Episodes Of Polymorphic Ventricular Tachycardia Research Articles

P5-111: Induction of torsades de pointes in association with epidural administration of bupivacaine

We report two cases of torsades de pointes (TdP) in association with epidural analgesia with bupivacaine (BUP). The first patient was a 36-year-old man who underwent surgical repair of an incarcerated hiatal hernia and gastric perforation, complicated by hepatic and renal impairment and mild electrolyte imbalance which was promptly corrected. During the postoperative course, shortly after administration of epidural BUP, he developed QRS widening and QT prolongation with recurrent episodes of polymorphic ventricular tachycardia and TdP.

Brugada and long QT-3 syndromes: two phenotypes of the sodium channel disease.

Brugada and long QT-3 syndromes are two allelic diseases caused by different mutations in SCN5A gene inherited by an autosomal dominant pattern with variable penetrance. Both of these syndromes are ion channel diseases of the heart manifest on surface electrocardiogram by ST-segment elevation in the right precordial leads and prolonged QT(c) interval, respectively, with predilection for polymorphic ventricular tachycardia and sudden death, which may be the first manifestation of the disease. Brugada syndrome usually manifests during adulthood with male preponderance, whereas long QT3 syndrome usually manifests in teenage years, although it can also manifest in adulthood. Class IA and IC antiarrhythmic drugs increase ST-segment elevation and predilection for polymorphic ventricular tachycardia and ventricular fibrillation in Brugada syndrome, whereas these agents shorten the repolarization and QT(c) interval, and thus may be beneficial in long QT-3 syndrome. Beta-blockade also increases the ST-segment elevation in Brugada syndrome but decreases the dispersion of repolarization in long QT-3 syndrome. Mexiletine, a class IB sodium channel blocker decreases QT(c) interval as well as dispersion of repolarization in long QT-3 syndrome but has no effect on Brugada syndrome. The only effective treatment available at this time for Brugada syndrome is implantable cardioverter defibrillator, although repeated episodes of polymorphic ventricular tachycardia can be treated with isoproterenol. In symptomatic patients of long QT-3 syndrome in whom the torsade de pointes is bradycardia-dependent or pause-dependent, a pacemaker could be used to avoid bradycardia and pauses and an implantable cardioverter defibrillator is indicated where arrhythmia is not controlled with pacemaker and beta-blockade. However, the combination of new devices with pacemaker and cardioverter-defibrillator capabilities appear promising in these patients warranting further study.

Brugada syndrome with atypical ECG: downsloping ST-segment elevation in inferior leads

We present an unusual case of a young Thai immigrant, symptomatic, who had suffered prior episodes of syncope with strong family background: male, first-degree relatives, younger than 45 years old who had died suddenly. The rest ECG, with the patient asymptomatic at the time, showed persistent ST-segment elevation, in inferior leads and “mirror” image in the anterior wall, which were not modified with sublingual nitrates, in absence of demonstrable structural heart disease by chest X-rays and echocardiogram, hypothermia, ischemia, or electrolytic disorders. Holter monitoring revealed at dawn, a short episode of polymorphic ventricular tachycardia of short onset extrasystole coupling, which evolved into asystole and sudden cardiac death. We believe this is a sudden unexplained death syndrome, although we did not have a chance to conduct a genetic study.

Transmural electrophysiological heterogeneities underlying arrhythmogenesis in heart failure.

Although expression of numerous ion channels is altered in heart failure (HF), mechanisms by which dysfunction at the ionic and molecular levels lead to ventricular tachyarrhythmias in HF are unknown. Previously, we found that transmural heterogeneities of repolarization play a critical role in the genesis of polymorphic ventricular tachycardia (PVT) when QT interval was prolonged in LQT2. Because QT interval is also prolonged in HF, we hypothesized that transmural heterogeneities are a mechanism of PVT in HF. Optical action potentials were measured simultaneously from cells spanning the entire transmural wall of arterially perfused canine wedge preparations. Wedges were isolated from dogs without (control, n=5) and with HF (n=8) produced by rapid ventricular pacing. In HF, action potential duration (APD) prolongation was markedly heterogeneous across the transmural wall, and was characterized by disproportionate APD prolongation of midmyocardial (M) cells. APD prolongation of M cells accounted for QT-interval prolongation, and caused significant increases (P<0.01) in spatial gradients of repolarization across the ventricular wall from 4.3+/-2.1 (control) to 12.4+/-3.5 ms/mm (HF). Enhanced gradients were directly responsible for development of functional conduction block, leading to PVT in 63% of HF wedges but in no controls (P<0.03). Moreover, intramural decremental conduction and block of the premature impulse, preceded each episode of PVT, and always occurred at the border between M-cell and subepicardial zones, where repolarization gradients were highest. Selective prolongation of APD within M cells underlies several key features of the HF phenotype, including QT-interval prolongation, transmural heterogeneity of repolarization, and susceptibility to conduction block and reentrant PVT.

Polymorphic Reentrant Ventricular Tachycardia in the Isolated Rabbit Heart Studied by High-Density Mapping

The role of dispersion of refractoriness and reentry for the genesis of polymorphic ventricular tachycardia (VT) has recently become emphasized. We investigated the mechanisms of polymorphic arrhythmias in a 2D preparation confining an area of prolonged refractoriness. In 16 Langendorff-perfused rabbit hearts, a sheet of left ventricular epicardium was obtained by a cryoprocedure. Enhanced spatial heterogeneity in a refractory period was created by cooling a central region (diameter=12 mm). This markedly prolonged the refractory period (by 36+/-14 ms) inside but only slightly prolonged it (by 5+/-11 ms) outside the cooled area (n=6). During a control procedure, programmed stimulation with up to 3 premature stimuli induced an episode of monomorphic VT in only 1 of 10 hearts. During regional cooling, episodes of polymorphic VT with a maximum duration of 35 seconds could be induced in all hearts. High-resolution mapping (229 electrodes) of epicardial activation revealed that polymorphic VT was caused by a functional reentrant circuit located partially within the region of prolonged refractoriness. The reentrant wavefront was continuously shifting along the border of the cooled region, resulting in beat-to-beat changes in the excitation pattern. Spontaneous termination of polymorphic VT occurred either by a shift of the reentrant circuit outside the cooled region or by a block in the central common pathway during figure-of-8 reentry in the region of prolonged refractoriness. A shifting functional reentrant circuit was the underlying mechanism of polymorphic VT in a substrate of enhanced spatial heterogeneity of refractoriness.

Taquicardia ventricular inducible en un paciente con síncope recurrente tras operación de Senning

A 17 year old man with transposition of the great vessels who had two episodes of late recurrent syncope following Senning repair 2 months before hospital registration. One episode required basic cardiopulmonary reanimation. Holter monitoring documented isolated polytopic and coupled ventricular extrasystoles. Programmed left ventricular pacing induced polymorphous ventricular tachycardia, which converted to monomorphic sustained ventricular tachycardia after intravenous procainamide. A cardioverter defibrillator was implanted in left ventricle by intravenous approach. Twelve months later the patient presented an episode of polymorphic ventricular tachycardia and one appropriate therapy from the defibrillator discharge was done.

Fetus with long QT syndrome manifested by tachyarrhythmia: a case report

We encountered a fetus who exhibited transient (at most 30 s), repeated episodes of tachyarrhythmia (240 bpm). This female neonate was born at 36 weeks of gestation and showed a markedly prolonged QT interval and transient, repeated episodes of polymorphic ventricular tachycardia. Congenital long QT syndrome was diagnosed. Retrospective analysis of the videotape showing fetal cardiac movement revealed that atrio-ventricular dissociation was present prenatally and thus, the fetal tachyarrhythmia was due to ventricular tachycardia. To our knowledge, there are few reports of a fetus with the long QT syndrome who exhibited ventricular tachycardia in utero. In the presence of unexplained fetal tachyarrhythmia, long QT syndrome should be considered as a possible underlying cause disorder. The presence of atrio-ventricular dissociation may be useful in prenatal diagnosis of long QT syndrome.

Short‐and Long‐Term Performance of a Tripolar Down‐Sized Single Lead for Implantable Cardioverter Defibrillator Treatment: A Randomized Prospective European Multicenter Study

A new, thinner (10 Fr) and more flexible, single-pass transvenous endocardial ICD lead, Endotak DSP, was compared with a conventional lead, Endotak C, as a control in a prospective randomized multicenter study in combination with a nonactive can ICD. A total of 123 patients were enrolled, 55 of whom received a down-sized DSP lead. Lead-alone configuration was successfully implanted in 95% of the DSP patients vs 88% in the control group. The mean defibrillation threshold (DFT) was determined by means of a step-down protocol, and was identical in the two groups, 10.5 +/- 4.8 J in the DSP group versus 10.5 +/- 4.8 J in the control group. At implantation, the DSP mean pacing threshold was lower, 0.51 +/- 0.18 V versus 0.62 +/- 0.35 V (p < 0.05) in the control group, and the mean pacing impedance higher, 594 +/- 110 omega vs 523 +/- 135 omega (p < 0.05). During the follow-up period, the statistically significant difference in thresholds disappeared, while the difference in impedance remained. Tachyarrhythmia treatment by shock or antitachycardia pacing (ATP) was delivered in 53% and 41%, respectively, of the patients with a 100% success rate. In the DSP group, all 28 episodes of polymorphic ventricular tachycardia or ventricular fibrillation were converted by the first shock as compared to 57 of 69 episodes (83%) in the control group (p < 0.05). Monomorphic ventricular tachycardias were terminated by ATP alone in 96% versus 94%. Lead related problems were minor and observed in 5% and 7%, respectively. In summary, both leads were safe and efficacious in the detection and treatment of ventricular tachyarrhythmias. There were no differences between the DSP and control groups regarding short- or long-term lead related complications.

Torsades de pointes following radiofrequency catheter His ablation

A case of polymorphic ventricular tachycardia torsade de pointes type, appearing in a 70-year-old female following radiofrequency catheter His ablation, is presented. The substrate was slow rate with ventricular bigeminy and QT prolongation which appeared after ablation. The same phenomenon reappeared after permanent VVIR pacemaker implantation with a basal rate of 55 beats/min. One episode of polymorphic ventricular tachycardia deteriorated into ventricular fibrillation, requiring a 360-J DC shock. Raising the pacemaker rate to 80 beats/min abolished the arrhythmias.

Bradycardia‐Induced Polymorphic Ventricular Tachycardia After Atrioventricular Junction Ablation for Sinus Tachycardia‐Induced Cardiomyopathy

In a patient with severe left ventricular dysfunction resulting from chronic nonparoxysmal sinus tachycardia, rate control and improvement in left ventricular function were achieved with atrioventricular junction ablation and ventricular pacemaker implantation. Within 12 hours after the ablation procedure, several episodes of polymorphic ventricular tachycardia that may have been triggered by the abruptly decreased heart rate occurred. Recurrence of polymorphic ventricular tachycardia was prevented by an increase in pacing rate.

Sudden cardiac death and polymorphous ventricular tachycardia in pationts with normal QT intervals and normal systolic cardiac function

This study delineates the clinical spectrum of 15 patients with polymorphic ventricular tachycardia and normal QT intervals in the absence of apparent structural heart disease, adverse drug effects, or electrolyte disturbances. Patients presented with either palpitations (n = 2), presyncope (n = 5), syncope (n = 4), no symptoms (n = 1), or aborted sudden death (n = 3). Mean age was 41 years (range 20 to 64), and mean follow-up 38 months (range 4 to 109). Left ventricular function was normal as determined by either echocardiogram (n = 9) or left ventriculography (n = 9). Episodes of polymorphic ventricular tachycardia (VT) were analyzed in terms of the preceding interval, and the relation of the initiating coupling interval to the QT interval (coupling interval/QT interval = polymorphic VT index). The mean QT for the group as a whole was 0.41 +/- 0.02 second. Patients could be separated into 3 distinct groups. Four patients had polymorphic VT reproducibly induced by exercise and initiated by late-coupled beats (mean polymorphic VT index 1.27 +/- 0.21). Isoproterenol induced polymorphic VT in 3 of 4 patients, and all 4 responded to chronic beta blockade. Two patients had polymorphic VT during episodes of coronary artery spasm, and both responded to calcium channel blockade. Polymorphic VT unrelated to exertion or coronary vasospasm occurred in 9 patients. Tachycardia onset was initiated by closely coupled beats (mean polymorphic VT index 0.95 +/- 0.16), and was preceded by a pause in 4 patients, and no pause in 5 patients. Sudden death occurred in 5 of 9 patients with the shortest polymorphic VT indexes.(ABSTRACT TRUNCATED AT 250 WORDS)

944-116 Focal Activation Patterns of Cesium Chloride Induced Torsades-de Pointes Tachycardias

‘Torsades-de-pointes’ tachycardias are probably initiated by early after depolarizations causing triggered activity. Whether successive beats with their constantly changing amplitude and axis result from focal or reentrant mechanisms has not yet been elucidated. Three dimensional mapping was carried out in 4 beagle dogs with polymorphic ventricular tachycardia (PVT) induced by repetitive (every 10 minutes) doses of cesium chloride (CsCI, 1 mmo/lkg i.v.). Bradycardia was produced by radiofrequency ablation of the AV node. Bipolar left and right ventricular electrograms were simultaneously recorded from 240 endo-, epi- and intramyocardial sites through 60 pins containing 4 bipolar electrodes each (interelectrode distance 2 mm, distance between pins 10–15 mm). One (3 dogs) or two (1 dog/ doses of CsCI produced various episodes of PVT, nine of which were analyzed (6.8 ± 2.7 consecutive beats). PVT originated from various left (n = 3) or right (n = 6) ventricular endocardial sites. Slow conduction or conduction block was not evident, total ventricular activation time during consecutive beats was 75 ± 12 msec. Initiation and continuation of PVT appeared to be exclusively due to focal mechanisms. Three different activation patterns were observed: (1) Changing foci from beat to beat, with variable coupling intervals (n = 2); (2) Two competing endocardial foci firing at variable rates (n = 3); (3) Periodically changing foci, replacing each other after gradual slowing of respective intrinsic rates (n = 4) Compatible with triggered activity elicited in Purkinje fibers, CsCI induced PVT demonstrate a focal activation pattern with an endocardial site of earliest activation. Local foci may initially speed up and then slow down in rate. Competing foci apparently rather trigger than suppress activation of each other

Results and efficiency of programmed ventricular stimulation with four extrastimuli compared with one, two, and three extrastimuli.

Conventional programmed ventricular stimulation protocols are inefficient compared with more recently proposed protocols. The purpose of the present study was to determine if additional efficiency could be derived from a 6-step programmed ventricular stimulation protocol that exclusively uses four extrastimuli. The subjects were 209 consecutive patients with coronary artery disease and documented sustained monomorphic ventricular tachycardia, nonsustained ventricular tachycardia, aborted sudden death, or syncope. These patients underwent 159 electrophysiological tests in the absence of antiarrhythmic drug therapy and 105 electrophysiological tests in the presence of antiarrhythmic therapy. Programmed stimulation was performed with two protocols in random order in each patient. Both protocols used an eight-beat drive train, 4-s intertrain pause, and basic drive cycle lengths of 350, 400, and 600 ms. The 6-step protocol started with coupling intervals of 290, 280, 270, and 260 ms, which were shortened simultaneously in 10-ms steps until S2 was refractory. The 18-step protocol used one, two and three extrastimuli in conventional sequential fashion. The end points were 30 s of sustained monomorphic ventricular tachycardia, two episodes of polymorphic ventricular tachycardia requiring cardioversion, or completion of the protocol at two right ventricular sites. There was no significant difference in the yield of sustained monomorphic ventricular tachycardia using the two protocols, regardless of the clinical presentation or treatment with antiarrhythmic drugs. Polymorphic ventricular tachycardia occurred with the 18-step protocol twice as frequently as with the 6-step protocol (6% versus 3%, P < .001). The duration of the 18-step protocol was significantly longer than that of the 6-step protocol in patients with inducible ventricular tachycardia (5.5 +/- 7 versus 2.3 +/- 2 minutes, P < .001), as well as in patients without inducible ventricular tachycardia (25.4 +/- 7 versus 6.9 +/- 2 minutes, P < .001). A stimulation protocol that exclusively uses four extrastimuli improves the specificity and efficiency of programmed ventricular stimulation without compromising the yield of monomorphic ventricular tachycardia in patients with coronary artery disease.

Siblings of schizophrenia probands: Presence of neuropsychological impairments

Chronic kidney disease (CKD) patients undergoing hemodialysis (HD) have a high risk of sudden cardiac death (SCD). A unique risk factor may be a longer interval between HD sessions (interdialytic period). Inherent in conventional HD (thrice-weekly) are two 48-hour short breaks (SIDP) and one 72-hour long break (LIDP) between HD sessions.We used an implantable cardiac monitor (ICM) to define the incidence and timing of significant arrhythmias in an HD population.Fifty CKD patients undergoing HD with left ventricular ejection fraction >35% had an ICM inserted, with intensive follow-up to record SCD events and predefined bradyarrhythmias and tachyarrhythmias.Mean age of the patients was 67 ± 11 years; 72% were male, and the mean follow-up was 18 ± 4 months. There were 8 unexpected SCDs (16%), all during the LIDP. The terminal event was severe bradycardia with asystole in each recorded case. No episodes of polymorphic ventricular tachycardia (VT) occurred. A total of 7686 arrhythmia events were recorded in 43 patients (86%), including bradycardia in 15 patients (30%), sinus arrest in 14 (28%), second-degree atrioventricular block in 4 (8%), nonsustained VT in 10 (20%), and new-onset paroxysmal atrial fibrillation in 14 (28%). The LIDP was the highest-risk period for all arrhythmias (P < .001). The arrhythmia event rate per hour was greatest during the first pre-HD period of the week compared with any other peri-HD period (P < .001).Risk of SCD and significant arrhythmias is greatest during the LIDP. SCD was attributable to severe bradycardia and asystole. Interventions to prevent this type of SCD or shorten the LIDP deserve further evaluation.URL: https://www.anzctr.org.au (Unique identifier: ACTRN12613001326785).

A comparison of the long-term effects of sotalol and atenolol on QT interval and arrhythmias after myocardial infarction

In order to dissociate the Class III effects of sotalol on QT interval and arrhythmias from those of chronic beta-receptor blockade, we compared the effects of sotalol 160 mg b.d. and atenolol 50 mg b.d. in a double-blind crossover study of 103 patients followed for one year after discharge following acute myocardial infarction. Sotalol caused a highly significant lengthening of the absolute and corrected QT (QTc) interval over atenolol which was apparent by day 6 and persisted unchanged throughout the follow-up period. The increase in QT interval averaged 43 ms (9%). Sotalol blunted the increase in ventricular premature beat frequency on ambulatory monitoring which occurred with atenolol, although direct comparison of arrhythmia frequency between the groups receiving atenolol and sotalol revealed no significant difference. Marked lengthening of QTc interval (greater than 500 ms) was observed on 29 occasions in patients receiving sotalol, most commonly at day 6, but no episodes of polymorphic ventricular tachycardia were recorded. The Class III action of sotalol persists over and above any response to beta-blockade during a one-year follow-up period. In a population with a low incidence of spontaneous arrhythmias, however, there was only a modest difference in antiarrhythmic efficacy between atenolol and sotalol. Episodes of marked lengthening of QT interval induced by sotalol in the absence of other adverse factors need not be arrhythmogenic.

A comparison of the long-term effects of sotalol and atenolol on QT interval and arrhythmias after myocardial infarction

In order to dissociate the Class III effects of sotalol on QT interval and arrhythmias from those of chronic beta-receptor blockade, we compared the effects of sotalol 160 mg b.d. and atenolol 50 mg b.d. in a double-blind crossover study of 103 patients followed for one year after discharge following acute myocardial infarction. Sotalol caused a highly significant lengthening of the absolute and corrected QT (QTc) interval over atenolol which was apparent by day 6 and persisted unchanged throughout the follow-up period. The increase in QT interval averaged 43 ms (9%). Sotalol blunted the increase in ventricular premature beat frequency on ambulatory monitoring which occurred with atenolol, although direct comparison of arrhythmia frequency between the groups receiving atenolol and sotalol revealed no significant difference. Marked lengthening of QTc interval ( >500 ms) was observed on 29 occasions in patients receiving sotalol. most commonly at day 6, but no episodes of polymorphic ventricular tachycardia were recorded. The Class III action of sotalol persists over and above any response to beta-blockade during a one-year follow-up period. In a population with a low incidence of spontaneous arrhythmias, however, there was only a modest difference in antiarrhythmic efficacy between atenolol and sotalol. Episodes of marked lengthening of QT interval induced by sotalol in the absence of other adverse factors need not be arrhythmogenic.

Epicardial mapping during induction of nonsustained polymorphic ventricular tachycardia in a 7-day-old canine myocardial infarction model

Programmed electrical stimulation and epicardial mapping were performed to study electrophysiologic mechanisms for induction of nonsustained polymorphic ventricular tachycardia in 29 dogs with 7-day-old myocardial infarction. Nine dogs had 15 different episodes of reproducible monomorphic ventricular tachycardia (11 sustained and 4 nonsustained) (group A). Seven episodes of polymorphic ventricular tachycardia (group B) were induced in six dogs, three of which degenerated into ventricular fibrillation. Epicardial activation time during premature stimulation at the time of tachycardia induction was more prolonged in group A than in group B (183 ± 43 vs 123 ± 35 msec, p < 0.01). Furthermore, induction of ventricular tachycardia was preceded by the development of functional block in 13 of 15 group A tachycardias, but in only three of seven group B tachycardias. During polymorphic ventricular tachycardia, epicardial activation patterns were radial from the earliest epicardial activation site, similar to those observed during left ventricular endocardial pacing. QRS polymorphism was associated with a beat-to-beat variation in the earliest epicardial activation site. In conclusion, inducibility of nonsustained polymorphic ventricular tachycardia is less dependent on the epicardial activation sequence than on monomorphic ventricular tachycardia.

Hypokalemia as a cause of cardiac arrest: Results of electrophysiologic testing and long-term follow-up

Hypokalemia is known to cause malignant ventricular arrhythmias.‘.” It is occasionally discovered in patients resuscitated from cardiac arrest.“-: Do these patients require antiarrhythmic drug therapy or is maintenance of normal potassium levels adequate to prevent recurrent cardiac arrest? We performed electrophysiologic studies in 10 patients with cardiac arrest associated with hypokalemia. The clinical and laboratory features are summarized in Table I. Six patients presented with ventricular fibrillation, two presented with monomorphic ventricular tachycardia, and two presented with polymorphic ventricular tachycardia with morphologic features suggesting torsade de pointes. Six patients had at least one episode of polymorphic ventricular tachycardia on post resuscitation rhythm strips. All had diuretic induced hypokalemia (2.2 to 3.3 mEq/L) and all had prolonged corrected QT intervals