Onset Of Ventricular Tachycardia Research Articles

Scaling Characteristics of Heart Rate Time Series Before the Onset of Ventricular Tachycardia

Ventricular tachycardia (VT) provokes sudden cardiac death (SCD), which is a major cause of mortality in developed countries. Implantable cardioverter-defibrillators (ICDs) are an efficient therapy for SCD prevention. In this study we analyze heart rate variability (HRV) in data stored by ICDs. In 29 patients exhibiting VT episodes, the last 1000 normal beat-to-beat intervals are analyzed and compared to an individually acquired control time series (CON). HRV analysis is performed with standard parameters of time and frequency domain as suggested by the HRV Task Force. For scaling analyses of heart rate time series, the fractal dimension is analysed, applying Higuchi's algorithm (HFD). Furthermore, detrended fluctuation analysis (DFA) is performed. None of the standard HRV parameters shows significant differences between CON and VT. Before the onset of VT, the scaling characteristics by means of HFD and DFA are significantly changed. In conclusion, scaling analysis reveals changes in autonomic heart rate modulation preceding VT.

The Magnitude of Sinus Cycle Length Change During Ventricular Tachycardia is Predictive of Successful Antitachycardia Pacing

Despite the wide use of antitachycardia pacing (ATP) in patients with implantable cardioverter defibrillators (ICDs), predictors of ATP success remain poorly understood. We hypothesize that the degree of sympathoexcitation, as measured by the sinus cycle length (SCL) shortening during ventricular tachycardia (VT), is a predictor of ATP success. The charts of 462 patients with dual-chamber ICDs were reviewed. A total of 88 events in 26 patients met the inclusion criteria and were analyzed. The mean SCL during the 4 seconds preceding the VT onset (SCL-baseline), and during the 4 seconds prior to ATP delivery (SCL-VT) was measured. The percent shortening in SCL was calculated as ((SCL-baseline) - (SCL-VT))/(SCL-baseline) x 100. Patients were classified into the ATP-success and ATP-failure groups depending on the VT(s) response to ATP. Using a t-test analogue for clustered data, patients in the ATP-success group exhibited a greater shortening in SCL when compared with the ATP-Failure group (5.8% compared to 4.7%, P = 0.007). The successful ATP events displayed an average SCL shortening of 6.0% compared to 1.8% in the unsuccessful ATP events (P = 0.029). When the events were analyzed, the sensitivity and specificity of a shortening in SCL of >10% in predicting ATP success were 0.29 and 1. We have shown that the SCL change during VT, a marker of the autonomic changes that accompany a tachycardia, is useful in predicting ATP success. Our findings suggest that analysis of the SCL during VT might play a role in future programming of ATP in patients with ICDs.

Triggers of Sustained Monomorphic Ventricular Tachycardia Differ Among Patients with Varying Etiologies of Left Ventricular Dysfunction

The mechanisms underlying the initiation of sustained ventricular tachycardia (VT) have not been fully elucidated. The extent to which reentry, abnormal automaticity, and triggered activity play a role in VT differs depending on the etiology of left ventricular dysfunction. By analyzing electrograms from implantable cardioverter defibrillator (ICD), we sought to determine whether there were differences in VT initiation patterns between patients with ischemic and nonischemic cardiomyopathy. We analyzed ICD electrograms in patients with ejection fractions < 40% who had sustained VT over a 27-month period. The trigger for VT onset was classified as a ventricular premature beat (VPB), supraventricular tachycardia, or of "sudden onset." The baseline cycle length, VT cycle length, coupling interval, and prematurity ratio were recorded for each event. The prematurity ratio was calculated as the coupling interval of the VT initiator divided by the baseline cycle length. Sixty-three VT events in 14 patients met the inclusion criteria. A VPB initiated the VT in 58 episodes (92%), 1 episode (2%) was initiated by a supraventricular tachycardia, and 4 episodes (6%) were sudden onset. The prematurity ratio was significantly higher (P < 0.05) in patients with ischemic cardiomyopathy (0.751 +/- 0.068) as compared to patients with nonischemic cardiomyopathy (0.604 +/- 0.139). VPBs initiated most sustained VT episodes. A significantly higher prematurity ratio was observed in the ischemic heart disease group. This may represent different mechanisms of VT initiation in patients with ischemic versus nonischemic heart disease.

Performance of Crucial Resuscitation Maneuvers during Simulated Pediatric Cardiopulmonary Arrests: The Effect of an Educational Intervention

BACKGROUND: Outcomes from in-hospital pediatric cardiopulmonary arrest remain bleak with only ∼ 24% of children surviving to one-year post-arrest. Timely initiation of basic and advanced life support is crucial to improving survival. Several studies have shown that pediatric residents feel uncomfortable in managing cardiopulmonary arrests, however there are few studies objectively assessing resident resuscitation skills. OBJECTIVE: 1) Document the proportion of pediatric residents that successfully defibrillate a human patient simulator within 3 minutes of simulated pulseless ventricular tachycardia (VT). 2) Compare the proportion that do so pre and post-educational intervention. METHODS: Prospective, before and after educational intervention study. In 2004, pediatric residents participated in individual mock codes at a tertiary care university using a high fidelity simulator. Each mock code included a standardized scenario of a conscious patient progressing to pulseless VT. Time to initiation of chest compressions, to the first defibrillation, and the proportion of residents successfully performing these maneuvers was evaluated. Following the 2004 sessions, deficiencies in resuscitation skills were identified. Monthly teaching sessions focused on leadership skills and timely initiation of ventilation, chest compressions and defibrillation were initiated. In 2005, the mock codes were repeated and the performance of the residents was compared pre and post educational intervention. RESULTS: In 2004, 72/80 (90%) and in 2005, 60/80 (75%) of pediatric residents participated in these individual mock codes. Level of training was similarly distributed each year. In 2004, 21/72 of pediatric residents failed to initiate or direct a nurse to initiate compressions on the “pulseless patient” during the entire 15 minute scenario vs. 4/60 in 2005, (29% vs. 7%; p = 0.002). Of the 21 residents who never did compressions in 2004, 14/21 (67%) recognized the patient was pulseless but eventually defibrillated, 6/21 (28%) defibrillated prior to checking a pulse and 1/21 (5%) never checked a pulse, started compressions or defibrillated. The mean time [+/- standard error] elapsed between onset of pulseless VT and initiation of compressions (substituting 15 minutes for those that never initiated compressions) decreased significantly: (2004: 365 [+/- 45 seconds] vs. 2005: 154 [+/- 30 seconds], p < 0.001). More residents failed to defibrillate the mannequin within 3 minutes of pulseless VT the first year, (2004: 35/72 (49%) failed vs. 2005: 23/60 (38%); p = 0.17). In addition, more residents were never able to able to successfully defibrillate the mannequin the first year, (2004: 4/72 (6%) failed vs. 2005: 0/60 (0%); p = 0.06). The mean time elapsed until successful defibrillation of VT in 2004 was 267 [+/- 25 seconds] vs. 2005: 186 [+/- 14], p = 0.006. CONCLUSION: At our institution, individual annual competency assessments were initiated in 2004. These mock codes revealed alarming deficiencies in resident resuscitation skills. Implementation of an educational intervention focused on identified deficiencies was associated with a higher likelihood of successfully performing crucial resuscitation maneuvers. Further research to determine whether improved ability to deliver high quality basic and advanced life support in a simulated setting translates to improved patient outcomes is warranted. Conflict of Interest: Authors indicated they have nothing to disclose.

Ventricular tachycardia and cardiac sarcoidosis: correspondence between MRI and electrophysiology

A 44-year-old woman with a history of histologically proved pulmonary and mediastinal sarcoidosis and chronic atrial fibrillation presented with palpitations followed by syncope. Clinical examination was normal except for arrhythmia and discrete swelling of the ankles. ECG showed the onset of ventricular tachycardia (VT) [ventricular rate 210 b.p.m. and left bundle branch block (BBB) contour and horizontal axis] with sudden hypotension and lipothymia leading to external defibrillation. Subsequent ECG tracings showed sinus rhythm (50 b.p.m.) and complete right BBB. Biology …

Canine model of paroxysmal atrial fibrillation and paroxysmal atrial tachycardia

Both autonomic nerve activity and electrical remodeling are important in atrial arrhythmogenesis. Therefore, dogs with sympathetic hyperinnervation, myocardial infarction (MI), and complete atrioventricular block (CAVB) may have a high incidence of atrial arrhythmias. We studied eight dogs (experimental group) with MI, CAVB, and sympathetic hyperinnervation induced either by nerve growth factor infusion (n = 4 dogs) or subthreshold electrical stimulation (n = 4 dogs) of the left stellate ganglion. Cardiac rhythm was continuously monitored by a Data Sciences International transmitter for 48 (SD 27) days. Three normal control dogs were also monitored. Six additional normal dogs were used for histology control. Paroxysmal atrial fibrillation (PAF) and paroxysmal atrial tachycardia (PAT) were documented in all dogs in the experimental group, with an average of 3.8 (SD 3) episodes/day, including 1.3 (SD 1.6) episodes of PAF and 2.5 (SD 2.2) episodes of PAT. The duration averaged 298 (SD 745) s (range, 7-4,000 s). There was a circadian pattern of arrhythmia onset (P < 0.01). Of 576 episodes of PAF and PAT, 236 (41%) episodes occurred during either sustained or nonsustained ventricular tachycardia (VT). Among these 236 episodes, 53% started before VT, whereas 47% started after the onset of VT. Normal dogs did not have either PAF or PAT. The hearts from the experimental group had a higher density of nerve structures immunopositive (P < 0.01) for three different nerve specific markers in both right and left atria than those of the control dogs. We conclude that the induction of nerve sprouting and sympathetic hyperinnervation in dogs with CAVB and MI creates a high yield model of PAF and PAT.

Detection of Repolarization Alternans With an Implantable Cardioverter Defibrillator Lead in a Porcine Model

Mechanistic links have been suggested between repolarization alternans (RPA) and the onset of ventricular tachycardia (VT) and/or fibrillation. Endocardial detection of RPA may, therefore, be an important step in future device-based treatments of arrhythmias. Here, we investigate if RPA could be detected during acute ischemia using an implantable cardioverter defibrillator (ICD) lead (tip to distal coil) located in the right ventricular apex. In 18 pigs, the right coronary (n = 10) or left anterior descending coronary (n = 8) artery was occluded for 10 min using a balloon catheter, followed by reperfusion for 30 min, and re-occlusion for 30 min. RPA magnitude, computed using the modified moving average (MMA) method, showed a sharp increase in all 18 animals, from a mean baseline level of 1.9 +/- 1.3 mV to 3.0 +/- 1.3 mV during first occlusion (p < 0.001). RPA magnitude showed a prominent increase in 10 animals during re-occlusion, from a mean baseline level of 1.7 +/- 1.0 mV to 3.3 +/- 1.5 mV (p < 0.001). The protocol was terminated during the first two stages of occlusion and reperfusion for the remaining 8 animals due to the occurrence of ventricular fibrillation (VF). These results confirm that RPA increases under ischemic conditions and that it is possible to detect and track RPA dynamics with an ICD lead that is positioned in a clinically realistic location. Such an approach may be useful in formulating improved arrhythmia detection and control algorithms.

795 Electrocardiogram after successful primary angioplasty: does it still matter?

@Background: elevated heart rate preceding the onset of ventricular tachycardia (VT), suggesting an increased sympathetic tone, has been reported to reduce the success of antitachycardia pacing (ATP) therapy in patients with implantable cardioverter defibrillators (ICD). Based on the data of the Variability Learned from Implantable Defibrillators (VALID) study, we aimed to assess the impact of autonomic tone on ATP effectiveness in ICD recipiens. Methods and results: a total of 36 out of 226 VALID-study patients implanted with a Biotronik ICD(Phylax XM or Microphylax+) were considred for the present sub-study. These devices have extended memory capacities (18000 RR intervals) that offerred the ability of analyzing heart rate variability (HRV) before the begening of the arrythmia. All the patients had ischemic heart disease. ATP programming was standardized within VT zones. During follow-up, 106 VTs recurred in these patients, 95 were terminated by ATP (ATP+) and ATP was unseccessful in 11 VTs (ATP-). HRV parameters were analyzed during the 30 minutes preceding VT onset. Two time- and three frequency-domain indices were derived semi-automatically: the standard deviation of normal RR intervals (SDNN), the proportion of adjacent normal RR intervals differing by > 50 ms (pNN50), the low-frequency (LF) power reflecting sympathetic tone, the high-frequency (HF) power reflecting parasympathetic activity, and the LF/HF power ratio. The following table summarizes the main

Sympathovagal Balance Prior to Onset of Repetitive Monomorphic Idiopathic Ventricular Tachycardia

Repetitive monomorphic idiopathic (RMI) ventricular tachycardia (VT) occurs typically in patients without structural heart disease, originates in most cases from the right ventricular outflow tract, and can often be induced by exercise or isoproterenol. This study analyzed the dynamic changes in autonomic tone immediately before the spontaneous onset of RMIVT using frequency-domain heart rate variability (HRV) indices. We analyzed the ambulatory electrocardiographic recordings from 6 men and 8 women (mean age: 43 +/- 18 years; mean number of VT runs per day: 134 +/- 213; mean VT rate: 194 +/- 40 bpm; median VT run length: 4 cycles) with RMIVT. A total of 36 clusters of nonsustained episodes of RMIVT preceded by >/=1 hour of sinus rhythm without VT were analyzed (25 minutes before the onset of RMIVT divided into five 5-minute periods; 8 minutes before onset of RIMVT divided into eight 1-minute periods). During 25 minutes preceding the onset of VT, the mean RR interval decreased from 767 +/- 118 to 723 +/- 105 ms (P = 0.015) and the low-frequency (LF)/high-frequency (HF) ratio increased from 2.24 +/- 0.79 to 2.49 +/- 1.0 (P = 0.03). During the 8 minutes before VT onset, the mean RR interval decreased from 745 +/- 118 to 718 +/- 102 ms (P = 0.001) and the LF components increased from 205 +/- 72 to 253 +/- 113 ms (P = 0.014). No change in HF components was observed during the 25 or 8 minutes periods preceding the RMIVT onset. The changes in HRV indices suggest a strong time-dependent primary activation of sympathetic tone prior to the occurrence of RMIVT. Withdrawal of vagal tone does not appear essential to the initiation of RMIVT clusters.

CLOSTRIDIUM TETANUS INFECTION IN 13 DOGS AND ONE CAT

Clostridium tetani infection is uncommon in dogs and cats. Up to this point in time just single case reports have been published in veterinary medicine. The goal of this retrospective study was to describe the clinical features and outcome of 13 dogs and one cat affected with Clostridium tetani. The medical records of the last ten year were reviewed. Dogs and cats that were identified as being infected with Clostridium tetani on the basis of characteristic clinical signs and/or bacterial culture from infected wounds were eligible for study inclusion. Thirteen dogs and one cat met the criteria for study inclusion. Six different breeds and mix‐breed dogs were affected, German Shepherd dogs (n=4, 29%) and Labrador retriever (n=3, 21%) were the most frequently affected breeds. Observed clinical complications were ventricular aspiration pneumonia (n=7), laryngeal spasm (n=6), hypersalivation (n=4), ventricular tachycardia (n=3), and third degree AV block (n=1). Median days from onset of clinical signs until first signs of improvement were 10 days (range: 9–12 days). Median hospitalisation time was 18 days (range: 14–22 days). Six animals showed full recovery and 8 animals died or were euthanized. Death was associated with acute onset of ventricular tachycardia in 2 dogs, 1 dog died with non‐responsive third degree AV‐block, 3 dogs died after developing aspiration pneumonia, and 1 dog died of unknown causes.

Forecasting of Life Threatening Arrhythmias Using the Compression Entropy of Heart Rate

Ventricular tachycardia (VT) provoking sudden cardiac death (SCD) are a major cause of mortality in the developed countries. The most efficient therapy for SCD prevention are implantable cardioverter defibrillators (ICD). In this study heart rate variability (HRV) measures were analyzed for short-term forecasting of VT in order to improve VT sensing and to enable a patient warning of forth-coming shocks. The last 1000 normal beat-to-beat intervals before 50 VT episodes stored by the ICD were analyzed and compared to individually acquired control time series (CON). HRV analysis was performed with standard parameters of time and frequency domain as suggested by the HRV Task Force and furthermore with a newly developed and optimized nonlinear parameter that assesses the compression entropy of heart rate (Hc). Except of meanNN (p = 0.02) we found no significant differences in standard HRV parameters. In contrast, Hc revealed highly significant (p = 0.007) alterations in VT compared with CON suggesting a decreased complexity before the onset of VT. Compression entropy might be a suitable parameter for short-term forecasting of life-threatening tachycardia in ICD.

Effect of elevated heart rate preceding the onset of ventricular tachycardia on antitachycardia pacing effectiveness in patients with implantable cardioverter defibrillators

The incorporation of antitachycardia pacing (ATP) into implantable cardioverter defibrillators (ICDs) has provided a better tolerated alternative to shocks. ATP has been shown to be effective in terminating approximately 80% to 90% of spontaneous ventricular tachycardia (VT) episodes. Although ATP is routinely used, little is known about predictors of ATP failure. Based on the evaluation of stored electrograms, we aimed to prospectively follow patients with ICDs, and to analyze parameters affecting ATP effectiveness. One hundred eighteen consecutive patients received ICDs for standard indications. Before discharge, empirical, standardized ATP therapy was programmed in all patients within VT zones. A total of 1,218 spontaneous tachycardia episodes occurred in 51 patients during a mean follow-up of 24.5 ± 12 months. Among these, 888 VTs were diagnosed. One hundred four fast VTs were detected in the ventricular fibrillation zone and treated with primary shock delivery. ATP was attempted 881 times in the remaining 784 VT episodes. ATP terminated 640 VTs successfully, ATP failed in 55 VTs finally reverted by shocks, and 89 VTs converted to a slower VT outside the VT zone. Fifty-one of these slower VTs reverted spontaneously, and 38 were redetected and treated. Finally, in primary intention-to-treat basis, ATP was successful in 691 VTs (88%) and unsuccessful in 93 VTs (12%). There was no influence of VT cycle length on ATP success rate. Furthermore, ATP efficacy was similar between patients with left ventricular ejection fraction ≤35% or >35%, between daytime and nighttime, as well as between patients with ischemic or nonischemic cardiomyopathy. A faster heart rate immediately preceding the onset of VT (103 ± 19 vs 78 ± 14 beats/min, respectively, hazard ratio 4.08, 95% confidence interval 2.11 to 7.89, p <0.001), and absence of β-blocker therapy (82% vs 93%, respectively, hazard ratio 2.71, 95% confidence interval 1.72 to 4.29, p = 0.02) were found, by Cox proportional-hazard analysis, to be the sole independent predictors of ATP ineffectiveness in ICD recipients. Thus, the present study identified both preceding sinus tachycardia (reflecting an increased sympathetic tone) and lack of β-blocker use as independent risk factors for reduced success of ATP therapy in terminating VT. Therefore, modification of sympathetic tone may be beneficial for patients with ICDs.

Circadian variation in ventricular tachycardia and atrial fibrillation in a medical-cardiological ICU.

To assess the diurnal distribution of ventricular tachycardia (VT) and atrial fibrillation (AF) in critically ill patients. Prospective observational study (episode-based design) in an eight-bed medical/cardiological ICU at a university hospital that also admits postoperative patients. 98 consecutive patients with AF ( n=55) or ventricular tachycardia ( n=43). There were a total of 218 arrhythmia episodes (83 AF, 136 VT). The time of arrhythmia onset was not evenly distributed. Circadian variation in VT but not AF onset was well represented by a sine wave function. Both VT and AF fibrillation showed a trough during the night. The distribution of VT and AF episodes did not differ significantly with or without analgosedation. In critically ill patients the onset of VT and AF over 24-h is nonuniformly distributed. In VT this circadian pattern of occurrence is well modeled by a sine wave function peaking between noon and 2 p.m. The circadian pattern is less clear for AF. The circadian variation is seen irrespective of the presence of absence of analgosedation for both arrhythmias.

Sustained ventricular tachycardia as a marker of inadequate myocardial perfusion during the acute phase of myocardial infarction.

Sustained ventricular tachycardia (VT) complicating the acute phase of myocardial infarction (AMI) is a quite rare event but with short-term unfavorable prognosis. The clinical characteristics as well as the therapeutic implications have not yet been well defined. This paper attempts to prove that VT may be considered a marker of inadequate myocardial perfusion after thrombolysis. To assess the clinic-electroangiographic characteristics and prognosis of patients with VT occurring within the first 4 days of an AMI, a case-control study was carried out in 23 patients from a total of 1,100 patients (1.9%) hospitalized with AMI between March 1993 and July 1997. These patients were compared with a control group of 131 patients hospitalized consecutively. A statistical analysis was made using the chi-square test, t-test, and logistic regression. There were no differences among groups with regard to age, gender, and area of necrosis. Average time for the onset of VT was 26 h (range 0-92 h). Sixteen patients underwent coronary angiography: 4 patients had left main coronary artery disease, 2 had single-vessel disease, 8 had lesions in two vessels, and 2 had triple-vessel disease. Univariate analysis showed that patients with VT had a higher incidence of creatine phosphokinase (CPK)-MB peak > 300 UI/l (61 vs. 30%; p<0.001), more frequent occurrence of previous AMI (48 vs. 17%; p<0.001), and acute intraventricular conduction disorders (26 vs. 4%; p<0.001). Furthermore, these patients suffered ischemia previous to VT more frequently (65 vs. 11%; p<0.0001), and had a greater mortality rate than that in the control group (35 vs. 4%; p<0.0001). In the multivariant analysis, the variables related to the occurrence of VT were CPK-MB peak > 300 IU/l (OR 5.9; 95% CI 1.6-21), acute intraventricular conduction disorders (OR 9.02; 95% CI 1.7-48), and ischemia immediately prior to VT (odds ratio [OR] 19.64; 95% confidence interval [CI] 5.3-73). Ventricular tachycardia may be considered a marker of inadequate myocardial perfusion after thrombolysis; therefore, a more aggressive revascularization treatment in these patients would be advisable. The profile of patients with AMI, hospitalized in the coronary care unit, who will likely suffer from VT is previous AMI, CPK-MB peak > 300, acute intraventricular conduction disorders, Killip > I, and ischemia previous to VT.

Heart rate variability before the onset of ventricular tachycardia: differences between slow and fast arrhythmias

Background: We tested whether or not heart rate variability (HRV) changes can serve as early signs of ventricular tachycardia (VT) and predict slow and fast VT in patients with an implantable cardioverter defibrillator (ICD). Methods and results: We studied the ICD stored 1000 beat-to-beat intervals before the onset of VT (131 episodes) and during a control time without VT (74 series) in 63 chronic heart failure ICD patients. Standard HRV parameters as well as two nonlinear parameters, namely ‘Polvar10’ from symbolic dynamics and the finite time growth rates ‘Fitgra9’ were calculated. Comparing the control and the VT series, no linear HRV parameter showed a significant difference. The nonlinear parameters detected a significant increase in short phases with low variability before the onset of VT (for time series with less than 10% ectopy, P<0.05). Subdividing VT into fast (cycle length ≤270 ms) and slow (>270 ms) events, we found that the onset of slow VT was characterized by a significant increase in heart rate, whereas fast VT was triggered during decreased heart rates, compared to the control series. Conclusions: Our data may permit the development of automatic ICD algorithms based on nonlinear dynamic HRV parameters to predict VT before it starts. Furthermore, they may facilitate improved prevention strategies.

T wave alternans as a predictor of spontaneous ventricular tachycardia in a canine model of sudden cardiac death.

We recently developed an ambulatory canine model of spontaneous ventricular tachycardia (VT) and sudden cardiac death by creating myocardial infarction, complete AV block, and infusion of nerve growth factor to the left stellate ganglion. Whether or not T wave alternans is associated with the spontaneously occurring episodes of VT in our model was unclear. Through intracardiac electrograms obtained from an implantable cardioverter defibrillator, we manually measured T wave amplitudes prior to VT and while the dogs were at rest (baseline, no VT). Of the 79 VT episodes analyzed, 28 (35.4%) exhibited repolarization alternans. In contrast, only 3 (4.7%) of 64 baseline data cases displayed alternans (P < 0.0001). The magnitude of T wave alternans for dogs that died of sudden cardiac death, dogs that did not die suddenly, and for the total 28 episodes that exhibited repolarization alternans were 4.8 +/- 2.8 mm, 4.9 +/- 3.5 mm, and 4.9 +/- 3.3 mm, respectively (P = NS). We also found the sensitivity, specificity, positive predictive value, negative predictive value, and relative risk of repolarization alternans in predicting VT to be 35.4%, 95.3%, 90.3%, 54.5%, and 1.98, respectively. The ventricular rate prior to VT (65 +/- 11 beats/min) was significantly higher than that at rest (49 +/- 12 beats/min; P < 0.0001). T wave alternans often occurred immediately before the onset of VT in dogs with myocardial infarction, complete AV block, and nerve growth factor infusion to the left stellate ganglion. Increased sympathetic activity might be responsible for the occurrence of the T wave alternans.

K(ATP) channel opening during ischemia: effects on myocardial noradrenaline release and ventricular arrhythmias.

Cardioprotection by K(ATP) channel openers during ischemia is well documented although ill understood. Proarrhythmic effects may be an important drawback. K(ATP) channel modulation influences neurotransmitter release during ischemia in brain synaptosomes. Therefore, we studied the effects of K(ATP) channel modulation on myocardial noradrenaline release and arrhythmias in ischemic rabbit hearts. Isolated rabbit hearts were perfused according to Langendorff and stimulated. Local electrograms were recorded and K+-selective electrodes were inserted in the left ventricular free wall. Cromakalim (3 microM) or glibenclamide (3 microM) was added 20 min prior to induction of global ischemia. After 15, 20, or 30 min of ischemia, hearts were reperfused and noradrenaline content of the first 100 ml of reperfusate was measured. Cromakalim (n = 16) prevented the second rise of extracellular [K(+)] in accordance with its cardioprotective effect. Cromakalim significantly reduced noradrenaline release after 15 min (mean, 169 +/- SEM 97 pmol/gr dry weight vs. control 941 +/- 278; p < 0.05) and 20 min of ischemia (230 +/- 125 pmol/gr dry wt vs. control 1,460 +/- 433; p < 0.05), but after 30 min of ischemia, the difference in noradrenaline release was no longer significant (cromakalim 2,703 +/- 1,195 pmol/gr dry wt vs. control 5,413 +/- 1,310; p = 0.08). Ventricular fibrillation or ventricular tachycardia occurred in 10 of 13 control hearts (77%) (n = 19), in six of 10 glibenclamide-treated hearts (60%) (n = 15), and in six of 14 cromakalim-treated hearts (43%) (p = NS). Cromakalim significantly accelerated onset of ventricular tachycardia or fibrillation (mean +/- SEM onset after 12.5 +/- 1.6 min ischemia vs. control 16.2 +/- 0.7 min; p < 0.05). Noradrenaline release occurred only in cromakalim-treated hearts with early-onset arrhythmias whereas no noradrenaline release was observed in cromakalim-treated hearts without ventricular tachycardia or fibrillation. Our results show that activation of the K(ATP) channel by cromakalim during ischemia reduces myocardial noradrenaline release and postpones the onset of irreversible damage, contributing to the cardioprotective potential of K(ATP) openers during myocardial ischemia.

Sustained ventricular tachycardia in children after repair of congenital heart disease.

To investigate an association between surface electrocardiographic (ECG) parameters and sustained ventricular tachycardia (VT) in children after repair of congenital heart disease (CHD), data were obtained and analyzed in three groups (group I, 7 postoperative patients with episode of sustained VT (4 tetralogy of Fallot (TOF), 2 double outlet right ventricle (DORV), 1 truncus arteriosus); group II, 14 children with postoperative TOF not associated with VT; group III, 14 normal children). Mean age at the onset of sustained VT was 129+/-77 months (range 60-232); mean age at corrective surgery, 44+/-33 months (range 10-102); mean follow-up period after surgery, 84+/-74 months (range 20-185); the duration from repair to the onset of sustained VT, range 1-185 months. Compared to group II and III, group I showed longer QRS duration (group I, 137+/-10 msec; group II, 114+/-22 msec; group III, 65+/-12 msec) and shorter corrected J to Tmax interval (group I, 209+/-24 msec; group II, 272+/-44 msec; group III, 249+/-18 msec). QT and corrected QT, J to Tmax interval, and their dispersions in group I and II are significantly different from those of group III. In conclusion, QRS duration and corrected J to Tmax interval could be helpful to predict ventricular tachycardia in postoperative CHD.

Anti-arrhythmic effects of levcromakalim in the ischaemic rat heart: a dual mechanism of action?

The action of pharmacological openers of K ATP channels depends on the availability and levels of various intracellular nucleotides. Since these are subject to change during myocardial ischaemia, K ATP channel openers may affect ischaemic and non-ischaemic tissue differentially. Using a recently developed dual coronary perfusion method, we investigated the effects on arrhythmias of the prototypical K ATP channel opener levcromakalim when applied selectively to ischaemic and/or non-ischaemic tissue. A novel perfusion cannula was used to independently perfuse the left and right coronary beds of hearts isolated from rats. Selective infusion of levcromakalim (3, 10 or 30 μM) into the left coronary bed in the absence of ischaemia did not induce ventricular arrhythmias. Regional zero-flow ischaemia was induced by cessation of flow to the left coronary bed and hearts received levcromakalim selectively into either the left, right, or both coronary beds. When applied selectively to the ischaemic left coronary bed, levcromakalim (3, 10 or 30 μM; n=10/group) delayed the onset of ventricular tachycardia in a dose-dependent manner (by 21*, 43* and 112%* at 3, 10 and 30 μM; * P<0.05 vs. control). When applied only to the non-ischaemic right coronary bed, levcromakalim reduced the incidence of ventricular tachycardia during later phases of ischaemia (from 100% in controls to 30%*). When present in both coronary beds, levcromakalim had a striking anti-arrhythmic effect — the overall incidence of ventricular tachycardia being reduced from 100% in controls to 20%*. We conclude that levcromakalim may have an anti-arrhythmic effect when applied either to ischaemic or non-ischaemic tissue but that the mechanisms may differ depending on the metabolic state of the heart.

Idiopathic ventricular tachycardia in infancy and childhood: A multicenter study on clinical profile and outcome

OBJECTIVESThe present study intended to evaluate the clinical profile and outcome in a large cohort of pediatric patients with idiopathic ventricular tachycardia (VT).BACKGROUNDVentricular tachycardia (VT) without underlying heart disease is rare in childhood. Limited information is available with regard to outcome and indications for long-term antiarrhythmic treatment.METHODSA retrospective multicenter study was conducted. Patient data were obtained from the individual centers using a standardized questionnaire.RESULTSNinety-eight pediatric patients with episodes of VT in the absence of structural heart disease were included. Mean age at first manifestation of the arrhythmia was 5.4 years (range 0.1 to 15.1), with 27% of the patients having had VT already in infancy. Clinical symptoms or echocardiographic signs of left ventricular dysfunction were observed initially in 36% of the patients, of which one third (12% of the whole population) presented with severe symptoms (heart failure or syncope). After a mean follow-up of 47 months (range 12 to 182), no patient had died. Twenty-five patients had never been treated with antiarrhythmic drugs. Sixty-three patients were free of VT and did not take antiarrhythmic drugs at last follow-up. Prognosis was better when VT occurred during the first year of life (VT resolution in 89%) compared with VT occurrence beyond the first year of life (VT resolution in 56%: p < 0.01). The clinical profile was more favorable for patients with presumed right VT (VT resolution in 76%, symptoms in 25% of patients) compared with patients with presumed left VT, where VT resolution occurred in 37% and symptoms in 67% of patients (p < 0.01).CONCLUSIONSVT in children with a normal heart carried a good prognosis. Outcome was better after onset of VT during infancy and when VT originated in the right ventricle. A restrictive use of antiarrhythmic agents might be justified in a large proportion of these patients.