia can be reproduced at electrophysiologic study.Background. Failure rates have been high in several recent studies in which prevention of ventricular tachyarrhythmias was guided by suppression of premature ventricular complexes or induced ventricular tachycardias.Methods. Digital waveform analysis was used to distinguish events of ventricular tachycardia initiated by configurationally distinct, possibly triggering, complexes (type 1) from events in which the initial QRS waveforms were identical to subsequent complexes, suggesting no requirement for premature ventricular beats (type 2).Results. Of 1,102 episodes of spontaneous ventricular tachycardia, 73 (6.6%) were type 1; 1,012 were type 2 (91.8%); and 17 (1.5%) were uncertain. Of 59 patients only 14 (24%) had only type 1 episodes (group 1), whereas 37 patients (63%) had predominantly type 2 events (group 2) (p < 0.0001). Sustained ventricular tachycardia was inducible in all group 1 patients, and in most (57%) the induced rhythm was similar to the spontaneous rhythm. Ventricular tachycardia could not be induced in 7 patients from group 2 (19%), and in 18 patients (49%) the induced and spontaneous rhythms were dissimilar. Recurrence of arrhythmia rates differed according to the guidance method in group 2.Conclusions. Discrepancies between observed and predicted modes of initiation of ventricular tachycardia and between spontaneous and induced rhythms could result in inappropriate guidance and subsequent failure of antiarrhythmic treatment.

705-2 Catheter Ablation of the Mitral Isthmus for Ventricular Tachycardia Associated with Inferior Infarction

Catheter ablation (CA) of ischemic sustained monomorphic ventricular tachycardia (SMVT) remains problematic due to the presence of multiple potential functional circuits. We identified 3 pts with SMVT and a posterior akinetic/dyskinetic segment in whom anatomic constraints on the reentrant circuit facilitated CA. Each pt had 2-40 episodes of spontaneous SMVT in the previous month despite amiodarone. SMVT had either a LBBB (rS in V1, R in V6) right superior axis morphology (M), or a RBBB (R in V1, QS in V6) left superior axis M. Both M were reproducibly induced in each pt (cycle length [CL] 600-320 ms). In each pt, both M appeared to share a similar slow conduction zone in the inferobasal left ventricle adjacent to the mitral valve annulus. During SMVT of either M, these sites were characterized by diastolic potentials with electrogram-ORS intervals of 115-251 ms (24-58% of SMVT CL) and concealed entrainment during pacing associated with stimulus-ORS intervals of 105-411 ms (23-92% of SMVT CL). Application of radiofrequency energy (50 W for 90-120 s) at one of these sites in each pt (figure) resulted intermination of SMVT within 2-12 complexes. Following CA, neither M couldbe induced in any pt. In 1 pt, SMVT with a third nonclinical ORS M (CL 250 ms) remained inducible. All pts had implantable defibrillators with RR interval and/or electrogram storage. During 1-5 mo follow-up, no pt has had spontaneous SMVT or shocks. An isthmus of surviving myocardium adjacent to the mitral valve annulus may constitute a critical region of slow conduction in some pts with inferior MI and recurrent SMVT, providing a vulnerable and anatomically localized target for CA. Characteristic SMVT morphologies may identify candidates for this approach.

Efficacy and Adverse Effects of Moracizine for Ventricular Tachycardia

Moracizine (mean dose 792 ± 84mg, range 600 to 900 mg/day) was evaluated in 18 patients aged 62 ± 7 years for spontaneous nonsustained (n = 3) or sustained monomorphic (n = 12) ventricular tachycardia, cardiac arrest (n = 1) or syncope (n = 2). All patients had spontaneous or induced sustained monomorphic ventricular tachycardia. Diagnoses included coronary artery disease (n = 7) and dilated cardiomyopathy (n = 4), valvular heart disease (n = 2), myocarditis (n = 1), or a combination of these (n = 4). The mean left ventricular ejection fraction was 32 ± 9% (range 15 to 52%). Prior to moracizine, antiarrhythmic drug administration included a mean of 2 ± 1 trials with class IA (n = 17), IB or IA + IB (n = 6) or IC (n = 5) antiarrhythmic drugs, or amiodarone (n = 3). Prior antiarrhythmic drugs were discontinued for either the occurrence of noncardiac side effects or lack of efficacy. On moracizine, new sustained monomorphic ventricular tachycardia occurred in 3 patients with previous nonsustained ventricular tachycardia; spontaneous sustained monomorphic ventricular tachycardia recurred in 5 (and appeared to be worse in at least 2) patients with previous sustained monomorphic ventricular tachycardia; sustained monomorphic ventricular tachycardia was induced in all 11 patients undergoing repeat electrophysiology testing and was more difficult to terminate in 2 patients; 1 patient with an implantable defibrillator died suddenly after receiving multiple implantable defibrillator shocks while on moracizine despite recent electrophysiology testing demonstrating satisfactory defibrillation thresholds. Serious arrhythmic events occurred in 7 patients within 7 days of therapy with the drug. In this patient population with inducible or spontaneous sustained monomorphic ventricular tachycardia, moracizine was not effective and caused frequent, serious (usually early) pro-arrhythmic effects.

Prevention of Spontaneous Sustained Ventricular Tachycardia in the Postinfarction Dog by Left Stellate Ganglionectomy

Suppression of Sustained VT by Left Stellectomy. Holter monitoring and ventricular pacing were used to examine control, right stellate ganglionectomy, and left stellate ganglionectomy treatment groups, 6‐24 hours after left anterior descending coronary artery ligation in dogs. In nine of 27 controls (33%), spontaneous ventricular triplets (358 ± 8 beats/min) initiated sustained monomorphic ventricular tachycardia (386 ± 16 beats/min), followed by ventricular fibrillation at 12.6 ± 1.4 hours. Ventricular pacing produced sustained monomorphic ventricular tachycardia in 13 of 18 survivors (73%) at 24 hours. Left but not right stellectomy performed 15 minutes before coronary artery ligation reduced the incidence of spontaneous sustained monomorphic ventricular tachycardia (2 of 27, 7%, P = 0.06; 7 of 27, 26%, P = 0.50, respectively) and reduced the maximal ventricular triplet rate (332 ± 12, P &lt;0.05 and 358 ± 10 beats/min, respectively, P = NS vs control). Neither left nor right stellectomy altered the incidence of ventricular triplets during the 6‐24 hour period (153 ± 58 and 222 ± 55/hour, respectively, vs control, 177 ± 59/hour, P = NS) nor prevented pacing‐induced sustained monomorphic ventricular tachycardia in the survivors at 24 hours (20 of 24, 75%; and 16 of 20, 80%, P = NS). The data demonstrate that left but not right stellectomy reduces spontaneous sustained ventricular tachycardia and ventricular fibrillation during the 6‐24 hour period following coronary artery ligation in the dog. Left stellectomy reduces the triggers for sustained monomorphic ventricular tachycardia (rapid ventricular triplets) without altering the underlying reentrant substrate for sustained ventricular tachycardia.

Long-term intracoronary ethanol administration electrophysiologic and morphologic effects

The long-term intracoronary infusion of ethanol was used to evaluate the potential of ethanol to produce myocardial injury and cardiac rhythm disturbances. In 22 dogs, electrophysiologic testing was performed 48 hr after the cessation of alcohol administration. Multiple premature ventricular beats occurred spontaneously in 3 dogs with spontaneous sustained monomorphic ventricular tachycardia observed in 1 dog. Provocative ventricular pacing produced ventricular tachycardia lasting 20 or more beats in 13 animals with sustained tachycardia observed in 3 animals. Provocative ventricular pacing in the presence of lidocaine or epinephrine produced sustained ventricular tachycardia in an additional 4 dogs. The electrophysiologic properties of Purkinje fibers from the zone receiving ethanol were altered when compared to the control zone. The resting membrane potential was decreased (−76±2 mV vs. −85±1 mV, p<0.001) with a decrease in action potential amplitude (91±4 vs. 109±2 mV, p<0.001) and phase 0 upstroke (231±27 vs. 456±25 V/sec, p<0.02). Prolonged refractoriness was observed in the ethanol zone without a prolongation of action potential duration. Intramural lesions observed within the left circumflex distribution varied from focal acute myofibrillar degeneration and necrosis to severe local scarring. The data suggest that intracoronary ethanol administration at human abuse levels of blood alcohol concentrations produces histologic and electrophysiologic injury in the canine heart. The electrophysiologic changes provide a substrate sufficient for the induction and maintenance of ventricular arrhythmia.

Mechanism of prevention of sudden death by nadolol: Differential actions on arrhythmia triggers and substrate after myocardial infarction in the dog

Electrocardiographic monitoring and provocative ventricular pacing were used to evaluate control and nadolol treatment groups 6 to 24 hours after left anterior descending coronary artery ligation in the dog. During the 6 to 24 hour period, the control group (n = 20) developed ventricular triplets at rates exceeding 270/min. Seven dogs spontaneously developed sustained monomorphic ventricular tachycardia (421 +/- 12 beats/min) at 13 +/- 2 hours. Sustained monomorphic ventricular tachycardia was present for 38 +/- 8 seconds before ventricular fibrillation developed. One dog developed recurrent monomorphic ventricular tachycardia, with six episodes lasting from 8 to 72 seconds (375 to 425 beats/min). At 24 hours, ventricular pacing produced sustained monomorphic ventricular tachycardia (378 +/- 12 beats/min) in 9 of 13 surviving animals. Nadolol administration 6 hours after coronary artery ligation (n = 19) lowered both the rate (241 +/- 8 versus 328 +/- 8 beats/min; p = 0.001) and the incidence (8 +/- 6 versus 198 +/- 61 per hour; p = 0.004) of rapid ventricular triplets and prevented sudden arrhythmic death (0%; p = 0.005). Nadolol failed to prevent sustained monomorphic ventricular tachycardia (88%; 365 +/- 12 beats/min) produced by ventricular pacing. The data suggest that nadolol prevents spontaneous sustained monomorphic ventricular tachycardia by selectively suppressing the arrhythmia trigger (rapid ventricular triplets) without altering the underlying arrhythmia substrate.