Early Ventricular Tachycardia Research Articles

Hyperglycemia and risk of ventricular tachycardia among patients hospitalized with acute myocardial infarction

BackgroundLittle is known about the association of hyperglycemia with the development of ventricular tachycardia (VT) in patients hospitalized with acute myocardial infarction (AMI) which we examined in the present study. The objectives of this community-wide observational study were to examine the relation between elevated serum glucose levels at the time of hospital admission for AMI and occurrence of VT, and time of occurrence of VT, during the patient’s acute hospitalization.MethodsWe used data from a population-based study of patients hospitalized with AMI at all central Massachusetts medical centers between 2001 and 2011. Hyperglycemia was defined as a serum glucose level ≥ 140 mg/dl at the time of hospital admission. The development of VT was identified from physicians notes and electrocardiographic findings by our trained team of data abstractors.ResultsThe average age of the study population was 70 years, 58.0% were men, and 92.7% were non-Hispanic whites. The mean and median serum glucose levels at the time of hospital admission were 171.4 mg/dl and 143.0, respectively. Hyperglycemia was present in 51.9% of patients at the time of hospital admission; VT occurred in 652 patients (15.8%), and two-thirds of these episodes occurred during the first 48 h after hospital admission (early VT). After multivariable adjustment, patients with hyperglycemia were at increased risk for developing VT (adjusted OR = 1.48, 95% CI = 1.23–1.78). The presence of hyperglycemia was significantly associated with early (multivariable adjusted OR = 1.39, 95% CI = 1.11–1.73) but not with late VT. Similar associations were observed in patients with and without diabetes and in patients with and without ST-segment elevation AMI.ConclusionsEfforts should be made to closely monitor and treat patients who develop hyperglycemia, especially early after hospital admission, to reduce their risk of VT.

Impact of timing of recurrence following catheter ablation of scar-related ventricular tachycardia on subsequent mortality.

Catheter ablation (CA) has an established role in scar-related ventricular tachycardia (VT), but the risk of recurrences is substantial and the appropriate intensity of postablation monitoring unknown. The implication of timing of postablation VT recurrence has not been adequately investigated. We studied 120 consecutive patients with scar-related VT (age 60 ± 15 years, left ventricular ejection fraction 39 ± 16%, 52% ischemic etiology) with at least 2 years of follow-up. Timing of VT recurrence was classified as very early (<1 month), early (1-6 months), or late (>6 months). At 24 months follow-up, 53 (44%) patients had recurrent VT, with eight (15%) having very early recurrence, 17 (32%) early recurrence, and 28 (53%) late recurrence. Mortality rates at 2 years were significantly higher in patients with very early VT recurrence (38%) compared to those with early (12%), late (7%), and no (3%) recurrences (log-rank P<0.001). Very early VT recurrence was associated with an increased risk of death (odds ratio=5.68, 95% confidence interval = 1.06-30.62, P=0.04), while recurrent VT beyond 6 months was not associated with increased risk of mortality (P=0.94). Timing of VT recurrence following CA of scar-related VT impacts subsequent risk of mortality. Patients experiencing VT recurrence within 1-6 months from the procedure are at particularly high risk. These data support the importance of intense postablation monitoring for at least 6 months after the procedure to identify patients with early VT recurrence who may benefit from additional therapeutic interventions to improve outcomes.

Early Ventricular Tachycardia or Fibrillation in Patients With ST Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention and Impact on Mortality and Stent Thrombosis (from the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction Trial)

The prevalence and impact of early ventricular arrhythmias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) occurring before mechanical revascularization for acute ST segment elevation myocardial infarction (STEMI) treated with percutaneous coronary intervention are poorly understood. We sought to investigate the association between early VT/VF and long-term clinical outcomes using data from the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction trial. Among 3,602 patients with STEMI, 108 patients (3.0%) had early VT/VF. Baseline clinical characteristics were similar in patients with versus without early VT/VF. Patients with early VT/VF had shorter symptom-to-balloon times and lower left ventricular ejection fraction and underwent more frequent thrombectomy compared with patients without early VT/VF. Adjusted 3-year rates of all-cause death (15.7% vs 6.5%; adjusted hazard ratio 2.62, 95% confidence interval 1.48 to 4.61, p <0.001) and stent thrombosis (13.7% vs 5.7%; adjusted hazard ratio 2.74, 95% confidence interval 1.52 to 4.93, p <0.001) were significantly higher in patients with early VT/VF compared with patients without early VT/VF. In conclusion, in the Harmonizing Outcomes with Revascularization and Stents in Acute Myocardial Infarction trial, VT/VF occurring before coronary angiography and revascularization in patients with STEMI was strongly associated with increased 3-year rates of death and stent thrombosis. Further investigation into the mechanisms underlying the increased risk of early stent thrombosis in patients with early VT/VF is required.

Ventricular Tachycardia Ablation in Severe Heart Failure: An International Ventricular Tachycardia Ablation Center Collaboration Analysis.

Ventricular tachycardia (VT) radiofrequency ablation has been associated with reduced VT recurrence and mortality, although it is typically not considered among New York Heart Association class IV (NYHA IV) heart failure patients. We compared characteristics and VT radiofrequency ablation outcomes of those with and without NYHA IV in the International VT Ablation Center Collaboration. NYHA II-IV patients undergoing VT radiofrequency ablation at 12 international centers were included. Clinical variables, VT recurrence, and mortality were analyzed by NYHA IV status using Kaplan-Meier analysis and Cox proportional hazard models. There were significant differences between NYHA IV (n=111) and NYHA II and III (n=1254) patients: NYHA IV had lower left ventricular ejection fraction; more had diabetes mellitus, kidney disease, cardiac resynchronization implantable cardioverter-defibrillator, and VT storm despite greater antiarrhythmic drug use (P<0.01). NYHA IV subjects required more hemodynamic support, were inducible for more and slower VTs, and were less likely to undergo final programmed stimulation. There was no significant difference in acute complications. In-hospital deaths, recurrent VT, and 1-year mortality were higher in the NYHA IV group, in the context of greater baseline comorbidities. Importantly, NYHA IV patients without recurrent VT had similar survival compared with NYHA II and III patients with recurrent VT (68% versus 73%). Early VT recurrence (≤30 days) was significantly associated with mortality, especially in NYHA IV patients. Despite greater baseline comorbidities, VT radiofrequency ablation can be safely performed among NYHA IV patients. Early VT recurrence is significantly associated with subsequent mortality regardless of NYHA status. Elimination of recurrent VT in NYHA IV patients may reduce mortality to a level comparable to NYHA II and III with arrhythmia recurrence.

Correlates and prognosis of early recurrence after catheter ablation for ventricular tachycardia due to structural heart disease.

Catheter ablation for ventricular tachycardia (VT) from structural heart disease has a significant risk of recurrence, but the optimal duration for in-hospital monitoring is not defined. This study assesses the timing, correlates, and prognostic significance of early VT recurrence after ablation. Of 370 patients (313 men; aged 63.0±13.2 years) who underwent a first radiofrequency ablation for sustained monomorphic VT associated with structural heart disease from 2008 to 2012, sustained VT recurred in 81 patients (22%) within 7 days. In multivariable analysis, early recurrence was associated with New York Heart Association classification ≥III (odds ratio [OR] 1.90, 95% confidence interval [CI] 1.03-3.48; P=0.04), dilated cardiomyopathy (OR 1.93, 95% CI 1.03-3.57; P=0.04), prevalence of VT storm before the procedure (OR 2.62, 95% CI 1.48-4.65; P=0.001), a greater number of induced VTs (OR 1.24, 95% CI 1.07-1.45; P=0.006), and acute failure or no final induction test (OR 1.88, 95% CI 1.03-3.40; P=0.04). During a median of 2.5 (1.2, 4.0) years of follow-up, early VT recurrence was an independent correlates of mortality (hazard ratio 2.59, 95% CI 1.52-4.34; P=0.0005). Patients who have early recurrences of VT after ablation are a high risk group who may be identifiable from their clinical profile. Further study is warranted to define the optimal treatment strategies for this patient group.

High-density substrate-guided ventricular tachycardia ablation: Role of activation mapping in an attempt to improve procedural effectiveness

Advanced techniques of electroanatomical mapping efficiently guide ventricular tachycardia (VT) ablation strategies; in this context, the adjunctive value of combining activation mapping (AMap) to improve accuracy has not been elucidated. To investigate whether conventional AMap further contributes to the identification of critical sites of VT reentry and whether this translates into a more effective ablation outcome in a cohort of patients undergoing VT ablation. We prospectively enrolled 126 patients (mean age 65.3 ± 10.5 years; left ventricular ejection fraction 33.3% ± 7.2%) with ischemic (n = 89) or idiopathic (n = 37) dilated cardiomyopathy undergoing endocardial (n = 105) or endo-epicardial (n = 21) electroanatomical mapping and ablation. A substrate-guided strategy targeting surrogate markers of reentry was accomplished in all patients, but the feasibility and efficacy of AMap was preliminarily assessed for all induced VTs focusing on early VT suppression obtained during radiofrequency delivery. VT-free survival was assessed by ICD interrogation. AMap successfully guided ablation in 62 of 104 (59.6%) patients with inducible VT(s). At 1 year, 6 of 126 (4.8%) patients died; VT recurred in 28 of 126 (22.2%) patients. No significant difference in VT recurrence rate was observed between patients in whom AMap proved effective versus those in whom substrate-guided ablation was not corroborated by AMap (16 of 62 [25.8%] vs 12 of 64 [18.8%]; log-rank test, P = .3). Our findings support the efficacy of a substrate-guided strategy targeting specific markers of arrhythmogenicity identified during sinus rhythm. AMap proves highly efficient acutely but does not improve overall VT-free survival, suggesting that in patients with advanced cardiac disease, life-threatening arrhythmias can be successfully treated by ablation in sinus rhythm, thus limiting procedural risks.

The Role of Preventive Ablation of Ventricular Tachycardia in the Patient with Coronary Artery Disease, Reduced Left Ventricular Function, and a New Implantable Cardioverter Defibrillator Implant.

Most patients referred for ventricular tachycardia (VT) ablation have already suffered multiple therapies for recurrent VT, typically in the form of implantable cardioverter defibrillator (ICD) shocks. Recent landmark trials have looked at these populations and suggest potential usefulness of early, preventive ablation of VT in patients with ischemic cardiomyopathy. In this review the potential role of early VT ablation in patients with ischemic cardiomyopathy, current controversies regarding VT ablation in this population, and ongoing and future research that may further inform clinical decision making regarding optimal timing of ablation in these patients are discussed.

The Relation Between Early Ventricular Tachycardia and QT Dispersion in Patients with Acute Myocardial Infarction Treated with Thrombolytic Therapy.

In this study, we investigated the influence of increased QT dispersion (defined as maximal QT interval minus minimal QT interval) on the occurrence of early nonsustained ventricular tachycardia (NSVT) in patients with acute myocardial infarction (AMI) who received thrombolytic therapy. In the retrospective analysis of 96 patients with clinical reperfusion criteria, 36 had NSVT within the first 12 hours after the onset of thrombolytic therapy (group A), and 60 patients did not have NSVT during the same period (group B). On admission ECG, QT and QT(c) dispersion and the amount of jeopardized myocardial area (Aldrich score) were calculated. In group A, Aldrich score was significantly higher (21.4 +/- 7.2% vs 14.2 +/- 4.9%; p < 0.005). There were significantly higher QT dispersion values on admission (83.3 +/- 23.4 vs 67.5 +/- 23.7 msec; p < 0.005), at 24th hour (87.1 +/- 12.6 vs 72.1 +/- 27.4 msec; p < 0.005) and on the 10th day (63.5 +/- 31.2 vs 49.5 +/- 14.3 msec; p < 0.005) in group A. In subgroup analysis of group A, patients with NSVT between 6-12 hours (group A2) had significantly higher Aldrich score and QT dispersion values at all above time points compared to patients with NSVT between 0-6 hours (group A1) after AMI. In conclusion, in this study we found a strong relation between the occurrence of NSVT within 12 hours and increased QT dispersion on admission ECG in patients with AMI who received thrombolytic therapy. This relation was even stronger for the subgroup of patients with NSVT within 6-12 hours. Thus, these results may indicate that NSVT is related to increased QT dispersion which is secondary to larger jeopardized myocardial area in patients with AMI. </hea

Predictors of ventricular tachyarrhythmia in high-risk myocardial infarction patients treated with primary coronary intervention

Background. We investigated the association between clinical characteristics, angiographic data and ventricular arrhythmia in patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI)Methods. In patients with STEMI (n=225), a Holter analysis was performed the first 12 hours after primary PCI.Results. A total of 151 (66%) patients had >/=1 episode of ventricular tachycardia (VT). Age <70 years (RR 4.9, 95% CI 1.8 to 12.7), TIMI 0-1 pre-PCI (RR 2.6, 95% CI 1.1 to 6.1) and peak CK (RR 3.5, 95% CI 1.9 to 5.8) were independent predictors of VT. One-year mortality was 7%, no association between mortality and presence of early VT was found.Conclusion. Ventricular tachycardia is common in the first 12 hours after primary PCI for STEMI. Independent predictors of VT are younger age, TIMI 0-1 flow prior to PCI and larger infarct size. The presence of early VT was not significantly associated with one-year mortality. (Neth Heart J 2010;18:122-8.).

The association between early ventricular arrhythmias, renin-angiotensin-aldosterone system antagonism, and mortality in patients with ST-segment-elevation myocardial infarction: Insights from global use of strategies to open coronary arteries (GUSTO) V

The long-term prognostic significance of early (<48 hours) ventricular fibrillation (VF) or sustained ventricular tachycardia (VT) in patients with an acute myocardial infarction remains controversial. Emerging data suggest that some of the benefit of renin-angiotensin-aldosterone system (RAAS) antagonism may be derived from a reduction in the incidence of these arrhythmias in the setting of acute myocardial infarction. We assessed the relationship between early VF/VT (defined as within 48 hours after admission) and mortality in 16,588 patients from global use of strategies to open coronary arteries (GUSTO) V trial. Furthermore, we examined the relationship between baseline use of angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB), early VF/VT, and mortality. Early VF or VT occurred in 732 (4.4%) patients. Compared to patients without VF/VT, those experiencing early VF or VT had a significant increase in 30-day mortality (22% vs 5%, P < .001). Baseline use of an ACEI/ARB was associated with a decreased incidence of early VF/VT (odds ratio 0.65, 0.47-0.89, P = .008). A lower 30-day mortality was seen in patients with early VF/VT on baseline ACEI/ARB compared with patients with early VF/VT not receiving an ACEI/ARB at baseline (17.7% vs 24.2%, respectively, P = .04). The association between baseline RAAS antagonism and mortality persisted after adjustment for multiple confounders. In patients presenting with acute myocardial infarction, early VF/VT identifies those at increased risk for 30-day mortality. Baseline use of RAAS antagonists is associated with a reduced incidence of malignant arrhythmias. Identifying how this association impacts short-term mortality in this patient population requires further prospective evaluation.

Postoperative ventricular tachycardia in patients with congenital heart disease: diagnosis and management

Ventricular tachycardia (VT) after palliative repair of congenital heart disease is relatively rare. Despite this rarity, VT is a known cause of early, intermediate and late morbidity and mortality in these patients. A number of factors have been linked to the development of VT in this unique patient population. The purpose of this article is to provide a concise overview regarding the etiology, diagnosis and treatment of VT in patients with congenital heart disease. In-depth information will be provided to aid diagnosis and the treatment of early postoperative VT. The use of additional diagnostic methods such as echocardiography, cardiac catheterization and electrophysiology studies to risk assess patients with postoperative VT will also be discussed. In addition, I examine the long-term management strategies for VT in these patients, from medical management and cardiovascular surgery to implantation of cardioverter-defibrillators.

The isolated blood-perfused rat heart: an inappropriate model for the study of ischaemia- and infarction-related ventricular fibrillation.

1. Well-characterized in vivo and in vitro models exist for the study of ischaemia- and infarction-related ventricular fibrillation (VF). In rats in vivo, VF appears to occur in distinct acute ischaemia- (early) and infarction-related (late) phases. Interestingly, isolated buffer-perfused rat hearts do not develop late VF. This raises the possibility that unidentified components of the blood may be responsible for late VF. We thus sought to characterize an isolated blood-perfused rat heart in order to investigate the possible influence of blood components on arrhythmias arising from ischaemia and infarction. 2. Hearts, excised from male Wistar rats, were perfused in the Langendorff mode with blood from support rats (male Wistar, 350-430 g) via an extracorporeal circuit. Perfused hearts underwent left coronary artery occlusion for 240 min or a sham procedure (n=10 group(-1)). 3. Only 10% of ischaemic hearts developed late VF (90-240 min). Tissue myeloperoxidase activity (an index of neutrophil accumulation) increased during ischaemia from 0.017+/-0.004 (six fresh hearts) to 0.056+/-0.005 units mg protein(-1) (P<0.05) at 240 min, but values were similar in sham hearts (0.083+/-0.013). Likewise, the decline (-1 vs 240 min of ischaemia shown) in circulating total white blood cells from 6.8+/-0.5 to 1.9+/-0.2 x 10(3) micro l(-1) and in platelets from 441+/-32 to 274+/-16 x 10(3) micro l(-1) (both P<0.05) was similar in time-matched sham hearts (data not shown). 4 Surprisingly, only 10% of ischaemic hearts developed early VF (0-90 min), although the incidence of early ventricular tachycardia was 100% in these hearts (P<0.05 vs sham hearts). Blood K+ values were normal (hyperkalaemia suppresses VF). 5 Although late VF was absent in blood-perfused hearts, it would be premature to conclude from this that late VF is not mediated by blood components. This is because the similar neutrophil accumulation in ischaemic and sham hearts, the decline in numbers of circulating blood components, and the unexpected paucity of early VF all question the validity of the model.

The relation between early ventricular tachycardia and QT dispersion in patients with acute myocardial infarction treated with thrombolytic therapy

The relation between early ventricular tachycardia and QT dispersion in patients with acute myocardial infarction treated with thrombolytic therapy

The Relation Between Early Ventricular Tachycardia and QT Dispersion in Patients with Acute Myocardial Infarction Treated with Thrombolytic Therapy

In this study, we investigated the influence of increased QT dispersion (defined as maximal QT interval minus minimal QT interval) on the occurrence of early non-sustained ventricular tachycardia (NSVT) in patients with acute myocardial infarction (AMI) who received thrombolytic therapy. In the retrospective analysis of 96 patients with clinical reperfusion criteria, 36 had NSVT within the first 12 hours after the onset of thrombolytic therapy (group A), and 60 patients did not have NSVT during the same period (group B). On admission ECG, QT and QTc dispersion and the amount of jeopardized myocardial area (Aldrich score) were calculated. In group A, Aldrich score was significantly higher (21.4 ± 7.2% vs 14.2 ± 4.9%;p < 0.005). There were significantly higher QT dispersion values on admission (83.3 ± 23.4 vs 67.5 ± 23.7 msec;p < 0.005), at 24th hour (87.1 ± 12.6 vs 72.1 ± 27.4 msec;p < 0.005) and on the 10th day (63.5 ± 31.2 vs 49.5 ± 14.3 msec;p < 0.005) in group A. In subgroup analysis of group A, patients with NSVT between 6–12 hours (group A2) had significantly higher Aldrich score and QT dispersion values at all above time points compared to patients with NSVT between 0–6 hours (group A1) after AMI. In conclusion, in this study we found a strong relation between the occurrence of NSVT within 12 hours and increased QT dispersion on admission ECG in patients with AMI who received thrombolytic therapy. This relation was even stronger for the subgroup of patients with NSVT within 6–12 hours. Thus, these results may indicate that NSVT is related to increased QT dispersion which is secondary to larger jeopardized myocardial area in patients with AMI.

Role of the Purkinje system in spontaneous ventricular tachycardia during acute ischemia in a canine model.

A role for the Purkinje system in the development of spontaneous ventricular tachycardia (VT) during acute ischemia has been suspected but not proved. We used a three-dimensional activation mapping system incorporating Purkinje signals to characterize the mechanism and site of origin of spontaneous VT occurring in the first 30 minutes after coronary artery occlusion in a dog model. The left anterior descending coronary artery was occluded in 48 dogs after instrumentation of the risk zone with 21 multipolar plunge needles, each recording 6 bipolar electrograms through the myocardial wall. VT of Purkinje origin was defined as a focal endocardial VT with a Purkinje potential identified before muscle potential on the electrode recording the earliest activity. Purkinje potentials were identified on an average of 10 of the 21 plunge needles. During atrial pacing at cycle lengths of 300 to 700 ms, a total of 25 VTs were observed from 18 of the 48 dogs (37.5%). Of the VTs, 15 (60.0%) were of focal Purkinje origin, 1 (4.0%) of focal endocardial origin, 2 (8.0%) of focal midmyocardial origin, and 2 (8.0%) of focal epicardial origin; 3 (12.0%) had a reentrant mechanism, whereas in 2 (8.0%), the mechanism could not be defined. The mean cycle length of all VTs was 265+/-17 ms (mean+/-SEM, n=25). Of the 25 VTs, 19 originated from an ischemic area as defined by significant decreases in voltages of muscle electrograms at the time of occurrence of the VT, 4 originated from an ischemic border zone, and the origin of 2 could not be determined. In this model, VT with a focal mechanism is commonly seen in the early ischemic period. Sixty percent of the VTs were of focal Purkinje origin as characterized by three-dimensional activation mapping. The results of this study indicate that Purkinje tissue may play an important role in the development of early ischemic VT.

Role of late potentials in identifying patients at risk for ventricular tachycardia after surgical correction of congenital heart disease

This study evaluates the role of late potentials in identifying patients with sustained ventricular tachycardia (VT) after surgery for congenital heart defects using right ventriculotomy. Nine patients with early (1 to 12 months) or late VT (spontaneous in 7 [induced during electrophysiologic study in 6 of the 7] and induced in 2) and 104 patients without VT were studied. All patients had complete right bundle branch block. Late potentials were quantified by 3 time-domain parameters of the signal-averaged electrocardiogram: total filtered QRS duration, root-mean-square voltage in the last 40 ms, and low-amplitude signal duration of the terminal filtered QRS complex. Root-mean-square voltage filtered at 80 to 250 Hz was lower in patients with than without VT (9 ± 6 vs 16 ± 8 μV, p < 0.01). By multivariate analysis, more complex surgery (i.e., insertion of extracardiac conduits, Kawashima operation, etc.), lower root-mean-square voltage, and higher Lown grade (2 to 5) of ventricular arrhythmias on routine postoperative Holter recordings were the only independent predictors of VT (p < 0.001, < 0.05, and < 0.05, respectively). A combination of more complex surgery, root-mean-square voltage <14 μV, and Lown grade 2 to 5 ventricular arrhythmias was highly predictive of VT (positive predictive value 75%). Conversely, patients without complex surgery and with root-mean-square voltage of >13 μV were not likely to develop VT (negative predictive value 100%). Late potentials are an independent predictor of VT and may improve the identification of patients at low and high risk of VT after surgery for congenital heart defects using right ventriculotomy.

Comparison of high energy direct current and radiofrequency catheter ablation of the atrioventricular junction

Objectives. The goal of the study was to determine short- and long-term success and complications of radiofrequency atrioventricular (AV) junction catheter ablation and to compare these with those of high energy direct current catheter ablation.Background. Catheter ablation of the AV junction with radiofrequency or direct current energy is an accepted treatment for drug-refractory supraventricular tachycardias. Few data are available on the long-term success and effects of radiofrequency ablation or its comparison with direct current ablation.Methods. Fifty-four patients who underwent attempted AV junction ablation with radiofrequency energy were followed up for a mean of 24 ± 8.4 months. These patients were retrospectively compared with 49 patients who underwent attempted AV junction ablation with direct current energy and were followed up for a mean of 41 ± 23 months.Results. The early success rate at the time of discharge for radiofrequency ablation was 81.5%, which was not statistically different from that for direct current ablation (85.7%). Fewer sessions were required to achieve complete AV block in the radiofrequency group (1.05 ± 0.23) (mean ± SD) compared with the direct current group (1.21 ± 0.41) (p = 0.02). Although overall complication rates were similar for both groups (9.3% in the radiofrequency group and 8.2% in the direct current group), there was a trend toward more life-threatening early complications in those patients who received direct-current shocks (6.8%) than in those who underwent radiofrequency ablation alone (2.3%) (p = 0.1). Early sudden death (one patient), early ventricular tachycardia (two patients) and cardiac tamponade (one patient) were seen only in those patients who underwent ablation with direct current energy, whereas pulmonary embolism (one patient) was the only early life-threatening complication in the radiofrequency group. During follow-up, the rate of recurrence of AV conduction was the same (5%) for both the direct current and radiofrequency groups. In the direct current group, one patient died suddenly 2 weeks after the procedure and another had a cardiac arrest due to ventricular tachycardia 6 h after the procedure. In the radiofrequency group, two patients died suddenly at 11 and 7 months, respectively. Two patients, one who had unsuccessful radiofrequency ablation and required direct current ablation, were resuscitated from ventricular tachycardia.Conclusions. Radiofrequency energy appears to be as efficacious as and perhaps safer than direct current energy for AV junction ablation.

Ventricular Tachycardia in an Isolated Guinea Pig Ventricular Free Wall Model of Ischemia and Reperfusion

Electrical activity from endo- and epicardium was recorded from isolated segments of right ventricular free walls of guinea pigs using standard differential microelectrode techniques and a high-gain electrocardiogram (ECG). Stimulation was applied to the endocardium. Tissues were exposed to ischemic conditions for 10 min and then were reperfused with "normal" Tyrode's solution. Early premature beats or rapid ventricular tachycardia (VT) occurred in 36% of hearts during "ischemia" and 79% of hearts on reperfusion. Endocardial activation was not significantly slowed by ischemic conditions or reperfusion. However, transmural conduction times increased, and muscle action potential durations decreased during ischemic conditions and early reperfusion. Rapid VT began with alternating activation of endo- and epicardium, and continuous low-voltage ECG activity bridging diastole. Activation of epicardium was essential for occurrence of early premature beats and rapid VT. Hyperkalemia during ischemia promoted arrhythmias during "ischemia," but not during reperfusion. Oscillatory afterpotentials (OAP) also occurred during reperfusion (36%), but not during "ischemia". Our study provides an isolated tissue model that reproducibly generates tachycardias, and that permits study of ischemia and reperfusion-induced transmembrane activity and defects in transmural conduction.

Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: Studies on the site of origin and mechanism

The electrophysiologic and arrhythmic properties of isolated infarcted right ventricle (RV) were studied in 17 dogs during the first 24 hours after complete occlusion of the right coronary artery (RCA). During the 16-to-20-hour post occlusion period, spontaneously occurring sustained monomorphic ventricular tachycardia (VT) was present in all 17 dogs. Overdrive ventricular pacing (cycle lengths 200 to 250 msec) caused significant suppression of the VT when the rate of the VT was slower than 150 bpm (range 120 to 145 bpm) (n = 9), but had negligible effect when VT rate was higher than 150 bpm (range 160 to 245 bpm (n = 8). Overdrive pacing could not terminate either the slow or the fast tpe of VT. Bipolar intramural electrograms have showed electrical activity in the infarcted RV zone to precede Q wave of the VT by 15.4 ± 5.8 msec regardless of VT rate. Microelectrode studies on isolated RV endocardial infarcted tissues 24 hours after RCA occlusions have shown the presence of spontaneous repetitive activity at a rate of 87 ± 47 bpm, which was overdrive suppressed in dogs with slow VT, and spontaneous activity at a rate of 115.2 ± 36 bpm ( p < 0.05) which was not overdrive suppressed in dogs with fast VT. Maximum diastolic potential, action potential amplitude, and Vmax of surviving subendocardial Purkinje fibers (SEPF) in the infarct zone were slightly but significantly depressed ( p < 0.05), and they manifested enhanced phase 4 depolarization, giving rise to automatic impulse initiation. Although action potential duration of these fibers was somewhat prolonged ( p < 0.05), no conduction delay occured. Histopathologic examinations have shown necrosis of the basal two thirds of the RV, with no left ventricular involvement. Electron microscopy revealed lipid accumulation in the surviving SEPF as the sole abnormality. We conclude (1) that occlusion of the RCA in the dog is associated with high survival rate despite extensive necrosis involving exclusively the RV and (2) that VT seen during the 20 to 24 hours after occlusion arise in the infarcted zone of the RV, by an enhanced automatic mechanism in the surviving SEPF, possibly caused by cytoplasmic lipid accumulation. This model, by virtue of its high survival rate and frequency of late VTs, should be useful in providing clues to determine factors involved in the genesis of early VT VF and for the evaluation of new pharmacologic agents during the 20- to 24-hour VT period.

Prolonged QT interval at onset of acute myocardial infarction in predicting early phase ventricular tachycardia

The prospectively assessed time course of changes in ventricular repolarization during acute myocardial infarction (AMI) is reported in 32 patients admitted 2.0 ± 1.8 (SD) hours after AMI onset. The initial corrected QT interval (QT c) upon hospitalization was longer (0.52 ± 0.07 seconds) in the 14 patients developing ventricular tachycardia (VT) within the first 48 hours as compared to QT c (0.47 ± 0.03 seconds) in the eight patients with frequent ventricular premature beats (VPBs) and to QT c (0.46 ± 0.03 seconds) in the 10 patients with infrequent VPBs ( p < 0.001; analysis of variance). By the fifth day after AMI onset, the QT c shortened significantly only in the VT group, suggesting a greater initial abnormality of repolarization in these patients. All 32 patients had coronary anglography, radionuclide ventriculography, and myocardial perfusion scintigraphy before hospital discharge. Significant discriminating factors related to early phase VT in AMI included initially longer QT and QT c intervals, faster heart rate, higher peak serum levels of creatine kinase, acute anterior infarction, anglographically documented proximal stenosis of the left anterior descending coronary artery, and scintigraphic evidence of hypoperfusion of the interventricular septum. Prior infarction, angina pectoris, hypertension, multivessel coronary artery disease, and depressed left ventricular ejection fraction did not provide discrimination among the three different ventricular arrhythmia AMI groups. We conclude that (1) the QT interval is frequently prolonged early in AMI, (2) the initial transiently prolonged ventricular repolarization facilitates and predicts complex ventricular tachyarrhythmias within the first 48 hours of AMI, (3) jeopardized blood supply to the interventricular septum frequently coexists, and (4) therapeutic enhancement of rapid recovery of the ventricular repolarization process merits investigation for prevention of VT in AMI.