Idiopathic verapamil-sensitive sustained left ventricular tachycardia

Idiopathic verapamil-sensitive left ventricular tachycardia (VT) has characteristic QRS configurations during VT: right bundle-branch block with either left axis or right axis (less common) deviation. QRS duration is relatively narrow (0.13-0.16s) and frequently endocardial activation prior to QRS is recorded during VT, which is the basis of its being called fascicular tachycardia. The mechanism is probably reentry, but the nature of the slow conduction necessary for the occurrence of reentry is quite different from that of other sustained monomorphic VT associated with structural heart disease. Chronic oral verapamil therapy is the drug of choice for alleviation of symptoms. Long-term prognosis is good.     

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms.

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infused at a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 +/- 4 vs. 7.4 +/- 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 +/- 78 vs. 450 +/- 81 ms, p = NS) and QRS duration (184 +/- 38 vs. 185 +/- 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Idiopathic verapamil-sensitive left ventricular tachycardia complicated by right ventricular outflow tract ventricular tachycardia and ventricular fibrillation.

Idiopathic ventricular tachycardias (VTs) are generally divided into those arising from the right ventricle and those arising from the left ventricle. There has been few reports of two morphologically distinct VT occurring in patients with no apparent structural heart disease. We report a patient with verapamil-sensitive left VT with a right bundle branch block pattern that spontaneously changed to VT with a left bundle branch block pattern. Ventricular fibrillation was induced by the application of programmed stimulation. Although it is unclear if our patient with pleomorphic VT has ventricular vulnerability, it is necessary to investigate further and follow him carefully.     

Sequential transvenous pacing and shock therapy for termination of sustained ventricular tachycardia

Rapid ventricular pacing and transvenous shocks are both effective in terminating sustained ventricular tachycardia (VT) only in selected patients. We prospectively examined efficacy and safety of an algorithm for VT termination combining rapid ventricular pacing with low and moderate energy transvenous shocks in patients with sustained VT. Sixty-three VT episodes in 23 patients, mean age 64 +/- 12 years, were treated with the algorithm. Bursts of rapid ventricular pacing and transvenous shocks were delivered with a Medtronic 6880 catheter positioned in the right ventricular apex. VT episodes with cycle lengths greater than 270 msec (group A) were treated with sequential therapy with rapid ventricular pacing (90%, 80%, and 70% of VT cycle length), low energy transvenous shocks (0.5 to 2.7 J), and moderate energy (2.7 to 10 J) transvenous shocks. Rapid VT episodes with cycle lengths less than 270 msec (group B) were treated with moderate energy transvenous shocks directly. Forty-one of 48 (85%) VT episodes in group A and 6 of 15 (40%) VT episodes in group B were successfully terminated by this algorithm. There was no difference in clinical or arrhythmia characteristics between responders and nonresponders in either group A or group B to the algorithm. VT acceleration was observed in 12% of episodes in group A and in 47% of episodes in group B. We conclude that an algorithm combining rapid ventricular pacing with low and moderate energy transvenous shocks is effective for VT termination in episodes with a cycle length greater than 270 msec and can reduce the need for transthoracic cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)     

External cardiac programmed stimulation for noninvasive termination of sustained supraventricular and ventricular tachycardia

To examine the feasibility of using a noninvasive temporary pacemaker for termination of well-tolerated supraventricular (SVT) and ventricular tachycardia (VT), a standard external demand pacemaker was modified to allow stimulation with single or multiple extrastimuli and overdrive pacing. To evaluate the efficacy, safety and tolerance of external cardiac programmed stimulation, a standard arrhythmia termination protocol was used in 223 tachycardias in 22 patients. The technique of external cardiac programmed stimulation was used in 209 episodes of SVT in 13 patients. It terminated 95% of the episodes with success in 19 of 20 episodes of atrioventricular nodal reentrant tachycardia and 179 of 189 episodes of atrioventricular reciprocating tachycardia. Of 198 episodes of SVT terminated by the technique 168 (85%) were terminated by a single extrastimulus and 28 (14%) by double extrastimuli. Only 2 episodes of SVT required overdrive pacing for termination. External cardiac programmed stimulation did not result in atrial fibrillation or arrhythmia acceleration. Of 14 episodes of sustained monomorphic VT 5 were terminated by external cardiac programmed stimulation. One tachycardia was terminated by a single extrastimulus, 1 by double extrastimuli and 3 by overdrive pacing. Arrhythmia acceleration occurred once and was terminated by endocardial pacing. On 27 separate occasions patient evaluation of maximal discomfort included 4 ratings of mild, 10 of moderate, 11 of severe and 2 of intolerable discomfort. External cardiac programmed stimulation is effective and safe in patients with well-tolerated sustained supraventricular or ventricular arrhythmias.     

射频导管消融治疗维拉帕米敏感性左心室特发性室性心动过速

目的报告6例维拉帕米敏感的左心室特发性室性心动过速(室速)的折返路径标测结果和射频导管消融效果。方法6例(男4,女2)左心室特发性室速的患者,电生理检查常规插入右心室心尖与冠状静脉窦电极,并经左、右股动脉分别插入消融导管和10极冠状静脉窦标测电极至左心室,使后者可依次记录到希氏束电位(H)、左束支电位(LB)、左后分支的蒲氏纤维电位(P)和心室肌电位(V),室速时P电位领先。消融导管电极在P电位电极对附近寻找到P电位最领先的点实施消融。结果前三例中凡在未记录到P电位的点放电,虽然V波最早,都是无效点,而最后消融成功的点,都记录到最领先的P电位;后三例都必须记录到最领先的P电位后才放电,均1次放电成功。6例随访至今6~20个月,未服任何抗心律失常药均无室速发作。结论左心室标测法不仅对研究左心室特发性室速的折返路径有重要意义,而且对临床治疗也很有帮助,既可缩短手术时间,又可提高消融质量。     

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination

Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. In conclusion: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: Identification of drugs that exacerbate tachycardia and potential mechanisms

Eleven of 83 patients who had ventricular tachycardia (VT) and underwent serial electrophysiologic study (EPS) had a more severe VT induced while receiving a particular antiarrhythmic drug as compared to control study. For all patients only nonsustained VT was initiated during control study, while sustained VT occurred during drug testing with disopyramide (2 patients), quinidine (2 patients), amiodarone (4 patients), and encainide (7 patients), although spontaneous arrhythmias appeared well-controlled prior to repeat testing. Pacing techniques used to induce sustained VT were the same as those used in the control study in eight patients and “less aggressive” in three patients. Almost all episodes of sustained VT resulted in substantial hypotension, especially in patients who were taking encainide. Drugs associated with sustained VT increased the median tachycardia cycle length by 112 msec (p < 0.005) but increased the median ventricular effective refractory period by only 30 msec (p < 0.02). Assuming re-entry was responsible for VT, we postulate that drugs facilitated initiation of sustained VT by prolonging activation time but only minimally increasing refractoriness of the tachycardia circuit.     

射频消融左后分支治疗维拉帕米敏感性特发性室性心动过速

目的报道消融左后分支治疗左室特发性室性心动过速(简称室速)。方法对57例维拉帕米敏感性左室特发性室速患者进行电生理检查及射频消融,以窦性心律时产生左后分支阻滞和/或室速不再被诱发作为消融成功终点。结果57例中41例室速诱发条件稳定(71.9%),9例诱发条件不稳定(15.8%),7例不能被诱发(12.3%),所有患者均达消融成功终点。术后全部患者体表心电图Ⅰ导联出现R波降低,S波加深,呈rS形态或RS形态,Ⅱ、Ⅲ、aVF导联出现小q波,或在原有q波基础上加深,R波振幅明显增高,呈qR形态,额面电轴度数显著增加(54.06°±38.24°vs 90.55°±7.88°,P<0.001)。27例出现完全性左后分支阻滞改变(47.4%),30例为不完全性左后分支阻滞(52.6%)。1例1年后室速再发,左后分支阻滞消失,重复消融直至再次出现左后分支阻滞,术后室速未有再发。结论射频消融产生左后分支阻滞可作为左室特发性室速的消融成功终点,尤其适用于不易被常规电生理检查诱发的患者。     

Intravenous magnesium sulfate for acute termination of sustained monomorphic ventricular tachycardia associated with coronary artery disease

The efficacy of intravenous magnesium in terminating sustained monomorphic ventricular tachycardia was examined in this study. This therapy was found to be ineffective in aborting monomorphic ventricular tachycardia induced in the electrophysiology laboratory.     

心动过速终止后短暂心室复极异常和严重室性心律失常

目的 观察长时间心动过速终止后对心室复极和恶性室性心律失常发生的影响.方法 3例长时间心动过速(9 d～6个月)患者,两例为长时间发作室性心动过速(室速),其中1例为无休止性左心室特发性室速并诱发心动过速性心肌病;另1例为主动脉瓣换瓣术后5年发生束支折返性室速;第3例为持续性心房扑动伴心功能不良并因三度房室阻滞于10年前植入单腔起搏器.结果 3例患者在心动过速时并无晕厥和恶性室性心律失常发生,而在心动过速间隙或射频导管消融终止后均出现qr间期延长和恶性心律失常,其中1例持续心房扑动合并心力衰竭的患者最后死于多脏器功能衰竭;另两例室速射频导管消融治疗后1周QT间期逐渐恢复正常,分别随访20和39个月无室速和晕厥发作.结论 长时间心动过速后可导致短时间心室复极异常及恶性室性心律失常,应加强防范,防止发生心脏性猝死.     

Antiarrhythmic drug therapy for sustained ventricular tachycardia

VT may be observed to accompany a wide variety of heart diseases and occasionally no heart disease at all. The efficacy of drug therapy is dependent on antiarrhythmic effects and the mechanism underlying the patient's VT. Conventional antiarrhythmic agents appear to be effective in no more than one third of patients, but a substantial number of other potentially useful antiarrhythmic agents exist. Unfortunately, their effectiveness in treating sustained VT for the most part must still be proved. Other agents such as amiodarone appear effective, but ways to predict which patients will benefit remain unknown. Invasive and noninvasive techniques exist for assessing therapeutic efficacy, but determination of which is more appropriate awaits a wider experience and more direct comparison.     

Valsalva termination of ventricular tachycardia in myocardial infarction

A 66-yr-old patient with recurrent monomorphic ventricular tachycardias subsequent to a previous myocardial infarction is reported. The tachycardia could repeatedly be terminated by the Valsalva manoeuvre. Procainamide, infused shortly before, possibly had an additional effect. As far as we know, this is the first report of ventricular tachycardias, as a result of an old myocardial infarction, that could be terminated by the Valsalva manoeuvre.     

New-onset sustained ventricular tachycardia after cardiac surgery

BACKGROUND: The de novo occurrence of sustained ventricular tachycardia (VT) after CABG has been described, but the incidence, mortality rate, long-term follow-up, and mechanism are not well defined. METHODS AND RESULTS: This prospective study enrolled consecutive patients undergoing CABG at a single institution. Patients were followed up for the development of sustained VT, and a detailed analysis of clinical, angiographic, and surgical variables associated with the occurrence of VT was performed. A total of 382 patients participated, and 12 patients (3.1%) experienced >/=1 episode of sustained VT 4.1+/-4.8 days after CABG. In 11 of 12 patients, no postoperative complication explained the VT; 1 patient had a perioperative myocardial infarction. The in-hospital mortality rate was 25%. Patients with VT were more likely to have prior myocardial infarction (92% versus 50%, P<0.01), severe congestive heart failure (56% versus 21%, P<0.01), and ejection fraction <0.40 (70% versus 29%, P<0.01). When all 3 factors were present, the risk of VT was 30%, a 14-fold increase. Patients with VT had more noncollateralized totally occluded vessels on angiogram (1.4+/-0.97 versus 0.54+/-0.7, P<0.01), a bypass graft across a noncollateralized occluded vessel (1.50+/-1.0 versus 0.42+/-0.62, P<0.01), and a bypass graft across a noncollateralized occluded vessel to an infarct zone (1.50+/-1.0 versus 0.17+/-0.38, P<0.01). By multivariate analysis, the number of bypass grafts across a noncollateralized occluded vessel to an infarct zone was the only independent factor predicting VT. CONCLUSIONS: The first presentation of sustained monomorphic VT in the recovery period after CABG is uncommon, but the incidence is high in specific clinical subsets. Placement of a bypass graft across a noncollateralized total occlusion in a vessel supplying an infarct zone was strongly and independently associated with the development of VT.