Observations on the Initiation of Sustained Ventricular Tachycardia by Programmed Stimulation

We analyzed the initiation of sustained monomorphic ventricular tachycardia (VT) by programmed ventricular stimulation (PVS) in 50 consecutive patients who had clinical VT or aborted sudden cardiac death with remote myocardial infarction. In 25 of 50 patients, the first induced QRS complex of VT was morphologically identical to the succeeding QRS complexes of VT (type I). In 25 other patients, the first VT beat had a different morphology (type II). Type I had a significantly longer VT cycle length than type II (333 +/- 65 msec and 293 +/- 66 msec, P = 0.036). Type II VT initiation required more aggressive stimulation protocol than type I (type I: type II; number of extrastimulus required for induction 2.5 +/- 0.9 : 3.0 +/- 0.6, P = 0.026; shortest extrastimuli coupling interval 244 +/- 28 msec : 220 +/- 23 msec, P = 0.002). The interval between the last extrastimulus and the onset of the first VT beat was 408 +/- 88 msec in type I and 336 +/- 75 msec in type II (P = 0.004). Furthermore, there was good correlation between the VT cycle length and the interval from last extrastimulus to the onset of nonpaced beat in type I but not in type II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term reproducibility of ventricular tachycardia induction with electrophysiological testing in patients with coronary heart disease and depressed left ventricular ejection fraction

The Multicenter Automatic Defibrillator Implantation Trial (MADIT) has recently confirmed the role of programmed ventricular stimulation (PVS) to identify the high risk patients of sudden death after myocardial infarction and to prevent this risk. The purpose of this study was to evaluate the long-term reproducibility of PVS in these patients. Thirty patients with coronary heart disease without spontaneous documented sustained ventricular tachycardia (VT) underwent two programmed stimulations in the absence of antiarrhythmic drug treatment between 2 and 6 years (mean 4 years). No patient had a myocardial infarction or intervening cardiac surgery during this period. The protocol of study was similar using up to three extrastimuli in two sites of the right ventricle, delivered in sinus rhythm and driven rhythm (600 ms, 400 ms, respectively). On the first PVS, 17 patients had inducible sustained VT (group I). Thirteen patients did not have inducible VT (group II). On the second PVS all group I patients but one had inducible VT, but the cycle length was significantly modified in 11. In group II, five patients had inducible VT and in the other patients the PVS remained negative. In conclusion, in patients with coronary heart disease, but without documented VT, the long-term reproducibility of PVS was excellent in those with inducible VT (94%); the patients remain at risk of VT and a prophylactic implantable cardioverter defibrillator could be considered. In patients with initially negative study, reproducibility of PVS was lower (61.5%), probably because of the progressive remodeling after myocardial infarction. Therefore, the occurrence of new symptoms in patients with previously negative study requires a second programmed ventricular stimulation.     

Effects of Coronary Artery Bypass Grafting on Ventricular Arrhythmias: Results with Electrophysiological Testing and Long-Term Follow-Up

Myocardial revascularization was performed in 56 patients with coronary artery disease who presented with ventricular tachycardia (VT) (n = 39) or ventricular fibrillation (n = 17). There were 46 men and 10 women, aged 65 ± 10 years. Three vessel (n = 42) or left main disease (n = 4) was present in 82%. Left ventricular ejection fraction averaged 36%± 11%. Electrophysioiogical studies were performed preoperatively in all patients; 50 (89%) had inducible ventricular arrhythmias. Sustained monomorphic VT was induced in 40 patients (cycle length 284 ± 61 msec). Reproducible symptomatic nonsustained VT was induced in four patients and ventricular fibrillation in six patients, while six patients had no inducible arrhythmia. Preoperatively the patients with inducible VT failed 3.3 ± 1.2 drug trials during electrophysiological studies. In addition to coronary bypass, 22 patients also received an automatic implantable cardioverter defibrillator (ICD), 26 patients received prophylactic ICD patches, and 1 patient had resection of a false aneurysm. There were no perioperative deaths. Postoperative electrophysiological studies were performed in all 56 surgical survivors. Ventricular tachyarrhythmia could not be induced in the six patients who had no inducible VT preoperatively and in 13 of 40 (33%) with preoperatively inducible sustained VT or in 19 of 50 (38%) patients with any previously inducible ventricular arrhythmia, thus a totaJ of 25 patients (45%) had no inducible VT postoperatively. Of the remaining, 11 patients were treated with antiarrhythmic drugs alone, 11 had already received an ICD (combined with drugs in 7), and another 9 received the ICD postoperatively (combined with drugs in 4). At a mean foJJow-up of 28 ± 21 months there were 11 deaths (20%): 2 sudden, 5 nonsudden cardiac, and 4 noncardiac deaths. There were 16 nonfatal VT recurrences (29%): 14 among patients with persistently inducible arrhythmias, and onJy 2 among those with no inducible arrhythmia postoperatively (P = 0.004); 13 occurred in patients with an ICD (P = 0.01). Thus among these patients with malignant ventricular arrhythmias who underwent revascuJarization, 45% had no inducible arrhythmia postoperatively with 33% of those with preoperatively inducible sustained VT apparently rendered noninducible by revascularization, while the majority (70%) remained free of major arrhythmic events during long-term follow-up. We conclude that myocardial revascularization alone can result in no ventricular arrhythmia induction in selected patients with VT inducible prior to surgery. Long-term follow-up of such patients indicates a low sudden death and arrhythmia recurrence rate. Furthermore, in patients with persistently inducible ventricular tachyarrhythmias after coronary revascuJarization, the sudden death rate is low despite a high frequency of nonfatal arrhythmia recurrence when antiarrhythmic medications are guided by programmed stimulation or an ICD is used.     

Retrospective Analysis of Patients Undergoing One- or Two-Stage Strategies for Myocardial Revascularization and Implantable Cardioverter Defibrillator Implantation

Internal defibrillation leads were placed at time of coronary revascularization in 79 patients. In 34, an implantable cardioverter defibrillator (ICD) was placed simultaneously (group I). A two-stage strategy (selective implantation of the ICD in patients with postoperative spontaneous or inducible ventricular tachycardia [VT]) was followed in 45 patients (group II). Group I patients had failed more antiarrhythmic drug trials (2.9 +/- 1.6 vs 1.5 +/- 1.6; P = 0.02), including amiodarone (62% vs 20%; P less than 0.001). There were four operative deaths in each group. Postoperatively, VT was present in 27 group II patients (60%), 25 of whom received an ICD (two refused device implantation). Patients with postoperative VT had a lower left ventricular ejection fraction than those without VT (33 +/- 9 vs 47 +/- 16; P = 0.01). Actuarial survival at 1, 2, and 3 years was 88 +/- 6, 88 +/- 7, and 88 +/- 10 in group I; and 83 +/- 6, 76 +/- 7, and 76 +/- 11 in group II (NS). No patient without an ICD (based on the postoperative electrophysiological study [EPS]) died suddenly. Five patients (6%) had ICD system infection. Sudden death was largely prevented by either strategy, but relatively high rates of operative mortality and ICD system infection were observed. Prospective studies should identify patients more likely to benefit from one or another strategy.     

Ventricular Arrhythmia Inducibility Predicts Subsequent ICD Activation in Nonischemic Cardiomyopathy Patients: A DEFINITE Substudy

Objectives: We evaluated whether electrophysiologic (EP) inducibility predicts the subsequent occurrence of spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) in the Defibrillators in Nonischemic Cardiomyopathy Treatment Evaluation (DEFINITE) trial.
Background: Inducibility of ventricular arrhythmias has been widely used as a risk marker to select implantable cardioverter defibrillator (ICD) candidates, but is believed not to be predictive in nonischemic cardiomyopathy patients.
Methods: In DEFINITE, patients randomized to the ICD arm, but not the conventional arm, underwent noninvasive EP testing via the ICD shortly after ICD implantation using up to three extrastimuli at three cycle lengths plus burst pacing. Inducibility was defined as monomorphic or polymorphic VT or VF lasting 15 seconds. Patients were followed for a median of 29 ± 14 months (interquartile range = 2–41). An independent committee, blinded to inducibility status, characterized the rhythm triggering ICD shocks.
Results: Inducibility, found in 29 of 204 patients (VT in 13, VF in 16), was associated with diabetes (41.4% vs 20.6%, P = 0.014) and a slightly higher ejection fraction (23.2 ± 5.9 vs 20.5 ± 5.7, P = 0.021). In follow-up, 34.5% of the inducible group (10 of 29) experienced ICD therapy for VT or VF or arrhythmic death versus 12.0% (21 of 175) noninducible patients (hazard ratio = 2.60, P = 0.014).
Conclusions: In DEFINITE patients, inducibility of either VT or VF was associated with an increased likelihood of subsequent ICD therapy for VT or VF, and should be one factor considered in risk stratifying nonischemic cardiomyopathy patients.     

Late Ventricular Potentials and Spontaneous and Induced Ventricular Arrhythmias in Dilated or Hypertrophic Cardiomyopathies. A Prospective Study About 83 Patients

In a series of 83 patients with dilated (DCM) (n = 56) or hypertrophic cardiomyopathies (HCM) (n = 27), were performed 24-hour-Holter monitorings, exercise stress testings, noninvasive recordings of late ventricular potentials (LVP), and programmed ventricular stimulations (PVS) (sinus rhythm and three cycles of stimulation, two extrastimuli, two right ventricle sites) (n = 53). in order to appreciate the frequency of ventricular premature depolarisations (VPDs), to correlate these results with myocardial vulnerability to TV induction, and to compare electrophysiologic and hemodynamic results. Holter monitoring showed that 80% of group A patients had VPDs (75% Lown's grade 3 or over) and 63% in group B (37%≥ grade 3). LVP were found in 15/56 DCM, and 2/27 HCM; in comparison with a control group of 32 normal subjects, the prevalence of LVP was only significant for DCM group. LVP were more frequent in cases of VPD's ≥ Lown's grade 3 at Holter monitoring in DCM group, (33% versus 7% if VPDs ≤ Lown's grade 3) and HCM group (20% versus 0) but the correlation was not significant. Exercise stress testing, conducted only in group E, revealed about 20% of VPDs. PVS provoked ventricular arrhythmia (>5 QRS) in 13 out of 33 cases in group A and in 2 out of 20 cases in group B. There was no significant correlation between the results of these methods of study and those of hemodynamic or echocardiographic explorations except for cardiac index in group A flower when LVP were present, and VPDs ≥ grade 3 during Holter) and end diastolic diameter (larger when PVS provoked fewer ventricular arrhythmias). In group B, PVS induced monomorphic VT in 2/3 patients with syncopes. Thus: (1) ventricular arrhythmias are frequent in cardiomyopathies but LVP had a significant prevalence only in dilated forms; (2) in DCM monomorphic induced VT reproduce spontaneous crisis, whereas in HCM it is possible to provoke VT in patients with syncopes but without this clinical arrhythmia; (3) in DCM as in HCM, ventricular arrhythmia can be independent from hemodynamic disorders.     

Abnormal heart rate turbulence predicts the initiation of ventricular arrhythmias

BACKGROUND: Abnormal heart rate turbulence (HRT) reflects autonomic derangements predicting all-cause mortality, yet has not been shown to predict ventricular arrhythmias in at-risk patients. We hypothesized that HRT at programmed ventricular stimulation (PVS) would predict arrhythmia initiation in patients with left ventricular dysfunction. METHODS: We studied 27 patients with coronary disease, left ventricular ejection fraction (LVEF) 26.7 +/- 9.1%, and plasma B-type natriuretic peptide (BNP) 461 +/- 561 pg/mL. Prior to arrhythmia induction at PVS, we measured sinus cycles after spontaneous or paced premature ventricular contractions (PVCs) for turbulence onset (TO; % cycle length change following PVC) and slope (TS; greatest slope of return to baseline cycle). T-wave alternans (TWA) was also measured during atrial pacing. RESULTS: At PVS, abnormal TO (> or =0%) predicted inducible ventricular tachycardia (VT; n = 10 patients; P < 0.05). TO was greater in inducible than in noninducible patients (2.3 +/- 3.1% vs -0.02 +/- 2.8%, P < 0.05) and correlated with LVEF (P < 0.05) but not with BNP. TS did not differ between groups. Conversely, ambulatory HRT differed significantly from HRT at PVS (TO -0.55 +/- 1.08% vs 0.85 +/- 3.02%, P < 0.05; TS 2.63 +/- 2.09 ms/RR vs 8.70 +/- 6.56 ms/RR, P < 0.01), and did not predict inducible VT but trended (P = 0.05) to predict sustained VT on 739 +/- 179 days follow-up. TWA predicted inducible (P < 0.05) and spontaneous (P = 0.0001) VT but did not co-migrate with HRT. CONCLUSIONS: Abnormal HRT measured at PVS predicted the induction of sustained ventricular arrhythmias in patients with ischemic cardiomyopathy. However, HRT at PVS did not correlate with ambulatory HRT, nor with TWA, both of which predicted spontaneous ventricular arrhythmias. Thus, HRT may reflect the influence of autonomic milieu on arrhythmic susceptibility and is likely complementary to traditional arrhythmic indices.     

Is the Fascicle of Left Bundle Branch Involved in the Reentrant Circuit of Verapamil‐Sensitive Idiopathic Left Ventricular Tachycardia?

The exact reentrant circuit of the verapamil-sensitive idiopathic left VT with a RBBB configuration remains unclear. Furthermore, if the fascicle of left bundle branch is involved in the reentrant circuit has not been well studied. Forty-nine patients with verapamil-sensitive idiopathic left VT underwent electrophysiological study and RF catheter ablation. Group I included 11 patients (10 men, 1 woman; mean age 25 +/- 8 years) with left anterior fascicular block (4 patients), or left posterior fascicular block (7 patients) during sinus rhythm. Group II included 38 patients (29 men, 9 women; mean age 35 +/- 16 years) without fascicular block during sinus rhythm. Duration of QRS complex during sinus rhythm before RF catheter ablation in group I patients was significant longer than that of group II patients (104 +/- 12 vs 95 +/- 11 ms, respectively, P=0.02). Duration of QRS complex during VT was similar between group I and group II patients (141 +/- 13 vs 140 +/- 14 ms, respectively, P=0.78). Transitional zones of QRS complexes in the precordial leads during VT were similar between group I and group II patients. After ablation, the QRS duration did not prolong in group I or group II patients (104 +/- 11 vs 95 +/- 10 ms, P=0.02); fascicular block did not occur in group II patients. Duration and transitional zone of QRS complex during VT were similar between the two groups, and new fascicular block did not occur after ablation. These findings suggest the fascicle of left bundle branch may be not involved in the antegrade limb of reentry circuit in idiopathic left VT.     

Ventricular Tachycardia Surgery in 1992: Did the Automatic Defibrillator Change This Approach?

The role of ventricular tachycardia (VT) surgery has been changed since the automatic implantable cardioverter defibrillator (ICD) is available. We studied the follow-up of 131 patients who underwent mapping guided surgery due to recurrent VT refractory to antiarrhythmic drug treatment. There were 65 patients operated upon between 1980–1985 (group I) and 66 patients between 1986–1991 (group II). Ten patients (8%) died perioperatively (< 3 weeks after surgery) [7/65 patients, 11%, in group I and 3/66 patients, 5%, in group II (P = 0.15)]. During a mean follow-up of 41 ± 24 months, 38 of 121 patients died (31%), significantly more patients in group I (24/58 patients, 41%) than in group II (14/63 patients, 22%) (P < 0.05). In group I, there was a higher incidence of sudden (7/58 patients, 12%) or cardiac death (15/58 patients, 26%) than in group II (sudden death 4/63 patients, 6%, cardiac death 7/63 patients, 11%) (P < 0.05). There was a similar incidence of VT recurrences between group I(9/65 patients, 14%) and group II (9/66 patients, 14%). Our data show that the indication for VT surgery has changed since the ICD is available because of better patient selection.     

Long-Term Outcome Following Programmed Electrical Stimulation in Patients with High-Grade Ventricular Ectopy

To determine if programmed electrical stimulation (PES) could be utilized to identify patients with high-grade ventricular ectopy at low- or high-risk for sudden cardiac death, we performed PES in 40 patients with high-grade ventricular ectopy refractory to conventional antiarrhythmic agents. Twenty-one patients had a previous myocardial infarction, five had cardiomyopathy, six had hypertension, three had valvular heart disease and five had no known structural heart disease. The mean age was 50 years (range, 18 to 76). During programmed ventricular stimulation, eight patients had inducible sustained (more than 30 seconds) monomorphic ventricular tachycardia (Group I) but in 32 patients sustained ventricular tachycardia was not inducible (Group II). None of the five patients without structural heart disease were inducible while seven out of 21 (33%) patients with previous myocardial infarction had inducible ventricular tachycardia (VT). Antiarrhythmic therapy was instituted in patients with inducible VT; patients without inducible VT did not receive antiarrhythmic agents. In Group I, seven of the eight patients are alive (mean follow-up, 16 months) and in Group II, 28 of the 32 patients are alive (mean follow-up, 17 months). None of the five deaths were sudden. We conclude that in the absence of antiarrhythmic therapy, the incidence of sudden cardiac death is very low in patients with high-grade ventricular ectopy who do not have inducible monomorphic ventricular tachycardia during programmed ventricular stimulation.     

Dispersion in ventricular repolarization in patients with severe intraventricular conduction disturbances

Increased dispersion of repolarization, measured invasively or by QT interval measurements, is associated with an increased risk for ventricular arrhythmias and sudden death. Most studies on this issue have included patients with normal intraventricular conduction, and it is not known if this finding has a predictive value also in patients with intraventricular conduction disorders. An invasive electrophysiological study, including programmed ventricular stimulation and assessment of effective refractory periods at two RV sites, was performed in 103 patients with bifascicular block (mean age 67 +/- 12 years). QT dispersion was measured from standard 12-lead ECGs. In patients with inducible sustained polymorphic VT or VF the dispersion in refractoriness between the two RV sites was significantly greater (46 +/- 11 ms, n = 13) than in noninducible patients (14 +/- 14 ms, n = 84) and in patients with inducible sustained monomorphic VT (16 +/- 5 ms, n = 6) (P < 0.01). Similarly, QT dispersion was 104 +/- 46 ms, 66 +/- 31 ms, and 77 +/- 33 ms, respectively, in the three groups (P < 0.05). Dispersion in repolarization, neither measured invasively nor by QT interval measurements, predicted sudden death, all cause mortality, or ventricular arrhythmia during a mean follow-up period of 3 years. In patients with bifascicular block, there is a relation between the degree of dispersion of ventricular repolarization and the inducibility of polymorphic ventricular arrhythmia, but this outcome did not occur during follow-up.     

Incidence and initial characteristics of pilsicainide-induced ventricular arrhythmias in patients with Brugada syndrome

BACKGROUND: In patients with Brugada syndrome, class I antiarrhythmic drugs can trigger ventricular arrhythmias (VA). The incidence and initial characteristics of VA that developed after pilsicainide was examined in 28 patients with Brugada-type electrocardiographic (ECG) abnormalities and with a positive response in the pilsicainide test. The clinical outcome was also compared between patients with and without pilsicainide-induced VA. METHODS AND RESULTS: In all patients, pilsicainide increased ST segment elevation and accentuated type 1 ECG changes. Ventricular tachycardia (VT) developed in 3 patients and premature ventricular complexes (PVC) in 2 other patients. These 5 patients (group I) had higher ST segment elevation in lead V2 on the ECG at baseline and after pilsicainide and showed a longer QTc interval after pilsicainide than the other 23 patients (group II). However, there was no difference between the 2 groups regarding incidence of prior cardiac events, results of signal-averaged ECG, HV interval, inducibility of ventricular fibrillation by programmed electrical stimulation, or QRS duration. In 1 patient, PVC originated from 3 sites, 2 of which triggered polymorphic VT. The right ventricular (RV) outflow tract was the origin of 2 types of PVC, and other RV sites of 5 other types. During a 45 +/- 37 months follow-up, polymorphic VT recurred in 2 patients in group II. CONCLUSIONS: Pilsicainide induced VA in some patients with Brugada syndrome, but this result may not be used as a parameter of the risk stratification of Brugada syndrome. Multiple PVC induced by pilsicainide and triggering polymorphic VT originated from several RV sites is an important factor when considering patients for treatment with catheter ablation.     

Device Use Patterns and Clinical Outcome of Implantable Cardioverter Defibrillator Patients with Moderate and Severe Impairment of Left Ventricular Function

The beneficial effects of implanted cardioverter defibrillator (ICD) therapy in patients with malignant ventricular tachyarrhythmias and variable degrees of left ventricular (LV) dysfunction are debated. ICD use and patient survival were examined in 128 patients with malignant ventricular arrhythmias and moderate or severe LV dys function. Group I included 64 patients with moderate LV dysfunction (LV ejection fraction of > 30%) and group H, 64 patients with severe LV dysfunction (LV ejection fracfion of ≤ 30%). Follow-up period ranged from 1 to 78 months. The two groups were similar in age, incidence of coronary artery disease and presenting arrhythmia. The mean LV ejection fraction in group I was 44%± 8% and group II was 22%± 5% (P < 0.0001). At 4 years of follow-up, 66% of patients from group I and 62% from group II (P = NS) had ICD activation for presumed ventricular tachyarrhythmia. Survival was calculated using actuarial analysis. Arrhythmic or sudden death mortality at 4 years of follow-up was 4% in group I and 7% in group II (P = NS). Cardiac mortality was for group I, 7% (P < 0.05), 12% (fP < 0,01), 15% (P < 0.01), and 15% (P < 0.01) for follow-up years 1, 2, 3, and 4, respectively. For group II, cardiac mortality was 27%, 36%, 41%, and 41% for follow-up years for 1, 2, 3, and 4, respectively. The majority of cardiac deaths in both groups was observed in the first 2 years of follow-up. However, in both groups, cardiac mortality was comparable in patients who did (users) and did not (nonusers) experience appropriate ICD shocks. Thus, the incidence of long-term ICD use is comparable in patients with moderate and severe LV dysfunction. Cardiac mortality is higher in patients with severe LV dysfunction in the first 4 years of follow-up irrespective of device use. The comparable long-term clinical outcome of ICD users and non users in patients with moderate or severe LV dysfunction can be related to elimination of arrhythmic mortality. Long-term patient survival in ICD recipients with severe LV dysfunction remains substantial even at 4 years of follow-up.     

Initiating Sequences in Exercise Induced Idiopathic Ventricular Tachycardia of Left Bundle Branch-Like Morphology

Initiating Sequences in Exercise Induced Idiopathic Ventricular Tachycardia of Left Bundle Branch-Like Morphology. Initiating sequences for VT may infer the underlying arrhythmogenic mechanisms. This study examines the initiating sequences of exercise induced idiopathic VT of left bundle branch block-like (LBBB-like) morphology and makes an attempt to relate these to clinical aspects and the mechanisms of arrhythmia. Thirty-two patients (mean age 33.4 ± 13.2 years; 18 men) with exercise induced VT in the absence of structural cardiac abnormality on history, clinical examination, and noninvasive and invasive investigations were divided into two groups on the basis of the initiating sequence of VT on exercise. Group I consisted of patients with long-short sequence of RR intervals prior to the onset of VT (initiating/preinitiating cycle length ratio < 0.78). Group II consisted of patients without changes in cycle length prior to VT. Group I mechanism would suggest delayed afterdepolarizations (DADs) or reentry whereas group II mechanism triggered activity due to early afterdepolarizations. Fourteen patients (group I) had long-short sequence and 18 patients (group II) were without cycle length changes prior to VT initiated during exercise. VT axis was inferior in all 18 patients in group II but only in 9 patients in group I (P = 0.02). In these predefined patient groups, sustained monomorphic VT could not be initiated by programmed stimulation in any patient in group I, whereas four patients in group II had inducible VT. Patients in group II also had higher incidence of sustained VT on ambulatory monitoring (P < 0.05). The two groups did not differ in other respects. This study demonstrates the existence of at least two possible mechanisms of initiation of exercise induced idiopathic VT of LBBB-like morphology. VT initiated without cycle length changes is more common, more likely to have an inferior axis suggesting an outflow tract origin, and is probably related to triggered activity secondary to DADs. VT initiated with a long-short sequence is more often nonsustained and may have a superior axis suggesting an origin from the body or septal region of the ventricle. The two groups, therefore, exhibit differences in electrophysiological characteristics that may aid classification and therapy of this arrhythmia.     

Safety and efficacy of a dual chamber implantable cardioverter defibrillator capable of slow ventricular tachycardia discrimination: a randomized study

New developments in dual chamber implantable cardioverter defibrillators (ICD) have increased the specificity of therapy delivery. This study was performed to examine the performance of an algorithm, focusing on its ability to distinguish slow ventricular tachycardia (VT) from sinus rhythm or supraventricular tachyarrhythmias. The patient population included 77 men and 13 women, 63 +/- 11 years old, treated with ICDs after episodes of spontaneous or inducible ventricular tachyarrhythmias. They were randomized to programming of the ICD to a lower limit of VT detection at 128 beats/min (group I, n = 44), versus 153 beats/min II (group II, n = 46). The primary endpoint of the study consisted of comparing the specificity and sensitivity of the algorithm between the two groups of patients. Over a 10.1 +/- 3.5 months follow-up, 325 episodes were detected in the Tachy zone in group I, versus 106 in group II. The sensitivity and specificity of the algorithm in group I were 98.8% and 94.4%, respectively, versus 100% and 89% in group II (NS). A single episode of VT at a rate of 132 beats/min was diagnosed as SVT in group I. The sensitivity and specificity of the algorithm for tachycardias <153 beats/min were 97.4% and 94.5%, respectively. Overall VT therapy efficacy was 100% in both groups. The performance of this algorithm in the slow VT zone supports the programming of a long Tachy detection interval to document slow events, and allows to treat slow VT, if necessary, without significant risk of inappropriate interventions for sinus tachycardia.     

Catheter Ablation of Electrical Storm Due to Monomorphic Ventricular Tachycardia in Patients with Nonischemic Cardiomyopathy: Acute Results and Its Effect on Long‐Term Survival

Background: Electrical storm due to recurrent ventricular tachycardia (VT) in patients with implantable cardioverter defibrillator (ICD) can adversely affect their long‐term survival. This study evaluates the efficiency of the radiofrequency catheter ablation of electrical storm due to monomorphic VT in patients with idiopathic dilated cardiomyopathy (DCM) and assesses its long‐term effects on survival. Methods and Results: Between April 2004 and October 2008, 13 consecutive patients (nine men, mean age 56.8 ± 17.8 years) with DCM and electrical storm due to monomorphic VT who had ICD underwent 17 catheter ablation procedures, including four epicardial, at our center. Acute complete success was defined as the lack of inducibility of any VT at the end of procedure during programmed right ventricular stimulation and was achieved in eight patients (61.5%). During a median follow‐up of 23 months (range 3–63 months) nine patients (69%) were alive and eight patients (61.5%) were free from VT recurrence. Among those with acute complete (n = 8) and partial (n = 5) success, seven patients (87.5%) and one patient (20%) were free from any VT recurrence and ICD therapy, respectively (P = 0.025). Among those with acute complete and partial success, seven patients (87.5%) and two patients (40%) were alive, respectively (Mantel‐Cox test P = 0.082). Among those who had an initially failed endocardial ablation (n = 8), four underwent further epicardial ablation that was completely successful in three patients (75%). Conclusion: Catheter ablation in patients with DCM and electrical storm due to monomorphic VT who had an ICD prevents further VT recurrence in 61.5% of the patients. Complete successful catheter ablation may play a protective role and was associated with reduced mortality during the follow‐up period. More aggressive ablation strategies in patients with initially failed endocardial ablation might improve the long‐term survival of these patients; however, further studies are needed to clarify this issue. (PACE 2010; 33:1504–1509)     

Nontransmural Scar Detected by Magnetic Resonance Imaging and Origin of Ventricular Tachycardia in Structural Heart Disease

Background: Contrast-enhanced magnetic resonance imaging (CMR) identifies scar tissue as an area of delayed enhancement (DE). The scar region might be the substrate for ventricular tachycardia (VT). However, the relationship between the occurrence of VT and the characteristics of scar tissue has not been fully studied.
Methods: CMR was performed in 34 patients with monomorphic, sustained VT and dilated cardiomyopathy (DCM, n = 18), ischemic cardiomyopathy (ICM, n = 10), or idiopathic VT (IVT, n = 6). The VT exit site was assessed by a detailed analysis of the QRS morphology, including bundle branch block type, limb lead polarity, and precordial R-wave transition. On CMR imaging, the transmural score of each of the 17 segments was assigned, using a computer-assisted, semiautomatic technique, to measure the DE areas. Segmental scars were classified as nontransmural when DE was 1–75% and transmural when DE was 76–100% of the left ventricular mass in each segment.
Results: A scar was detected in all patients with DCM or ICM. Nontransmural scar tissue was often found at the VT exit site, in patients with DCM or ICM. In contrast, no scar was found in patients with IVT.
Conclusions: CMR clarified the characteristics and distribution of scar tissue in patients with structural heart disease, and the presence and location of scar tissue might predict the VT exit site in these patients.     

Efficacy of Antitachycardia Pacing in Patients Presenting with Cardiac Arrest

The efficacy of antitachycardia pacing (ATP) incorporated into implantable cardioverter defibrillators (ICDs) was assessed in 29 consecutive survivors of cardiac arrest, not attributable to acute myocardial infarction, ischemia, or drug and electrolyte effects. The cohort included 25 men and 4 women with a mean age of 65 years and a mean left ventricular ejection fraction of 29%. Seventeen patients had coronary artery disease, 11 had nonischemic dilated cardiomyopathy, and 1 had long QT syndrome. Programmed stimulation yielded monomorphic ventricular tachycardia (VT) in 17 patients, polymorphic VT in 6, and no inducible VT in 6. During a mean follow-up of 22 months, a total of 91 episodes of monomorphic VT occurred, 73 of which were successfully pace terminated (83%). Monomorphic VT amenable to pace termination recurred only in the group that had this arrhythmia inducible. The recurrent arrhythmias in the 12 patients having either no inducible VT or polymorphic VT were all rapid VTs, having a cycle length < 220 ms; and therefore, not amenable to pace termination. These results suggest that ATP incorporated into ICDs is useful in survivors of cardiac arrest and may significantly reduce the number of shocks that these patients would otherwise receive. Programmed stimulation may also help to define those patients who would receive the maximum benefit from ATP.     

The utility of quantitative body surface isoarea mapping for predicting ventricular tachyarrhythmias

Noninvasive techniques, such as the signal averaged ECG, have been used to assess risk of ventricular tachyarrhythmias (VT). However, these methods produce false positive and negative results. The purpose of this study was to develop body surface map algorithms which would enhance prediction of susceptibility to VT. Fifty-three patients referred for programmed electrical stimulation were enrolled in this study. All patients underwent signal averaged ECG, body surface map, programmed electrical stimulation. Group I patients had no sustained inducible VT and group II patients had either inducible sustained VT at electrophysiology study or previously documented spontaneous, sustained VT. For body surface map analysis, the difference between extrema on isoarea maps was calculated and defined as the gradient range. An abnormal body surface map was defined as a QRST gradient range ≤ 109 mv.ms. The mean QRST gradient range in group II was significantly < that in group I (P < 0.05). By logistic regression analysis, the presence of coronary artery disease, a QRST gradient range ≤ 109 mv.ms, an EF < 40% and a singal averaged ECG QRS duration > 114 ms predicted VT. The sensitivity, specificity, positive and negative predictive values for predicting VT susceptibility of an algorithm which combines the signal averaged ECG QRS duration and the QRST gradients were 0.93, 0.76, 0.79, and 0.91, respectively, while those for the signal averaged ECG alone were 0.52, 0.69, 0.63, and 0.59 for VT susceptibility. A combined body surface map-signal averaged ECG algorithm was more sensitive in detecting susceptibility to VT than the signal averaged ECG alone.     

Ventriculoatrial Conduction Capability and Prevalence of 1:1 Retrograde Conduction During Inducible Sustained Monomorphic Ventricular Tacbycardia in 305 Implantable Cardioverter Defibrillator Recipients

Retrograde Conduction During Inducible Sustained Monomorphic Ventricular Tachycardia in 305 Implantable Cardioverter Defibrillator Recipients. Despite the advent of dual chamber ICDs, differentiation of VT (SMVT) with 1:1 VA conduction will remain a challenge. In this study, VA conduction capability and prevalence of inducible sustained monomorphic (SM) VT with 1:1 VA conduction was assessed in 305 ICD recipients. SMVT with a mean cycle length (CL) of 304 ± 61 ms was induced in 161 (53%) patients. Twenty-six percent of the patients maintained 1:1 VA conduction to CL ≤ 400 ms during incremental ventricular pacing, regardless of presenting tachyarrhythmia or presence of inducible SMVT. Among ten patients who had inducible SMVT with possible 1:1 VA conduction (based on SMVT CL comparable to the shortest CL associated with 1:1 retrograde conduction during ventricular pacing), all seven with available intracardiac tracings had documented 1 :1 VA conduction during the induced SMVT—representing 4.4% of the patients with inducible SMVT (95% CI 1.2%-7.6%), and 2.3% of the entire ICD cohort (95% CI 0.6%-4.0%). We conclude that about one-fifth of ICD recipients possess 1:1 VA conduction to CL ≤ 400 ms and that inducible SMVT with 1:1 VA conduction can be demonstrated in a small hut nonnegligible proportion of ICD recipients. These data are relevant to the design of tachyarrhythmia-discrimination algorithms for dual chamber ICDs.