QT/RR Relationship in Patients after Remote Anterior Myocardial Infarction with Left Ventricular Dysfunction and Different Types of Ventricular Arrhythmias

Background: QT/RR relationship was found to be both rate‐dependent and rate‐independent, what suggests the influence of autonomic drive and other not‐autonomic related factors on it. The steeper QT/RR slope in patients after acute myocardial infarction (MI) was described, but the relationship to ventricular arrhythmias is unknown. The purpose of this study was to calculate differences in QT/RR relationship in patients after remote anterior MI with left ventricular dysfunction and different types of ventricular arrhythmias. Methods: The cohort of 95 patients (age: 63 ± 11 years, LVEF: 35 ± 9%) with previous anterior MI (mean 1.1 years) was divided into two well‐matched groups—50 patients without episodes of ventricular tachycardia (VT) or ventricular fibrillation (VF) (NoVT/VF: 39 males, 64 ± 12 years, LVEF 37 ± 8%) and 45 patients with VT and/or VF (all with ICD implanted) (VT/VF: 35 males, 62 ± 10 years, LVEF 34 ± 10%). No true antiarrhythmics were used. QT/RR slope was calculated from 24‐hour Holter ECG for the entire recording (E), daytime (D) and nighttime (N) periods. Results: Groups did not differ in basic clinical data (age, LVEF, treatment). QT/RR slopes were steeper in VT/VF than in NoVT/VF group in all analyzed periods: E ‐ 0.195 ± 0.03 versus 0.15 ± 0.03 (P < 0.001), N – 0.190 ± 0.03 versus 0.138 ± 0.03 (P < 0.001) and D ‐ 0.200 ± 0.04 versus 0.152 ± 0.03 (P < 0.001). No significant day‐to‐night differences were found in both groups. Conclusions: Steeper QT/RR slope and complete lack of day‐to‐night differences in VT/VF patients show inappropriate QT adaptation to the heart rate changes. The prognostic significance of this parameter needs prospective studies.     

Prevention of Recurrent Life-threatening Ventricular Arrhythmias by Temporary Cardiac Pacing

ABSTRACT Overdrive pacing has been applied in 26 patients to prevent frequent recurrent ventricular fibrillation (VF) and ventricular tachycardia (VT) occurring in the setting of ventricular extrasystole of 2–5 degrees graded by Lown. These patients had 3–47 recurrent attacks of VF and VT (11.4±2.4) which were not prevented with antiarrhythmic agents. Overdrive pacing was continued for 2–236 hours (21.3±3.7) and appeared to be effective in 23 (88.4%) of the 26 patients including those with prolonged QT intervals. Atrial pacing was more effective than ventricular overdriving and required stimulation at a slower rate. Antiarrhythmic therapy and overdrive pacing in combination were more effective than both used independently. Suppression of ventricular extrasystole and prevention of life-threatening arrhythmias were achieved by increasing the heart rate by 23.2±4.5 beats/min.     

QT and JT dispersion in patients with monomorphic or polymorphic ventricular tachycardia/ventricular fibrillation

The present study evaluates the repolarization abnormalities in patients with monomorphic sustained ventricular tachycardia (MVT) and polymorphic ventricular tachycardia/ventricular fibrillation (PMVT/VF) by measuring QT and JT dispersion on the surface electrocardiogram (ECG). QT dispersion is a predictor of ventricular arrhythmias in several clinical settings. However, the value of QT and JT dispersion in identifying patients at risk for PMVT/VF is controversial. Maximum QT (JT) interval duration and QT (JT) dispersion were compared between 20 healthy individuals, 12 patients with inducible MVT during programmed electrical stimulation and seven patients with PMVT/VF recorded during 24-hour ambulatory ECG or induced by programmed electrical stimulation. QT dispersion was 40 +/- 9 ms in the control group, 63 +/- 21 ms in the MVT group, and 79 +/- 31 ms in the PMVT/VF group. QT dispersion in both the MVT and PMVT/VF groups were significantly greater than in the control group (P <.001 and P <.0001, respectively); however, there was no significant difference between the MVT and PMVT/VF groups. JT dispersion was 41 +/- 14 ms in the control group, 69 +/- 14 ms in the MVT group and 103 +/- 37 ms in the PMVT/VF group. JT dispersion differed significantly between the study groups and was significantly increased in PMVT/VF group than in the control group or MVT groups (P <.0001 vs. the control group, P <.005 vs. the MVT group). Patients with PMVT/VF have a greater dispersion of ventricular repolarization time. Repolarization abnormalities are important for ventricular arrhythmogenesis and detectable on the surface ECG.     

Postextrasystolic Repolarization Abnormalities in ST‐U Segment in Patients with Ventricular Arrhythmias

Background: Changes in U‐wave amplitude after premature ventricular contractions (PVC) are known as prognostic markers in the long QT syndrome dependent on bradycardia. The purpose of the study was to find correlation between postextrasystolic ST‐U segment changes and a history of sustained ventricular tachycardia or ventricular fibrillation (VT/VF). Methods: The ST‐U segment configurations were taken from the 24‐hour ambulatory ECG. The comparison of the morphology of these segments was performed between sinus beats preceding PVC's and first postextrasystolic beats. Population: Two groups of patients were evaluated: 1) 32 patients with VT/VF history (VT/VF group), and 2) 36 patients with potentially malignant arrhythmia (structural heart disease with frequent PVCs and/or nonsustained VT‐nsVT) tnon‐VT/VF group). Results: We found T‐wave changes in 8 patients (25%) from the VT/VF group and in 12 patients (33.3%) from the nonVT/VF group (P = NS) and U‐wave changes in 13 patients (40.6%) and 3 patients (8.3%), respectively (P < 0.05). Other ECG indexes related to PVC's were also considered: RR interval, coupling interval (Cl), prematurity index (Pl), and postextrasystolic pause (PP). The analysis of these ECG indices revealed, when compared with patients without T‐U‐wave changes, that the occurrence of U‐wave changes was significantly related to longer RR interval of the sinus rhythm preceding PVC: 1025 ± 211 vs 918 ± 200 ms (P < 0.05). The prematurity index was lowest in patients with U‐wave changes: 0.54 ± 0.12 vs 0.65 ± 0.16 (P < 0.01) while postextrasystolic pauses leading to the postextrasystolic U‐wave changes were significantly longer: 1383 ± 223 vs 1130 ± 247 ms (P < 0.001). Cl did not differentiate patients: 556 ± 108 vs 584 ± 117 ms (P = NS). Conclusions: Postextrasystolic changes in ST‐U segment configuration are dependent on bradycardia, low prematurity index of the PVC, and the lengthening of the postextrasystolic pause. U‐wave changes more frequently appeared in patients with malignant arrhythmias. Follow‐up study is needed to assess if they might be predictive for the occurrence or reoccurrence of arrhythmic episodes. A.N.E. 2002;7(1):17–21     

Dispersion of the QT Interval in Subjects with Frequent Nonsustained Ventricular Arrhythmias and No Underlying Heart Disease: Arrhythmogenic Substrate or Mechanoelectrical Feedback of Arrhythmias?

Background: QT dispersion (QTd) on the ECG is thought to reflect the temporal and spatial inhomogeneity of repolarization in the underlying myocardium. In myocardial infarction, ischemia, and long QT syndromes, an increased QTd is associated with a propensity for malignant ventricular arrhythmias and sudden cardiac death. We investigated this feature of the repolarization process in subjects with frequent ventricular arrhythmias and structurally normal hearts. Methods: Forty‐nine patients referred for frequent, nonsustained ventricular arrhythmias (45 ± 14 years, ×± SD, 61% female) had normal ventricular dimensions and function, no late potentials, and normal ECG. They were compared with 30 controls (42 ± 13 years, 50% female). QTd was measured as the difference between the longest and the shortest QT in the six precordial leads at a paper speed of 50 mm/s. Results: In patients, QTc was similar to that of controls: 395 ± 21 versus 386 ± 20. However, QTd was greater: 49 ± 20 ms versus 32 ± 14 ms, P < 001. Moreover, 18 patients (36%) had QTd exceeding 60 ms—a value superior to the mean normal value of 2 SD—compared to only 1 control (3%) (P < 0.01). Finally, patients with more frequent ventricular arrhythmias had larger QTd. Conclusions: In patients with frequent nonsustained ventricular arrhythmias and otherwise normal hearts, QT interval dispersion is increased. We speculate that, instead of representing a specific electrophysiological substrate of arrhythmias, QT dispersion in this specific population could result from arrhythmias themselves through a possible mechanoelectrical feedback.     

Electrophysiologic characteristics at initiation of ventricular tachycardia and ventricular fibrillation in a canine infarct model

Local ventricular activation time and the conduction time during sinus rhythm at the induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) were investigated using a canine model of chronic myocardial infarction. Of 26 dogs studied, 15 had inducible VT, 10 had inducible VF, and 1 had no inducible arrhythmias. Bipolar local ventricular electrograms were recorded during sinus rhythm from 136 sites in 10 dogs with VT and 164 sites in 11 dogs with VF. Mean activation time in dogs with inducible VT was significantly longer than in dogs with inducible VF. Furthermore, simultaneous local ventricular electrograms were recorded during the induction of VT (74 episodes) or VF (38 episodes) from the infarct border zone at the endocardium (B-EN), the epicardium (B-EP), and normal sites (N-EN, N-EP). During VT induction, the activation time at N-EN and N-EP was significantly longer than during VF induction (N-EN: 94 ± 21, 70 ± 19 ms; N-EP: 83 ± 21, 64 ± 10 ms; p < 0.05). Conduction time was measured at the initiation of VT or VF induced by orthodromic or antidromic pacing. The conduction times of the last paced beat between N-EN and B-EP (35 ± 11, 62 ± 24 ms), N-EN and N-EP (35 ± 12, 14 ± 13 ms), B-EN and B-EP (16 ± 10, 38 ± 25 ms), and B-EP and N-EP (77 ± 27, 44 ± 12 ms) were significantly different in dogs with inducible VT (p < 0.05), but not in dogs with VF. Dispersion of effective refractory period was also observed in dogs with VT. Percent infarct in inducible VT was larger than in inducible VF (VT: 16 ± 5%; VF: 10 ± 2%; p < 0.001). These studies suggest that dogs with inducible VT have prolonged ventricular activation time and significantly different bidirectional conduction time during VT induction. This may serve as a substrate for reentry.     

Predictive Value of QT Dispersion for Ventricular Tachyarrhythmias in Patients with Implantable Cardioverter Defibrillator

Background: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization as a potential substrate for ventricular arrhythmias. Methods: QT dispersion was measured in the standard 12-lead ECG in 51 patients at the time of implantation of a third generation implantable cardioverter defibrillator (ICD) with automatic electrogram storage capability for electrical events triggering device therapy. In addition, QT dispersion was measured in 100 age- and sex-matched healthy controls. All 5 1 study patients with ICD were prospectively followed to determine possible associations between QT dispersion at implant and subsequent spontaneous ICD shocks for ventricular tachyarrhythmias (VT). Results: Rate-corrected QT dispersion and adjusted QTc dispersion, which takes account of the number of leads measured, were significantly greater in ICD patients compared to controls (76 ± 25 ms vs 46 ± 11 ms, and 24 ± 7 ms vs 14 ± 3 ms respectively, P < 0.0 1). During 15 ± 8 months follow-up, ventricular tachyarrhythmias occurred in 23 (45%) of 51 ICD patients. QTc dispersion and adjusted QTc dispersion were not significantly different between ICD patients with ventricular tachyarrhythmias and ICD patients without ventricular tachyarrhythmias during follow-up (74 ± 19 ms versus 77 ± 29 ms, and 23 ± 6 ms vs 25 ± 8 ms respectively). Conclusion: Increased QT dispersion measured in the 12-lead standard ECG does not appear to be a useful marker for future arrhythmic events in a mixed patient population with ICD.     

射频导管消融治疗特发性室性期前收缩触发的心室颤动／多形性室性心动过速

目的：探讨特发性室性期前收缩（早搏,PVC）触发心室颤动和（或）多形性室性心动过速（VF／PVT）的临床特点及射频导管消融治疗效果。方法：313例无器质性心脏病接受射频导管消融治疗的特发性PVC患者,其中6例发生了由PVC触发的VF／PVT,分析该6例患者的临床资料及射频导管消融治疗效果。结果：该6例患者动态心电图可记录到频发PVC[（16303±5854）次／d],PVC联律间期及基础QT间期分别为（412±44）ms和（407±10）ms。这些参数值在另外307例特发性PVC患者中分别为（15570±4743）次／d、（419±36）ms和（404±8）ms,两组间无显著性差异。313例患者中,有88例记录到由PVC触发的单形态室性心动过速（VT）。PVC触发VF／PVT患者中晕厥发生率（3／6）高于由PVC触发的单形态VT患者（4／88,4．5％,P〈0．05）,PVT的周长[（235±22）ms]则短于单形态VT组[（324±29）ms,P〈0．05]。针对触发VF／PVT的PVC消融后随访的10～36个月期间,所有6例患者未再发生晕厥、VF及心脏骤停。结论：恶性VF／PVT可能由一些特发性PVC诱发,射频导管消融PVC治疗可作为一项有效的治疗选择。     

Mode of Onset of Malignant Ventricular Arrhythmias in Idiopathic Ventricular Fibrillation

Mode of Onset of Idiopathic VF. Introduction : The mode of onset of malignant ventricular arrhythmias (ventricular tachycardia [VT] or ventricular fibrillation [VF] has been well described in patients with organic heart disease and in patients with the long QT syndromes. Less is known about the mode of onset of VF in patients with out-of-hospital VF who have no evidence of organic heart disease or identifiable etiology.
Methods and Results : We reviewed the ECGs of all our patients with Idiopathic VF. Documentation of the onset of spontaneous arrhythmias was available for 22 VK episodes in 9 patients (6 men and 3 women; age 41 ± 16 years). In all instances, spontaneous VF followed a rapid polymorphic VT, which was initiated by premature ventricular complexes (PVCs) with very short coupling intervals. The PVC initiating VF had a coupling interval of 302 ± 52 msec and a prematurity index of 0.4 ± 0.07. These PVCs occurred within 40 msec of the peak of the preceding T wave. Pause-dependent arrhythmias were never observed.
Concltision : Cardiac arrest among patients with idiopathic VF has a very distinctive mode of onset. Documentation of a polymorphic VT that is not pause dependent is of diagnostic value.     

射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

Electrocardiographic Markers of Late Sudden Death Risk in Postoperative Tetralogy of Fallot Children

Late Sudden Death Risk in Postoperative TOF. Following surgery for tetralogy of Fallot (TOP), children may develop late onset ventricular arrhythmias. Many patients have both depolarization and repolarization abnormalities, including right bundle branch block (RBBB) and QT prolongation. The goal of this study was to improve prospective risk-assessment screening for late onset sudden death. Resting ECG markers including QRS duration, QTc, JTc, and interlead QT and JT dispersion were statistically analyzed to identify those patients at risk for ventricular arrhythmias and sudden cardiac death. To determine predictive markers for future development of arrhythmia, we examined 101 resting ECGs in patients (age 12 ± 6 years) with postoperative TOF and RBBB, 14 of whom developed late ventricular tachycardia (VT) or sudden death. These ECGs were also compared with an additional control group of 1000 age- and gender-matched normal ECGs. The mean QRS (± SD) in the VT group was 0.18 ± 0.02 seconds versus 0.14 ± 0.02 seconds in the non-VT group (P < 0.01). QTc and JTc in the VT group was 0.53 ± 0.05 seconds and 0.33 ± 0.03 seconds compared with 0.50 ± 0.03 seconds and 0.32 ± 0.03 seconds in the non-VT group (P = NS). There was no increase in QT dispersion among TOF patients with VT or sudden death compared with control patients or TOF patients without VT, although JT dispersion was more common in the TOF groups. A prolonged QRS duration in postoperative TOF with RBBB is more predictive than QTc, JTc, or dispersion indexes for identifying vulnerability to ventricular arrhythmias in this population, while retaining high specificity. The combination of both QRS prolongation and increased JT dispersion had very good positive and negative predictive values. These results suggest that arrhythmogenesis in children following TOF surgery might involve depolarization in addition to repolarization abnormalities. Prospective identification of high-risk children may be accomplished using these ECG criteria.     

QT Dispersion as a Marker for Response to Quinidine in Patients with Ventricular Tachyarrhythmias

Objective: This study was undertaken to measure the effect of quinidine on QT dispersion and to determine whether changes in QT dispersion are associated with the acute response to quinidine in patients with ventricular tachycardia. Methods: In 36 patients with inducible ventricular tachycardia during programmed electrical stimulation (PES), QT and JT intervals were measured in all 12 leads of electrocardiograms recorded at baseline and after quinidine. QT/JT dispersion was calculated by subtracting the smallest from the largest interval; QTc and JTc dispersion were also calculated. Response to therapy was defined as the inability to induce a ventricular tachyarrhythmia during a repeat PES study. Results: Quinidine significantly prolonged the QTc and JTc intervals in the patients who responded to quinidine (n = 12) and in the nonresponders (n = 24). At baseline, QTc dispersion was similar in responders and nonresponders. However, quinidine increased QTc dispersion in nonresponders (from 78 ± 28 to 113 ± 40 ms, P < 0.05) but not in responders (from 81 ± 26 to 83 ± 42 ms). A similar pattern was seen for QT dispersion, JT dispersion, and JTc dispersion. Conclusion: QT dispersion increases in nonresponders, but not in responders to quinidine for ventricular tachycardia. This QT dispersion profile is distinct from the Class III antiarrhythmics and may explain results from large clinical trials and delineate a new safety and efficacy marker.     

Dofetilide reduces the frequency of ventricular arrhythmias and implantable cardioverter defibrillator therapies

Dofetilide Reduces VT/VF and ICD Therapies . Background: Patients with an implanted cardioverter defibrillator (ICD) and ventricular arrhythmias leading to ICD therapies have poor clinical outcomes and quality of life. Antiarrhythmic agents and catheter ablation are needed to control these arrhythmias. Dofetilide has only been approved for the treatment of atrial fibrillation. The role of dofetilide in the control of ventricular arrhythmias in patients with an ICD has not been established. Objective: Evaluate the safety and efficacy of dofetilide in a consecutive group of patients with an ICD and recurrent ventricular tachycardia (VT) and/ or ventricular fibrillation (VF) after other antiarrhythmic drugs have failed to suppress these arrhythmias. Methods: We studied 30 patients (age 59 ± 11; 5 women) with symptomatic VT or VF and ICDs for secondary prevention of sudden cardiac death. These patients had an average of 1.8 ± 4.5 episodes of VT/VF per month despite antiarrhymic therapy. Twenty‐one patients (70%) had recurrent appropriate ICD therapies prior to initiation of dofetilide, and 9 (30%) VTs below the programmed detection rate of the ICD. Twenty‐three patients (77%) had coronary artery disease. Mean ejection fraction was 30 ± 14% and 26/30 (87%) had congestive heart failure. All patients had previously failed 2 ± 1 antiarrhythmic drugs including amiodarone (n = 19) and sotalol (n = 10). Results: During the first month of treatment, 25 patients (83%) had complete suppression of VT/VF and of the 21 patients with ICD therapies 16 (76%) had no therapies during the first month of treatment. During a follow‐up period of 32 ± 32 months, dofetilide reduced the monthly episodes of VT/VF from 1.8 ± 4.5 to 1.0 ± 3.5 (P = 0.006). Monthly ICD therapies decreased from 0.9 ± 1.4 to 0.4 ± 1.7 (P = 0.037). In 9 patients that presented with slow VTs under the ICD detection zone, dofetilide reduced monthly VT/VF episodes from 0.7 ± 0.6 to 0.1 ± 0.1 (P = 0.01) and 6 (67%) had no further ICD therapies. Dofetilide was discontinued in 13 patients (43%) after 24 ± 30 months due to failure to control VT/VF (n = 7), placement of a left ventricular assist device (n = 3), catheter ablation (n = 1), heart transplantation (n = 1), and left ventricular restoration surgery (n = 1). There were 7 documented deaths (2 patients died suddenly; 3 patients of progressive heart failure; and 2 of non‐cardiac causes). Conclusions: In patients with an ICD and ventricular arrhythmias, dofetilide decreases the frequency of VT/VF and ICD therapies even when other antiarrhythmic agents, including amiodarone, have previously been ineffective. Recurrences still occur in some patients requiring catheter ablation, mechanical support, or heart transplantation. (J Cardiovasc Electrophysiol, Vol. 23 p. 296‐301, March 2012.)     

Dynamics of QT dispersion in acute myocardial infarction

BACKGROUND: We studied the dynamics of QT dispersion in patients with acute myocardial infarction, and compared them with those in controls. METHODS AND RESULTS: Serial electrocardiograms of patients admitted to our institute with acute myocardial infarction were analyzed for QT dispersion, and compared with those of healthy age- and sex-matched controls. QT dispersion from 12 leads was measured as maximum QT minus minimum QT interval in ms. The mean QT dispersion of 114 +/- 29.6 ms was significantly higher in patients with acute myocardial infarction on admission as compared to 51.45 +/- 5.56 ms in controls (p < 0.001). QT dispersion showed a dynamic change in patients with acute myocardial infarction who were thrombolyzed, being 109.11 +/- 5.77 ms, 87.59 +/- 5.88 ms, 75.89 +/- 18.33 ms, and 68.20 +/- 12.66 ms on admission, post-thrombolysis, and on days 3 and 7, respectively. During a similar time period, nonthrombolyzed patients showed a QT dispersion of 132.38 +/- 36.04 ms, 130.47 +/- 34.42 ms, 111.11 +/- 24.94 ms, and 106.25 +/- 27.64 ms, respectively: the difference between the 2 groups at all periods was significant (p < 0.01). Mean QT dispersion values in patients who developed ventricular tachycardia or ventricular fibrillation were significantly higher than in patients who did not develop ventricular tachycardia or ventricular fibrillation (p < 0.01). CONCLUSIONS: Mean QT dispersion is significantly increased after acute myocardial infarction, and shows a dynamic decrease with time, the difference being more marked in thrombolyzed patients. Mean QT dispersion levels are higher in patients with ventricular tachycardia and ventricular fibrillation compared to patients with acute myocardial infarction without these arrhythmias. The changes in QT dispersion are dynamic, and it may serve as a non-invasive marker of susceptibility to malignant ventricular arrhythmias.     

Long-term follow-up in patients with arrhythmogenic right ventricular cardiomyopathy

Long‐Term Prognosis in Patients with ARVC. Introduction: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a major cause of sudden cardiac death due to tachyarrhythmias. The purpose of this study was to investigate the long‐term prognosis in patients with ARVC and the incidence of rapid ventricular arrhythmias during follow‐up. Methods: Thirty ARVC patients (19 male, 63.3%, mean age 48 ± 15 years) fulfilling modified Task Force criteria 2010 were included. Of them, 13 patients (43.3%) received implantable cardioverter‐defibrillator (ICD) implantation. Rapid ventricular arrhythmia was defined as electrical storm or the occurrence of ventricular tachycardia (VT) or ventricular fibrillation (VF) with a cycle length of 240 ms or less that necessitate shock delivery to 2 or more times within a 24‐hour period. Results: With a mean follow‐up of 68 ± 10 months, 6 patients (20%) with ICD implantation had recurrent rapid VT/VF. One (3.3%) of them died of multiple shocks and SCD, and 5 (16.7%) had multiple ICD therapies due to VT/VF and electrical storm. The interval between the diagnosis of ARVC and occurrence of rapid VT/VF was 13.4 ± 4.9 months. Most (5/6, 83.3%) events of recurrent rapid VT/VF occurred within 2 years. Ablated patients who did not receive an ICD implant were totally free of rapid VT/VF. Conclusions: For patients with ARVC, long‐term prognosis is favorable. During a long‐term follow‐up, patients meeting the criteria for ICD implantation have a higher rate of rapid and potentially life‐threatening arrhythmias. However, early and clustered recurrence of rapid VT/VF in patients with an ICD is common, whereas late occurrence of rapid VT/VF is very rare. (J Cardiovasc Electrophysiol, Vol. 23, pp. 750‐756, July 2012)     

QT interval dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?

OBJECTIVE--To assess QT interval dispersion on the surface electrocardiogram in patients with sustained ventricular arrhythmias. DESIGN--A retrospective and prospective blinded controlled study of patients referred for investigation of ventricular arrhythmias at a tertiary cardiac centre. PATIENTS AND METHODS--89 consecutive patients with sustained ventricular arrhythmias due to chronic ischaemic heart disease, cardiomyopathy, or ventricular tachycardia (VT) in a normal heart. 32 patients did not meet the inclusion criteria; therefore 57 patients were compared with a control group of 40 patients with myocardial disease but no history of arrhythmias and 12 normal controls with no myocardial disease. Standard 12 lead electrocardiograms were enlarged, the QT intervals for each lead measured, and QT dispersion calculated. RESULTS--There was a significantly greater mean QT dispersion (77 ms) in patients with sustained ventricular arrhythmias compared with the control group (38 ms, p < 0.01). This held for all groups; after myocardial infarction VT (82 (22) ms v control 38 (10) ms; p < 0.01), dilated cardiomyopathy VT (76 (18) ms v control 40 (11) ms, p < 0.01), and normal heart VT (65 (7) ms v control 32 (8), p < 0.05). There was also a greater QT dispersion in patients with impaired left ventricular function and VT, with a correlation between left ventricular function and QT dispersion in patients with VT (r = 0.56, p < 0.01). CONCLUSION--QT interval dispersion may be a further non-invasive marker of susceptibility to ventricular arrhythmias.     

特发性右室流出道室性早搏触发多形性室性心动过速或心室颤动四例的临床特点

目的报道4例特发性右室流出道(RVOT)室性早搏(PVC)触发多形性室性心动过速/心室颤动(PVT/VF)的临床特点。方法 76例起源于RVOT的VT患者,其中4例为PVC触发PVT/VF,总结4例的临床资料并与另72例有关资料相比较。结果所有4例触发PVT/VF时的PVC与孤立PVC的形态一致,但2种PVC的联律间期发生了明显改变,其改变幅度均≥70 ms,其中2例缩短,2例延长。1例孤立PVC时的联律间期亦不恒定。72例PVC触发的单形VT患者每天PVC次数为15 427±1 109,QT间期为404±15 ms,孤立PVC联律间期为419±22ms。4例PVC触发PVT/VF患者中3例1天的PVC次数与72例PVC触发的单形VT患者平均PVC次数相当。4例患者的QT间期及孤立PVC联律间期与另72例患者相当。而4例PVT/VF的周长均小于280 ms,明显短于72例VT的平均周长(324±59 ms)。72例单形VT患者发生晕厥比率4.1%;4例PVT/VF患者中发生晕厥者2例。采用激动标测和起搏标测证实4例患者PVC均起源于RVOT间隔侧,经射频导管消融PVC取得成功。结论起源于RVOT的PVC触发PVT/VF具有PVC联律间期不恒定及PVT/VF的周长短的临床特征,射频导管消融治疗有效。     

Electrophysiologic manifestations of ventricular tachyarrhythmias provoking appropriate defibrillator interventions in high-risk patients with hypertrophic cardiomyopathy

Introduction: Our objective was to determine features of ventricular tachyarrhythmias triggering appropriate implantable cardioverter-defibrillator (ICD) interventions in hypertrophic cardiomyopathy (HCM).
Methods and Results: The study cohort was 68 high-risk HCM patients who received ICDs for primary sudden cardiac death prevention from 1995 to 2003. All episodes of sustained ventricular tachyarrhythmias identified by stored intracardiac electrograms were analyzed. Nine patients had 51 episodes of sustained ventricular tachyarrhythmic events that required device therapy (mean follow-up, 3.4 ± 2.2 years; cumulative event rate, 3.2% per year): five had 47 episodes of monomorphic ventricular tachycardia (VT); four each had one episode of ventricular fibrillation (VF). Sinus tachycardia or atrial fibrillation was the initiating rhythm in five of nine patients and in 43 of 51 episodes of events. Of the 17 episodes of monomorphic VT detected in the VT zone, 16 (94%) were terminated by antitachycardia pacing. Thirty episodes of monomorphic VT were detected in the VF zone and were terminated by defibrillation.
Conclusion: Sustained monomorphic VT is common in a high-risk cohort with HCM. Sinus tachycardia is often the initiating rhythm, suggesting that high sympathetic drive may be proarrhythmic when a susceptible substrate is present. Antitachycardia pacing is highly effective in terminating VT in this patient population.     

室早指数及临床意义的探讨

目的探讨室早指数对器质性病变患者发生恶性室性心律失常的预测价值。方法106例经动态心电图诊断为窦性心律伴发室性心律失常的患者,分为器质性与非器质性病变两组,统计室早个数、室速和室颤的发作阵次及诱发室速、室颤的室早联律间期、室早前次心搏的QT间期。结果106例患者中,平均24h室早总数12066±1105个;阵发室速662±79次,53例由RonT室早诱发,其中器质性病变46例(86.85%);阵发室颤39±5次,均发生于器质性病变者,其中11例(68.8%)由快速多形性室速诱发;器质性与非器质性病患者中诱发室速和(或)室颤的室早联律间期分别为340±15ms和420±20ms,室早前次心搏的QT间期分别为420±10ms和410±25ms,室早指数分别为0.90±0.10和1.00±0.15,两组比较有显著性差异(p<0.05)。结论当室早指数在0.78～0.83之间时,易诱发阵发性室速和室颤,尤其是器质性病变者,临床应给予足够的重视和治疗。     

Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia

Coupling Intervals and Polymorphic QRS Morphologies . Introduction: Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF. Methods and Results: The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT‐group) and 21 with monomorphic VT arising from the RVOT (MVT‐group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT‐group than in the MVT‐group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT‐group than that for the VT in the MVT‐group (P < 0.01). In the PVT‐group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321–3.659; P = 0.002). Conclusion: The smaller PIs of the first VT beat may result in a polymorphic QRS morphology. (Cardiovasc Electrophysiol, Vol. 23, pp. 521‐526, May 2012)