Relationship Between QT Interval Duration and Electrical Induction of Ventricular Tachycardia

The relation of inducible ventricular tachycardia (VT) to QT interval duration of ventricular paced rhythm has not been evaluated. To clarify this relation we measured corrected QT interval duration (QT_C) during sinus rhythm and QT interval duration during ventricular paced rhythm (QT-V) in patients with coronary artery disease without (non-VT group = group B) and with inducible VT (VT group = group A). Duration of QT-V was greater in the VT group (n = 20) compared with non-VT group (n = 20) during ventricular pacing at cycle lengths of 600 ms (424 ± 26 vs 396 ± 19 ms, P < 0.01), of 500 ms (407 ± 20 vs 383 ± 21 ms, P < 0.01), and of 400 ms (390 ± 21 vs 362 ± 17 ms, P < 0.001). During sinus rhythm the mean values of QT_C were similar in both groups (408 ± 25 vs 413 ± 20 ms, NSJ. During ventricular stimulation the percentage of patients with values of QT-V exceeding 380 ms was 35% in non-VT group and 95% in VT group (P <0.01) at cycle length of 500 ms and 5% versus 60%, respectively, (P < 0.01), at cycle length of 400 ms. Thus, a trend toward longer QT values of ventricular paced rhythm exists in patients with inducible VT.     

QT Variability Before and After Episodes of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

This study examined the changes in QT dynamics occurring during 5-minute intervals sampled immediately before and 1 hour after episodes of nonsustained ventricular tachycardia (VT) in patients with hypertrophic cardiomyopathy (HCM). Twenty-four hour Holter recordings were performed in 10 patients with HCM in the absence of antiarrhythmic medications and processed by the ELA Medical QT analysis software. All sinus complexes were averaged over 30-second segments and 2,880 templates were created. For each template, a mean corrected QT_ec (time interval between the onset of QRS and the end of the T wave) and QT_ac (time interval between the onset of the QRS and the peak of the T wave) were calculated, with their standard deviations (SDQT_e and SDQT_a) taken as indices of QT variability. The slopes of the regression line for the QT_e and QT_a against the corresponding RR also were calculated. Forty 5-minute segments were analyzed immediately before (sample A) and 1 hour after (sample B) 20 episodes of nonsustained VT. QT_ac was significantly longer in group A than in group R (321 ± 20 vs 312 ± 22, P < 0.0001) and SDQT_a was significantly lower (2.8 ± 1.2 vs 4.7 ± 3.7, P < 0.03). There were no significant differences in QT_ec, SDQT_e, QTe/RR and QT_a/RR before and after the episodes. Our data indicate that in patients with HCM, the averaged QT_ac is significantly longer and the QT_a variability significantly lower before episodes of nonsustained VT.     

Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy

BARANOWSKI, R., et al .: Analysis of the Corrected QT Before the Onset of Nonsustained Ventricular Tachycardia in Patients with Hypertrophic Cardiomyopathy. This study examined ventricular repolarization before the onset of 37 episodes of nonsustained ventricular tachycardia (NSVT) in 26 untreated patients with hypertrophic cardiomyopathy (HCM). Fourteen episodes were recorded in patients with a history of cardiac arrest or patients who died suddenly during follow-up. The QT interval was measured beat-by-beat on 24-hour ambulatory electrocardiograms. Mean 24-hour, hourly QTc and QTc of the last 10 beats prior to NSVT, consisted of 4–50 cycles (mean   9 ± 10   ), at the fastest rates of 100–175 beats/min (mean 122 ± 22) were analyzed. NSVT was more prevalent during nighttime (23 episodes), than during daytime (14 episodes,   P < 0.05   ). No significant differences were observed between mean 24-hour, mean hourly QTc during the hour with NSVT, and QTc of the last 10 cycles prior to onset of NSVT. QTc was significantly longer in patients with a history of sudden cardiac death (SCD) or who died suddenly during follow-up than in survivors. The 24-hour QT variability was higher in nonsurvivors than in survivors (   -39 ± 6   vs   33 ± 6 ms, P = 0.03   ). Episodes of NSVT in untreated patients with hypertrophic cardiomyopathy were more frequent during the nighttime. The 24-hour QT variability was higher in nonsurvivors than in survivors. (PACE 2003; 26[Pt. II]:387–389)     

Magnetocardiographic QT Interval Dispersion in Postmyocardial Infarction Patients with Sustained Ventricular Tachycardia: Validation of Automated QT Measurements

T dispersion is a measure of heterogeneity in ventricular repolarization. Increased ECG QT dispersion is associated with life-threatening ventricular arrhythmias. We studied if magnetocardiographic (MCG) measures of QT dispersion can separate postmyocardial infarction patients with and without susceptibility to sustained VT. Manual dispersion measurements were compared to a newly adapted automatic QT interval analysis method. Ten patients with a history of sustained VT (VT group) and eight patients without ventricular arrhythmias (Controls) were studied after a remote myocardial infarction. Single-channel MCGs were recorded from 42 locations over the frontal chest area and the signals were averaged. QT dispersion was defined as maximum — minimum or standard deviation of measured QT intervals. VT group showed significantly more QT and JT dispersion than Controls. QT_apex dispersions were 127 ± 26 versus 83 ± 21 ms (P = 0.004) and QT_end dispersions 130 ± 37 versus 82 ± 37 ms (P = 0.013), respectively. Automatic method gave comparable values. Their relative differences were 9% for QT_apex and 27% for QT_end dispersion on average. In conclusion, increased MCG QT interval dispersion seems to be associated with a susceptibility to VT in postmyocardial infarction patients. MCG mapping with automated QT interval analysis may provide a user independent method to detect nonhomogeneity in ventricular repolarization.     

Catecholaminergic Polymorphic Ventricular Tachycardia with QT Prolongation

The QT interval in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) is typically normal. However, CPVT patients are sometimes misdiagnosed as concealed long QT syndrome (LQTS), because patients with LQTS also manifest with syncope or sudden death following periods of exertion or extreme emotion. We report a CPVT patient with a pathogenic RyR2 mutation associated with a marked QT prolongation, which normalized after flecainide therapy.     

Ten-Years Follow-Up of 20 Patients with Idiopathic Ventricular Tachycardia

The follow-up and characteristics of 20 patients with ventricular tachycardia (VT) and no detectable heart disease is reported. These were 16 men and four women with a mean age of 44 years. Symptoms were present in 18 patients (eight had syncope and ten palpitations or dizziness), VT was sustained in 11 patients and a left bundle branch block morphology with inferior axis was found in 17 patients. In three patients, VT had a right bundle branch block morphology and left-axis deviation. The VT was inducible in 13 patients during the electrophysiological testing (EP) and was sustained in five patients. Medical treatment was introduced in 19 patients. During a mean follow-up of 10 years from the onset of the symptoms and 6 years from the EP testing, one patient died suddenly. He had stopped taking amiodarone 5 months before. In seven patients symptoms recurred and were due to discontinuation of therapy in two cases and inefficacy of previous effective treatment in five patients. After modification of the treatment (three cases), implantation of a pacemaker (one case) and catheter ablation (one case), all patients became asymptomatic. Eleven patients became asymptomatic with the first administered antiarrhythmic therapy. One patient continues to be asymptomatic in spite of discontinuation of his medical therapy. We conclude that patients with VT and no detectable heart disease have a good long-term prognosis and that appropriate therapy can be found in almost all patients.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.     

Relationship Between Spectral Measures of Heart Rate Variability and Ventricular Ectopic Activity in Patients with Idiopathic Ventricular Tachycardia

This study examines the relationship of hourly spectral measures of heart rate variability (HRV) to the occurrence of ventricular ectopic (VE) activity in 20 patients with idiopathic ventricular tachycardia and frequent VE's. Spectral measures of HRV were obtained from 24-hour Holler recordings from the patients in a drug free state and included the total energies in the spectrum, the low frequency components (1) (0.04–0.15 Hz) representing predominantly sympathetic lone with some contribution from the parasympathetic and high frequency components (H) (0. 15–0.4 Hz) representing mainly parasympathetic tone. A high H component (parasympathetic) was defined as area > 12 msec and high L components (sympathetic) as area > 30 msec. On an hourly analysis of spectral components in relation to VE activity, VE's occurred significantly more frequently during periods of low H and low L (F = 20.5, DF = 3, P < 0.0001). The number of VE's did not differ statistically in the other combinations of H and L components flow H, low L = 612.8 (50.1); high H, low L = 180.1 (36.8); low H, high L = 338.4 (58.9); high H, high L - 204.9 (17.7) VE's/hr (SEM). The results suggest that VE's are more frequent during periods of low H and low L and are diminished when either H or L are increased in patients with idiopathic ventricular tachycardia. The results would be consistent with the hypothesis that the parasympathetic nervous system has an electro physiologically stabilizing effect on the myocardium.     

Prevalence, Therapeutic Response, and Outcome of Ventricular Tachycardia in the Out-of-hospital Setting: A Comparison of Monomorphic Ventricular Tachycardia, Polymorphic Ventricular Tachycardia, and Torsades de Pointes

OBJECTIVE: To investigate out-of-hospital ventricular tachycardia (VT) cardiac arrest patients, comparing the prevalences and outcomes of the following VT subtypes among this population: monomorphic VT (MVT), polymorphic VT (PVT), and torsades de pointes (TdP, PVT with a prolonged QT interval). METHODS: This was a retrospective review from a fire department-based paramedic system of nontraumatic VT cardiac arrest patients (January 1991 to December 1994) with a supraventricular perfusing rhythm (SVPR) at some time during out-of-hospital care, with a measurable QT interval. QT interval was measured from an SVPR, and corrected QT interval (QTc) was calculated and considered prolonged if > 0.45 sec. VT was classified as polymorphic or monomorphic. TdP was defined as PVT with a prolonged QT interval. RESULTS: 196 patients were identified; six were excluded due to incomplete medical records, leaving 190 who met inclusion criteria and were used for data analysis. 117 (62%) patients had MVT, while 73 (38%) patients had PVT; of the 73 patients with PVT, 37 (51%) had normal QTc (non-TdP PVT) and 36 (49%) had prolonged QTc (TdP PVT). 97 (51%) patients had prolonged QTc (PQTc). Regardless of VT type (i.e., MVT vs PVT), 97 (51%) patients had prolonged QTc, with a mean QTc of 0.476+/-0.15 seconds prearrest and 0.464+/-12 seconds postarrest. Patients with PQTc were not more likely to have PVT (70 [37%] vs 76 [40%]; p = 0.705). No significant difference with respect to paramedic-witnessed arrests in each VT morphology group and each QT group was found. The overall hospital discharge rate was 28.4%. Regardless of VT type, patients had similar rates of out-of-hospital return of spontaneous circulation (ROSC) and hospital discharge; patients with PQTc were less likely to be discharged from the hospital (19.6% vs 37.6%; p = 0.01). 27.8% of TdP and 26.8% of non-TdP patients were discharged (p = 0.912). CONCLUSIONS: In this population of out-of-hospital VT arrest patients, MVT is the most common form of VT encountered; PVT and the subtype TdP are also seen in this population with approximately equal frequencies. All three rhythm types demonstrate similar responses to standard Advanced Cardiac Life Support therapy with equal rates of out-of-hospital ROSC and hospital discharge. PQTc may be a marker of poor clinical outcome in patients with out-of-hospital VT arrest.     

Idiopathic Recurrent Parasystolic Ventricular Tachycardia in a Child

An asymptomatic 3¹/₂-year-old boy demonstrated parasystolic ventricular tachycardia with AV dis-sociation, early sinus capture beats, marked variability in coupling intervals between conducted and ectopic beats, fusion beats, and interectopic intervals which were multiples of the ectopic cycle length. The arrhythmia initially responded to quinidine, reappeared over an 11-month observation period, and finally was suppressed at a high quinidine dose. An invasive and noninvasive work-up failed to demonstrate organic heart disease.     

经导管射频消融治疗特发性室性心动过速患者的护理

目的探讨经导管射频消融治疗特发性室性心动过速患者的护理方法。方法回顾性分析75例行导管射频消融治疗的特发性室性心动过速患者的临床资料。结果发生术后并发症3例,其中穿刺点血肿2例、心脏压塞1例,经精心治疗和护理后均痊愈出院。结论经导管射频消融治疗特发性室性心动过速患者安全有效,手术前后需要密切观察、精心护理、及时发现并协助处理各种并发症。     

Ambulatory Assessment of the QT Interval in Patients with Hypertrophic Cardiomyopathy: Risk Stratification and Effect of Low Dose Amiodarone

This study aims to assess the dynamics of the QT interval in patients with hypertrophic cardiomyopathy (HCM). Three consecutive QT intervals and the preceding RR intervals were measured on 24-hour ambulatory electrocardiograms at 30-minute intervals in ten high risk patients with HCM (sudden cardiac death [SCD] and/or documented ventricular fibrillation), aged 29 ± 17 years, compared with ten age and sex matched low risk patients with HCM (no syncope, no adverse family history, and no ventricular tachycardia on Holter monitoring), and ten normal subjects. Another ten patients who were on amiodarone therapy (200-mg daily) were also studied. Patients witb intraventricular conduction defects were excluded. There were 4,424 pairs of QT intervals and their preceding RR intervals were measured in this study. A nonsignificant prolongation in the QT interval and a significant prolongation in QT_c values (Bazett's and Fridericia's formulas) were demonstrated in patients with HCM compared with normals. There were no significant differences in the QT and QT_c between high and low risk patients. The slope of regression line for the QT against RR interval was significantly different between normals and HCM (0.1583 ± 0.040 vs 0.2017 ± 0.043. P < 0.05), but not between high and low risk patients. Amiodarone significantly prolonged the QT and QT_c without significantly altering the slope of the regression line (0.2017 ± 0.043 vs 0.2099 ± 0.037, NS). Our findings support the observations that there is a prolonged QT interval in patients with HCM and that there is no significant use dependent effect of amiodarone on ventricular repolarization. In conclusion, ambulatory assessment of the QT interval provides an alternative method for the assessment of ventricular repolarization and for the assessment of use dependent effects of anti arrhythmic drugs on ventricular repolarization during normal daily activities. However, this method does not help in the identification of patients at high risk of SCD in HCM.     

Amiodarone in the Management of Patients with Ventricular Tachycardia and Ventricular Fibrillation

Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximumtolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800–1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 ± 1.7 months (mean ± S. D.) of treatment with amiodarone at a mean daily dose of 588 ± 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5–9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 ± 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF overa follow-up period of 21.5 ± 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600–800 mg per day of amiodarone.     

Idiopathic polymorphic ventricular tachycardia with normal QT interval in a structurally normal heart

Polymorphic ventricular tachycardia (PVT) is a life-threatening arrhythmia that is typically related to long QT syndrome, organic heart disease, electrolyte abnormalities, cardiotoxic drugs, or adrenergic stimulation. A review of the literature reveals that PVT with normal QT interval and without underlying cause is quite rare. We report a case of idiopathic spontaneous PVT with structurally normal heart and without electrolyte abnormalities, drug reactions, or evidence of catecholamine induced arrhythmia. We also review the literature on the electrocardiographic characteristics and management of idiopathic PVT.     

儿茶酚胺敏感性室性心动过速患者的护理

目的探讨儿茶酚胺敏感性室性心动过速(catecholaminergic polymorphic ventricular tachycardia,CPVT)患者的护理特点。方法回顾性分析2005年6月至2011年6月宁波市医疗中心李惠利医院心内科收治的5例CPVT患者的临床资料,并总结其护理经验。结果β受体阻滞剂对大多数CPVT患者效果良好,但对长期足量应用β受体阻滞剂仍不能满意控制心律失常发生的患者,需要采用植入式心律转复除颤器(implantable cardioverter defibrillator,ICD)治疗。结论 CPVT患者护理各有特点,药物治疗为主的CPVT患者应重视解释疏导和心理护理,而安装植入式心律转复除颤器(implantable card-ioverter defibrillator,ICD)患者的应重视术后护理工作。     

Ventricular Pacing Induced Ventricular Tachycardia in Patients with Implantable Cardioverter Defibrillators

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 ± 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1–16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.     

Late Potentials Are Unaffected by Radiofrequency Catheter Ablation in Patients with Ventricular Tachycardia

Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averaged electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastolic potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 ± 50 msec; mean ± SEM) 13–180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in any patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 ± 4.0 msec postablation; 135.7 ± 4.5 msec preablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 ± 1.0 μV postablation; 5.9 ± 0.4 μV preablation). or in the duration of the low amplitude signal (69.2 ± 2.0 msec postablation; 62.7 ± 3.4 msec preablation). At follow-up electrophysiology study performed 14 ± 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up electrophysiology study.