Monomorphic Ventricular Tachycardia In Patients Research Articles

The year in cardiovascular medicine 2022: the top 10 papers in arrhythmias.

(A) Comprehensive clinical, electrocardiographic, and genetic overview of the various diseases associated with VA or SCD as reported in the 2022 ESC Guidelines for VA and SCD.1 The VA/SCD Guidelines provide many updated recommendations for the management of patients with congenital heart disease, idiopathic VF, acquired Long QT, Brugada and early repolarization syndrome, as well as catecholaminergic polymorphic VT, and short QT syndrome. (B) From the same Guidelines, an algorithm for the management of sustained monomorphic ventricular tachycardia in patients with chronic coronary artery disease.1 The algorithm also holdsin partfor non-ischaemic pathologies. Note, the new VA/SCD Guidelines promote VT ablation significantly. It may e.g. be performed to ameliorate or avoid ICD therapy, or to enhance resynchronization therapy by ablation of frequent monomorphic PVCs (extrasystolopathy). The trials PARTITA, PAUSE-SCD, and SURVIVE-VT, discussed in the present paper, all strengthen the recommendations for application of catheter ablation.57 (C) Exercise causes downregulation of genes coding intercalated disk proteins, as well as scaffolding and ion channel proteins, both in normal mice and PKP2 conditional knockouts. Consistent with PKP2-dependent muscle mass deficit, cardiac dimensions in human athletes carrying PKP2 mutations were reduced (data not shown), compared with matched controls. Exercise challenges a cardiomyocyte desmosomal reserve which, if impaired genetically (e.g. Plakophilin2 loss), can cause accelerated progression of the cardiomyopathy.3 Reprinted with permission.

Efficacy and tolerability of quinidine as salvage therapy for monomorphic ventricular tachycardia in patients with structural heart disease.

Quinidine is an effective therapy for a subset of polymorphic ventricular tachycardia and ventricular fibrillation (VF) syndromes; however, the efficacy of quinidine in scar-related monomorphic ventricular tachycardia (MMVT) is unclear. Between 2009 and 2020 a single VT referral center, a total of 23 patients with MMVT and structural heart disease (age 66.7 ± 10.9, 20 males, 15 with ischemic cardiomyopathy, mean LVEF 22.2 ± 12.3%, 9 with left ventricular assist device [LVAD]) were treated with quinidine (14 quinidine gluconate; 996 ± 321 mg, 8 quinidine sulfate; 1062 ± 588 mg). Quinidine was used in combination with other antiarrhythmics (AAD) in 19 (13 also on amiodarone). All patients previously failed >1 AAD (amiodarone 100%, mexiletine 73%, sotalol 32%, other 32%) and eight had prior ablations (median of 1.5). Quinidine was initiated in the setting of VT storm despite AADs (6), inability to tolerate other AADs (4), or recurrent VT(12). Ventricular arrhythmias recurred despite quinidine in 13 (59%) patients at a median of 26 (4-240) days after quinidine initiation. In patients with recurrent MMVT, VT cycle length increased from 359 to 434 ms (p = .02). Six (27.3%) patients remained on quinidine at 1 year with recurrence of ventricular arrhythmias in all. The following adverse effects were seen: gastrointestinal side effects (6), QT prolongation (2), rash (1), thrombocytopenia (1), neurologic side effects (1). One patient discontinued due to cost. Quinidine therapy has limited tolerability and long-term efficacy when used in the management of amiodarone-refractory scar-related MMVT.

Radiofrequency Catheter Ablation ofVentricular Tachycardia in Patients With Hypertrophic Cardiomyopathy andApical Aneurysm.

This study evaluated the characteristics and results of radiofrequency catheter ablation (RFCA) of ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM) and left ventricular apical aneurysm (AA). Monomorphic VT in patients with HCM and left ventricular AA has been reported. However, outcome data of RFCA are insufficient. Fifteen patients with HCM and AA who underwent RFCA for VT at 5 different institutions were included in this study. The data were evaluated retrospectively. Endocardial voltage mapping showed a low-voltage area (LVA), and late potential in the AA was recorded in 12patients (80%). Although epicardial or intramural origin of VT was suspected in 7 patients, endocardial RFCA successfully suppressed the VT at the LVA border (n= 10) or within the LVA (n= 2). In 2 of 3 patients without LVA at the endocardial site,linear RFCA at the anterior wall of the aneurysmal neck side was successful. In the remaining patient, endocardial RFCA of AA was not effective, and epicardial RFCA site was needed. In all patients, clinical VT became noninducible after RFCA. VTrecurrence was observed in 2 patients (13.3%) during the 12-month follow-up period. One patient underwent a second endocardial RFCA, and no VT recurrence was noted. In the other patient, VT recurred 3 months after RFCA and was successfully terminated by antitachycardia pacing of the implantable cardioverter-defibrillator. In patients with HCM and AA, endocardial RFCA of AA effectively suppressed monomorphic VT which was related to AA and resulted in satisfactory outcomes.

Pattern of initiation of monomorphic ventricular tachycardia and implications on tachycardia mechanism

The incidence of sudden cardiac death, predominantly caused by ventricular tachycardia and ventricular fibrillation, is high in patients with congestive heart failure. Implantable cardiac defibrillators have improved survival in this population but defibrillator shocks can lead to low quality of life and heart failure progression. The current management of recurrent ventricular tachycardia includes ablation and anti-arrhythmic drugs and both are associated with high recurrence rates. Better understanding the mechanism of ventricular tachycardia allowing individualization of treatment may improve outcomes. Re-entry is currently accepted as the mechanism of the majority of monomorphic ventricular tachycardias in patients with congestive heart failure, being responsible for more than 90% of the ventricular tachycardia in patients with ischemic cardiomyopathy. On the other hand, some studies show a greater participation of focal arrhythmias in the genesis of ventricular tachycardia in this population. The pattern of initiation of ventricular tachycardia is divided into sudden, when the first beat of the tachycardia is morphologically similar to the rest of the tachycardia, and non-sudden, when its morphology is dissimilar. An association between the pattern of the initiation and the mechanism of ventricular tachycardia has been proposed. The pattern of initiation of ventricular tachycardia is a readily available from data stored in current generation implantable cardiac defibrillators. The association with tachycardia mechanism may allow individualization of the therapy, however evidence is lacking and further research is required.

Ventricular tachycardia in repaired congenital heart disease.

Ventricular arrhythmias are an important cause of late morbidity and sudden cardiac death in the growing population of adults with repaired congenital heart disease. Risk stratification remains challenging because of the heterogeneity of the malformations and the surgical approaches. Therapeutic interventions depend on the type of ventricular arrhythmia, which can be polymorphic ventricular tachycardia (VT) or ventricular fibrillation in patients without ventricular scars, but also potentially fatal monomorphic reentrant VTs, typical for patients with ventricular scars or obstacles. Advances in surgical techniques have improved survival and have important implications for the arrhythmia substrates and prognosis. Over the past few decades, progress has been made to determine the anatomical basis for monomorphic VT in patients with ventricular surgical scars and patch material. These substrates can be currently identified and targeted during sinus rhythm by radiofrequency catheter or surgical ablation without the need for VT induction. The review provides an update on the evolving surgical approaches, the changing VA substrates, and the potential consequences for individualized risk assessment and tailored treatment.

Incidence and relevance of nonreentrant monomorphic ventricular tachycardia in patients with frequent implantable cardioverter defibrillator interventions.

Nonreentrant ventricular tachycardia (VT) originates in hearts without structural disease but occasionally can occur in patients with different cardiomyopathies equipped with an implantable cardioverter defibrillator (ICD). In a series of 142 ICD recipients with structural heart disease undergoing ablation for recurrent or incessant monomorphic VT, nonreentrant VTs were identified. Nonreentrant VTs were the cause of appropriate ICD interventions in 12 patients (8.4%). The underlying heart disease was nonischemic cardiomyopathy in eight patients, prior myocardial infarction in two patients, and valvular cardiomyopathy in two patients with a mean left ventricular ejection fraction of 42 ± 7%. Unresponsiveness to antitachycardia pacing and repetitive spontaneous re-initiation of the VT after defibrillation was the cause of frequent ineffective ICD interventions including repetitive ICD shocks in these patients. Using ICD interrogation, one or more episodes of a severe electrical storm (≥3 serial efficacious ICD shocks within 15 min) were more frequently documented in patients with nonreentrant VTs (10/12) than in patients with scar-related reentrant VTs (36/115). The origin of the nonreentrant VT was the left ventricular outflow tract in seven patients, the right ventricular outflow tract in three patients, and the tricuspid and mitral annulus in each one patient. Catheter ablation including epicardial mapping in 2 patients eliminated the nonreentrant VT in 11 of 12 patients and prevented recurrent VT storm. Repetitive nonreentrant VTs may be ineffectively treated by ICD interventions and can be the cause of an electrical storm in different cardiomyopathies.

Radio-frequency ablation as primary management of well-tolerated sustained monomorphic ventricular tachycardia in patients with structural heart disease and left ventricular ejection fraction over 30%

Patients with well-tolerated sustained monomorphic ventricular tachycardia (SMVT) and left ventricular ejection fraction (LVEF) over 30% may benefit from a primary strategy of VT ablation without immediate need for a 'back-up' implantable cardioverter-defibrillator (ICD). One hundred and sixty-six patients with structural heart disease (SHD), LVEF over 30%, and well-tolerated SMVT (no syncope) underwent primary radiofrequency ablation without ICD implantation at eight European centres. There were 139 men (84%) with mean age 62 ± 15 years and mean LVEF of 50 ± 10%. Fifty-five percent had ischaemic heart disease, 19% non-ischaemic cardiomyopathy, and 12% arrhythmogenic right ventricular cardiomyopathy. Three hundred seventy-eight similar patients were implanted with an ICD during the same period and serve as a control group. All-cause mortality was 12% (20 patients) over a mean follow-up of 32 ± 27 months. Eight patients (40%) died from non-cardiovascular causes, 8 (40%) died from non-arrhythmic cardiovascular causes, and 4 (20%) died suddenly (SD) (2.4% of the population). All-cause mortality in the control group was 12%. Twenty-seven patients (16%) had a non-fatal recurrence at a median time of 5 months, while 20 patients (12%) required an ICD, of whom 4 died (20%). Patients with well-tolerated SMVT, SHD, and LVEF > 30% undergoing primary VT ablation without a back-up ICD had a very low rate of arrhythmic death and recurrences were generally non-fatal. These data would support a randomized clinical trial comparing this approach with others incorporating implantation of an ICD as a primary strategy.

Foregoing ICD implantation in patients presenting with ventricular tachycardia: is catheter ablation alone sufficient?

This editorial refers to ‘Radio-frequency ablation as primary management of well-tolerated sustained monomorphic ventricular tachycardia in patients with structural heart disease and left ventricular ejection fraction over 30%’[†][1], by P. Maury et al. , on page 1479 Ventricular tachycardia (VT) in the setting of structural heart disease (SHD) and a reduced ejection fraction (EF) of ≤35% is commonly treated by insertion of an implantable cardioverter-defibrillator (ICD).1 While the strategy of secondary prevention reduces mortality, the presence of an ICD has no impact on recurrent episodes of VT. Hence, antiarrhythmic drug therapy is frequently established in order to prevent future arrhythmic events.2 Use of potent drugs such as amiodarone is hampered by a multitude of side effects, often leading to drug discontinuation by the patient.2 Since VT in patients with SHD is commonly due to macro-re-entry within the ventricles, catheter ablation has become an attractive means to terminate VT acutely ( Table 1 ). The first prospective randomized trial, SMART VT, demonstrated that patients with coronary artery disease (CAD) presenting with aborted sudden cardiac death, syncope, or unstable VT/ventricular fibrillation (VF) benefit from catheter ablation, resulting … [1]: #fn-2

Value of Electro‐Vectorcardiogram in Hypertrophic Cardiomyopathy

The electrocardiogram is an important tool for the initial diagnostic suspicion of hypertrophic cardiomyopathy in any of its forms, both in symptomatic and in asymptomatic patients because it is altered in more than 90 percent of the cases. Electrocardiographic anomalies are more common in patients carriers of manifest hypertrophic cardiomyopathy and the electrocardiogram alterations are earlier and more sensitive than the increase in left ventricular wall thickness detected by the echocardiogram. Nevertheless, despite being the leading cause of sudden death among young competitive athletes there is no consensus over the need to include the method in the pre-participation screening. In apical hypertrophic cardiomyopathy the electrocardiographic hallmarks are the giant negative T waves in anterior precordial leads. In the vectorcardiogram, the QRS loop is located predominantly in the left anterior quadrant and T loop in the opposite right posterior quadrant, which justifies the deeply negative T waves recorded. The method allows estimating the left ventricular mass because it relates to the maximal spatial vector voltage of the left ventricle in the QRS loop. The recording on electrocardiogram or Holter monitoring of nonsustained monomorphic ventricular tachycardia in patients with syncope, recurrent syncope in young patient, hypotension induced by strain, bradyarrhythmia, or concealed conduction are markers of poor prognosis. The presence of rare sustained ventricular tachycardia is observed in mid-septal obstructive HCM with apical aneurysm. The presence of complete right bundle branch block pattern is frequent after the percutaneous treatment and complete left bundle branch block is the rule after myectomy.

Prophylactic catheter ablation for induced monomorphic ventricular tachycardia in patients with implantable cardioverter defibrillators as primary prevention

Prophylactic catheter ablation (CA) has been established to reduce the incidence of appropriate implantable cardioverter-defibrillator (ICD) therapy (anti-tachycardia pacing or shock) in secondary prevention patients. The aim of this study was to determine whether prophylactic CA for induced ventricular tachycardia (VT) reduces the incidence of appropriate ICD therapy in primary prevention patients. We retrospectively investigated 66 consecutive patients with structural heart disease who had undergone ICD implantation as primary prevention and electrophysiological study. Patients with hypertrophic cardiomyopathy or no inducible monomorphic VT had been excluded, and the remaining 38 patients were divided into two groups; those who had undergone prophylactic CA for induced monomorphic VT (the CA group, n = 18), and those who had not undergone CA (the non-CA group, n = 20). During a mean follow-up of 50 ± 38 months, 1 patient (5%) received appropriate ICD therapy in the CA group and 13 (65%) in the non-CA group. Kaplan-Meier survival analysis revealed a significantly higher event-free survival rates for appropriate ICD therapy in the CA group compared with the non-CA group (P = 0.003). Among the patients, one patient (5%) in the CA group and nine patients (45%) in the non-CA group suffered appropriate shock (P = 0.018). Prophylactic CA for induced monomorphic VT reduces the incidence of appropriate ICD therapy including shock in primary prevention patients. These results indicate that prophylactic CA may be considered for structural heart disease patients who are candidates for ICD implantation as primary prevention.

Electrophysiological characteristics of ventricular tachyarrhythmias in cardiac sarcoidosis versus arrhythmogenic right ventricular cardiomyopathy

Recent evidence suggests that cardiac sarcoidosis (CS) and arrhythmogenic right ventricular cardiomyopathy (ARVC) can manifest very similarly. To investigate whether there are significant demographic and electrophysiological differences between patients with CS and ARVC. We prospectively compared patients with proven CS or ARVC who underwent radiofrequency catheter ablation of ventricular tachycardias by using 3-dimensional electroanatomical mapping. Furthermore, we evaluated whether the diagnostic criteria for ARVC would have excluded ARVC in patients with CS. Eighteen patients (13 men; mean age 44.9 years) were included. All 18 patients had mild to moderately reduced right ventricular ejection fraction. Patients with cardiac sarcoidosis (n = 8) had a significantly lower mean left ventricular ejection fraction (35.6±19.3 vs 60.6±9.4; P = .002). Patients with CS had a significantly wider QRS (0.146 vs 0.110s; P = .004). Five of 8 (63%) patients with CS fulfilled the diagnostic ARVC criteria. Ventricular tachycardias (VTs) with a left bundle branch block pattern were documented in all but one patient (with CS). Programmed ventricular stimulation induced an average of 3.7 different monomorphic VTs in patients with CS vs 1.8 in patients with ARVC (P = .01). VT significantly more often originated in the apical region of the right ventricle in CS vs ARVC (P = .001), with no other predilection sites. Ablation success and other electrophysiological parameters were not different. The current diagnostic ARVC guidelines do not reliably exclude patients with CS. Clinical and electrophysiological parameters that were characteristic of CS in our patients include reduced left ventricular ejection fraction, a significantly wider QRS, right-sided apical VT, and more inducible forms of monomorphic VT.

Sustained monomorphic ventricular tachycardia in patients with Brugada syndrome

Sustained monomorphic ventricular tachycardia in patients with Brugada syndrome

Ventricular Tachycardia and Sudden Cardiac Death

Ventricular tachycardia (VT), which most commonly occurs in patients with structural heart disease, can be associated with an increased risk of sudden death. The most common cause of ventricular fibrillation is acute coronary ischemia, whereas a myocardial scar from prior infarct is the most common cause of sustained monomorphic VT in patients with structural heart disease. More benign forms of idiopathic VT can also occur in the absence of structural heart disease. Treatment of VT involves both emergent management and prevention of recurrence with medical and device therapy. Appropriately selected patients who have experienced VT or those who are at risk of VT may be candidates for an implantable cardioverter-defibrillator. The left ventricular ejection fraction is most frequently used to stratify patients with either ischemic or nonischemic cardiomyopathy who are at risk of sudden death and may be candidates for a prophylactic defibrillator. Catheter ablation may also be an option for appropriately selected patients with many forms of VT. This article discusses the etiologies and management of VT and its association with sudden death.

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

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. 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%). 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.

Substrate Characterization and Catheter Ablation for Monomorphic Ventricular Tachycardia in Patients With Apical Hypertrophic Cardiomyopathy

VT Ablation in Apical Hypertrophic Cardiomyopathy. Monomorphic ventricular tachycardia (VT) is uncommon in apical hypertrophic cardiomyopathy (HCM). The purpose of this study was to define the substrate and role of catheter ablation for VT in apical HCM. Four patients with apical HCM and frequent, drug refractory VT (mean age of 46 ± 10 years, left ventricular [LV] ejection fraction; 54 ± 14%) underwent catheter ablation with the use of electroanatomic mapping. Endocardial mapping was performed in 4 patients and 3 patients underwent epicardial mapping. In 3 patients, VT was related to areas of scar in the apical LV where maximal apical wall thickness ranged from 14.5 to 17.8 mm, and 2 patients had apical aneurysms. Endocardial and epicardial substrate mapping revealed low voltage (<1.5 mV) scar in both endocardial and epicardial LV in 2 and only in the epicardium in 1 patient. Inducible VT was abolished with a combination of endocardial and epicardial ablation in 2 patients, but was ineffective in the third patient who had intramural reentry that required transcoronary ethanol ablation of an obtuse marginal vessel for abolition. The fourth patient had focal nonsustained repetitive VT from right ventricular outflow tract (RVOT), consistent with idiopathic RVOT-VT, that was successfully ablated. During follow-ups of 3-9 months, all patients remained free from VT. Monomorphic VT in apical HCM can be due to endocardial, epicardial or intramural reentry in areas of apical scar. Epicardial ablation or transcoronary alcohol ablation is required in some cases.

Catheter Ablation of Scar-Related Ventricular Tachycardia in Patients with Electrical Storm Using Remote Magnetic Catheter Navigation

A remote magnetic navigation system (MNS) has been used for ablation of ventricular arrhythmias. However, irrigated tip catheter has not been evaluated in large series of patients. To evaluate acute and long-term efficiency of the newly available irrigated tip magnetic catheter for radiofrequency (RF) ablation of scar-related ventricular tachycardia (VT) in patients with ischemic heart disease. Between January 2008 and October 2009, a total of 30 consecutive patients with ischemic heart disease (26 men, age 70.1 ± 8.7 years, left ventricular ejection fraction: 30 ± 9%) and electrical storm due to monomorphic VT underwent RF ablation using a remote MNS and a magnetic irrigated tip catheter. Acute success was defined as noninducibility of any monomorphic VT during programmed right and left ventricular stimulation, and obtained in 24 (80%) patients. A total of 1-6 VTs (mean 2.3 ± 1.2, 394 ± 108 ms, 210-660 ms) were inducible during each procedure. The duration of RF energy application was 41.2 ± 23.3 minutes, with total procedure and fluoroscopy times of 158 ± 47 minutes and 9.8 ± 5.3 minutes, respectively. No acute complications were observed during the procedures. During mean follow-up of 7.8 months, 21 patients (70%) had no recurrence of VT and received no implantable cardioverter defibrillator therapy. Among patients who were noninducible during programmed right ventricular stimulation (n = 25), ≥1 monomorphic VT was inducible during programmed left ventricular stimulation in four (16%) that was ablated successfully in three of them. Irrigated ablation of scar-related VT using remote MNS is an effective modality for management of the monomorphic VT in patients with ischemic cardiomyopathy with minimal radiation exposure. Programmed left (in addition to right) ventricular stimulation might be necessary to assess acute outcome of the ablation procedure.

Ventricular tachycardia and sudden cardiac death.

Ventricular tachycardia (VT), which most commonly occurs in patients with structural heart disease, can be associated with an increased risk of sudden death. The most common cause of ventricular fibrillation is acute coronary ischemia, whereas a myocardial scar from prior infarct is the most common cause of sustained monomorphic VT in patients with structural heart disease. More benign forms of idiopathic VT can also occur in the absence of structural heart disease. Treatment of VT involves both emergent management and prevention of recurrence with medical and device therapy. Appropriately selected patients who have experienced VT or those who are at risk of VT may be candidates for an implantable cardioverter-defibrillator. The left ventricular ejection fraction is most frequently used to stratify patients with either ischemic or nonischemic cardiomyopathy who are at risk of sudden death and may be candidates for a prophylactic defibrillator. Catheter ablation may also be an option for appropriately selected patients with many forms of VT. This article discusses the etiologies and management of VT and its association with sudden death.

Initation Modes of Spontaneous Monomorphic Ventricular Tachycardia in Patients With Chagas Heart Disease

We sought to demonstrate the mode of spontaneous onset of sustained monomorphic ventricular tachycardia in patients with Chagas' cardiomyopathy. We studied 222 stored electrograms in 14 patients with Chagas cardiomyopathy and spontaneous monomorphic ventricular tachycardia treated with a cardioverter defibrillator. Premature ventricular complexes before ventricular tachycardia were classified by morphology and number. The onset was considered "sudden" if no previous premature ventricular complexes were present, and "extrasystolic" if a ventricular extrasystole precedeed SMVT initiation. Prematurity was evaluated by the coupling interval and a calculated prematurity ratio (RR'/RR). Two-hundred and nine episodes (94%) were initiated by late-coupled premature ventricular complexes (prematurity ratio >0.5). The mean coupling interval of the initiating beat was 565+/-117 ms with a mean prematurity ratio of 0.72+/-0.15. A sudden onset was the most frequent pattern of ventricular tachycardia initiation (129 episodes, 58%). Among the extrasystolic onset (93 episodes, 42%), 48 were due to multiple premature ventricular complexes and 88 had a different QRS complex (electrogram) morphology of the ventricular extrasystoles than that recorded during the subsequent ventricular tachycardia. The arrhythmia was preceded by a short-long-short sequence in 95/222 episodes (43%). In implantable cardioverter defibrillator recipients with Chagas cardiomyopathy, spontaneous monomorphic ventricular tachycardia episodes are typically initiated by late-coupled premature ventricular complexes, which often show a short-long-short sequence.

Enhanced Infarct Border Zone Function and Altered Mechanical Activation Predict Inducibility of Monomorphic Ventricular Tachycardia in Patients with Ischemic Cardiomyopathy

To prospectively determine whether mechanical behavior of left ventricular wall segments that contain different degrees of scar tissue and are located at different distances from the interface between infarcted and noninfarcted myocardial tissue can help predict inducibility of monomorphic ventricular tachycardia (VT) in patients with ischemic cardiomyopathy. This HIPAA-compliant study was institutional review board approved; written informed consent was obtained from all patients. Forty-six patients (36 men, 10 women; mean age +/- standard deviation, 61.6 years +/- 11.9) with prior myocardial infarction (MI) and left ventricular dysfunction were referred for defibrillator implantation and underwent an electrophysiologic examination and tagged contrast-enhanced magnetic resonance (MR) imaging. Peak circumferential shortening strain (Ecc) and time to peak Ecc were measured in 12 segments from short-axis sections. Remote, adjacent, and border zones were defined according to increasing proximity to the MI. Patients in whom monomorphic VT could be induced (ie, inducible patients) were considered positive for inducibility. Relationships between inducibility of monomorphic VT, peak Ecc, and time to peak Ecc were analyzed with one-way analysis of variance and Bonferroni test. Inducible patients had more infarcted and border zone sectors and a shorter time to peak Ecc than did noninducible patients in the border zone and adjacent and infarcted regions (P < .001). Peak Ecc in the border zone of inducible patients (-11.42% +/- 0.46 [standard error]) was greater than that in noninducible patients (-10.18% +/- 0.38; P < .05). Ratio of Ecc in border zone and in remote regions was greater (P < .05) in inducible patients than in noninducible patients (1.31 +/- 0.27 vs 0.64 +/- 0.13, respectively). Enhanced border zone function defined as greater Ecc and earlier time to peak Ecc showed positive correlation to VT inducibility in patients with prior MI and left ventricular dysfunction.

Successful ablation of sustained monomorphic ventricular tachycardias in patients with Brugada syndrome

Successful ablation of sustained monomorphic ventricular tachycardias in patients with Brugada syndrome