Search

Background Anti-tachycardia pacing (ATP) delivered from an implantable device is an important tool to terminate ventricular tachycardia (VT). But its real-world efficacy for fast VT has not been fully studied. Methods Using the database of Nippon-storm study, effect of patient-by-patient basis ATP programming for fast VT (≥188 bpm) was assessed for the patients with structural heart diseases. Fast VTs were divided into three groups depending on heart rate (HR); Group A was 188-209 bpm, and Group-B and Group-C were 210-239 bpm and ≥240 bpm, respectively. Results During a median follow-up of 28 months, 202 fast VT episodes (209 ± 19 bpm) were demonstrated in the 85 patients. ATP terminated 151 of the 202 episodes (74.8%) in total. The success rate of the ATP was not different among the three groups: 73.3% in Group A, 80.6% in Group B, and 66.7% in Group C. ATP success rate of >50% and >70% was 77.6% and 64.7% of the patients, respectively. Left ventricular ejection fraction (LVEF) was significantly higher in the patients with rather than without successful ATP therapy, and receiver operating characteristic (ROC) analysis revealed that LVEF of 23% was the optimal cut-off value. ATP was less effective in patients taking amiodarone, but etiology of the structural heart diseases, indication of the device implantation, and all Electrocardiogram (ECG) parameters were not useful predictors for successful ATP therapy. Conclusions ATP highly terminated fast VT with wide HR ranges in patients with structural heart diseases, and should be considered as the first-line therapy for fast VT except for patients with very low LVEF.

An asymptomatic 15-year-old boy, who had a family history of sudden cardiac death, was referred for screening for cardiac disease. The 12-lead electrocardiogram at rest showed a short QT/QTc(Bazett)/QTc(Fredericia) interval of 320/388/364 ms, but the intervals were further shortened to 200/339/284 ms after the treadmill test concomitant with appearance of a peaked T wave. Other conventional cardiac examinations were normal, but effective refractory period was less than 180 ms in both ventricles, and double ventricular extrastimulation reproducibly induced nonsustained polymorphic ventricular tachycardia. Intravenous administration of epinephrine also induced a short QT interval and a peaked T wave, and a hump was manifested on the T wave of the first postpacing beat with a longer preceding R-R interval. Furthermore, a couple of premature ventricular complexes originated from a similar timing as the hump. Genetic analysis did not show the mutation in KCNQ1, KCNH2, KCNE1, KCNE2, KCNJ2, SCN5A genes but revealed single nucleotide polymorphism (C5457T) in SCN5A gene.

A 35-year-old man, who had an episode of aborted sudden cardiac death due to ventricular fibrillation, suffered from multiple storms of ventricular tachycardia (VT). Conventional cardiac examinations did not reveal any structural heart diseases, and he had been treated by an implantable cardioverter defibrillator since 2007. At the latest admission, epicardial but not endocardial voltage mapping revealed a small area of low voltage at the left ventricular (LV) postero-lateral wall where a delayed potential was recorded during sinus rhythm. Excellent pacemapping with a prolonged stimulus to QRS interval was obtained from the area, and a mid-diastolic potential was recorded during the VT. Radiofrequency application terminated the VT and any VT became noninducible after the ablation. In some patients diagnosed as LV-VT with no apparent heart disease, arrhythmogenic substrate may exist on the epicardial surface of the ventricle.

A storm of J wave-associated idiopathic ventricular fibrillation (VF) was observed in a 49-year-old man. Multiform premature ventricular complexes initiated the episodes of VF. Intravenous isoproterenol attenuated the J wave and suppressed the VF storm. After the implantation of a cardioverter defibrillator, VF was induced by programmed electrical stimulation at baseline, and it was terminated by a 25-J shock after an unsuccessful 15-J shock. During oral treatment with quinidine sulfate, 600 mg daily, the J wave was attenuated and VF became noninducible by programmed electrical stimulation. VF induced by a shock delivered on the T wave was terminated by a single 10-J shock. Mean F-F interval and dominant frequency of the VF were 162 ms and 6.8 Hz at baseline, and 210 ms and 5.0 Hz during the quinidine sulfate treatment. (PACE 2012; 35:e226–e230)

A 65-year-old recipient of an implantable cardioverter defibrillator suffering from ventricular noncompaction developed storms of ventricular tachycardia (VT). Epicardial voltage mapping revealed the presence of a large low-voltage area in the left ventricular apical and inferoposterior wall, and isolated delayed potential was recorded over 1.5 cm in the posterior border between low and normal myocardial voltage. Pacemapping at the delayed potential recording site produced two different QRS depending on pacing output strength, and these two QRS morphologies were similar to clinically documented VTs. During one of the VTs, a mid-diastolic potential was recorded from the site with the delayed potential, and rapid pacing produced concealed entrainment. After epicardial radiofrequency ablation of the isolated delayed potential, VTs were noninducible and the VT storm was suppressed.

Premature ventricular complexes (PVC) falling after the end of the T wave triggered ventricular fibrillation (VF) at night and monomorphic ventricular tachycardia (MVT) during daytime, in a recipient of implantable cardioverter defibrillator with Brugada syndrome. Treatment with bepridil (1) decreased the height of ST segment elevation in leads V1-V3, (2) completely eliminated VF, and (3) markedly decreased the incidence of PVC and MVT. Albeit rare, VF can be triggered by late-coupled PVC, due to a mechanism other than phase 2 reentry in some patients with Brugada syndrome.

In two patients with variant forms of Brugada electrocardiographic abnormalities, ST segment elevation, and reciprocal ST segment depression developed during intravenous administration of pilsicainide. In one patient, pilsicainide accentuated the ST segment elevation in leads I, aV(L), and V(1)-V(3) and caused ST segment depression in leads II, III, and aV(F). Coronary angiograms at the time of ST segment elevation were normal. In the other patient, pilsicainide accentuated the coved-type ST segment elevation in leads II, III, and aV(F) and caused ST segment depression in leads I, aV(L), and V(2)-V(5). Frequent premature ventricular complexes (PVCs) with two different left bundle branch block patterns developed during ST segment elevation. Intravenous isoproterenol returned the ST segment to baseline in both patients and suppressed the PVCs in the second patient. We hypothesize that a wide area of epicardial myocardium with large I(to) current might explain the reciprocal ST segment depression observed at the time of accentuated ST segment elevation.

We observed a case of idiopathic ventricular arrhythmias originating from the right ventricular outflow tract (RVOT). The origin of target premature ventricular contraction (PVC) and nonsustained ventricular tachycardia (VT) was within a wide low-voltage area around the RVOT. During radiofrequency (RF) application to the site of arrhythmia origin, polymorphic VT and ventricular fibrillation were repeatedly triggered by new PVC that had developed near the site of ablation. This electrical storm persisted >30 minutes after cessation of RF current delivery, and was suppressed by additional RF applications to the site of origin of the new PVC.

Background: In patients with Brugada syndrome, class I antiarrhythmic drugs can trigger ventricular arrhythmias (VA). The incidence and initial characteristics of VA that developed after pilsicainide was examined in 28 patients with Brugada-type electrocardiographic (ECG) abnormalities and with a positive response in the pilsicainide test. The clinical outcome was also compared between patients with and without pilsicainide-induced VA. Methods and Results: In all patients, pilsicainide increased ST segment elevation and accentuated type 1 ECG changes. Ventricular tachycardia (VT) developed in 3 patients and premature ventricular complexes (PVC) in 2 other patients. These 5 patients (group I) had higher ST segment elevation in lead V2 on the ECG at baseline and after pilsicainide and showed a longer QTc interval after pilsicainide than the other 23 patients (group II). However, there was no difference between the 2 groups regarding incidence of prior cardiac events, results of signal-averaged ECG, HV interval, inducibility of ventricular fibrillation by programmed electrical stimulation, or QRS duration. In 1 patient, PVC originated from 3 sites, 2 of which triggered polymorphic VT. The right ventricular (RV) outflow tract was the origin of 2 types of PVC, and other RV sites of 5 other types. During a 45 ± 37 months follow-up, polymorphic VT recurred in 2 patients in group II. Conclusions: Pilsicainide induced VA in some patients with Brugada syndrome, but this result may not be used as a parameter of the risk stratification of Brugada syndrome. Multiple PVC induced by pilsicainide and triggering polymorphic VT originated from several RV sites is an important factor when considering patients for treatment with catheter ablation.

A 17-year-old man was referred to our hospital for treatment of common paroxysmal atrial flutter. His electrocardiogram at rest showed subtle ST-segment elevation in leads II, III, and aV(F). Intravenous pilsicainide caused further ST-segment elevation in the inferior leads, new ST-segment depression in leads V2-V6, two distinct forms of premature ventricular complexes (PVCs) triggering short runs of polymorphic ventricular tachycardia (VT). An infusion of isoproterenol suppressed these arrhythmias and normalized the ST-segment. Pilsicainide may induce PVCs and polymorphic VT in atypical Brugada syndrome.

morphic Ventricular Tachycardia Focus on Transmural Ventricular Repolarization. Background: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg + + ) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). Methods: In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg + + was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg + + administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. Results: Mg + + rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg + + caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 ′ 22 to 45 ′ 18 ms within 30 seconds after Mg + + injection. However, this effect was transient, and, at 120 seconds after Mg + + administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 ′ 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg + + in this model. Conclusion: Since these effects were transient, a continuous intravenous infusion of Mg + + is preferred to prevent recurrences of VTA.

Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the J-point (ST(J)), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated ST(J) byor = 0.1 mV. Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented ST(J) byor = 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.

The aim of this study was to investigate the long-term efficacy and safety of electrophysiologic study (EPS)-guided sotalol administration combined with implantable cardioverter defibrillators (ICD) for ventricular tachyarrhythmias (VTA). This study enrolled 92 patients with both structural heart disease and sustained VTA. Sotalol was administered to 57 patients, and its efficacy was assessed by EPS. Long-term treatment was continued in combination with ICD in 31 patients (57%) whose VTA was no longer inducible (responder group) and in 16 patients whose VTA remained inducible (nonresponder group). The long-term outcomes were compared among the responder group, the nonresponder group, and 35 ICD recipients untreated with antiarrhythmic drugs (ICD-only group). During a mean follow-up of 44 +/- 33 months, the recurrence of VTA was not significantly different between all patients treated with sotalol (30%) and patients in the ICD-only group (46%). However, the recurrence of VTA was significantly lower in the responder (13%) than in the nonresponder (63%) or the ICD-only groups (46%). There was no significant difference in VTA recurrence between the nonresponder and the ICD-only groups. One patient each in the responder and the ICD-only groups died suddenly, and all-cause mortality was similar in the three groups. The incidence of inappropriate ICD discharges was less in the sotalol than in the ICD-only groups. No patient had to discontinue long-term sotalol treatment because of the adverse effects. In conclusion, sotalol reduced VTA recurrence in the responding patients and inappropriate ICD discharge. EPS may predict the efficacy of sotalol for VTA recurrence.

We report two cases of intermittent Wolff-Parkinson-White (WPW) syndrome. In one patient, early repolarization (ER) was masked during preexcitation whereas in the other, J wave-like notches were observed in the right precordial leads only during preexcitation. The clinical significance of ER is not apparent in WPW syndrome but some possible mechanisms are discussed. (PACE 2012; 35:e231–e233)

Leakage of electrical current from the body surface during a defibrillation shock delivery by an ICD device was evaluated in 27 patients with life-threatening ventricular tachyarrhythmias. All patients underwent the implantation of the Medtronic Jewel Plus ICD system, and the defibrillation shocks were delivered between the active can implanted in the left subclavicular region and the endocardial lead placed in the right ventricle. At the time of measurement of the effect of electrical energy delivery for defibrillation, the shocks were delivered in a biphasic form at the energy level of 20 or 30 J. During each delivery of the defibrillation shock, the electrical current to the body surface was measured through large skin electrodes (6.2 cm2) that were pasted at the following positions: (1) parallel position: the electrodes were placed at the left shoulder and the right low-chest, and the direction of the electrode vector was parallel to the direction of the defibrillation energy flow, and (2) cross position: the electrodes were placed at the right shoulder and the left low-chest, and the vector of the electrodes was roughly perpendicular to the direction of the energy flow. The energy leakages were measured in 80 defibrillation shocks. The peak leakage current during the shock delivery at energy of 30 J was 48 +/- 26 mA at the parallel position and 19 +/- 15 mA at the cross position (P = 0.0002). The energy leakage at a 30-J shock was 7.4 +/- 7.2 mJ at the parallel position and 1.4 +/- 2.3 mJ at the cross position (P = 0.0002). The actual maximum energy leakage was 105 mA, 29 mJ, and 106 V that appeared at the parallel position. The body surface leakage of the defibrillation energy of the ICD device was evaluated. The power of the energy leakage strongly depended on the angle between the alignment of the recording electrodes and the direction of the energy flow. The highest current leakage to the body surface reached a considerable level, but the energy leakage was small because of the short duration of the defibrillation shock.

Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the LV and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin-A (AP-A) model of long QT syndrome (LQTS). This may be related to the distribution of myocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid-myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP-A in dogs. Using constant pacing and single premature stimulation (S1S2), the ventricular repolarization pattern was analyzed from 256 unipolar electrograms. Activation-recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP-A increased regional ARI dispersion to 88.1 +/- 36.0 ms in the LV, to 72.9 +/- 35.7 ms in the IVS, and to 23.0 +/- 8.7 ms in the RV at the pacing cycle length (CL) of 1,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S1S2 interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repolarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger delta ARI and slower time constant (tau), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S1S2 protocol. S2 created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhythmogenicity of torsades de pointes is primarily due to dispersion of repolarization in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes.

In a patient with nonischemic ventricular tachycardia (VT), VT was entrained and the conduction time from the pacing site to the entrained local electrogram showed a rate dependent shortening and its degree affected by the pacing site. The QRS complex, which was entrained by the last pacing stimulus, was constant and identical to that of VT and no rate dependent facilitated conduction was observed when the heart was paced at similar paced cycle lengths during sinus rhythm. As the mechanism of the shortening of the conduction time through the reentrant circuit, a shift of the entrance seems most likely.

Procainamide depresses conduction velocity and prolongs refractoriness in myocardium responsible for reentrant VT, but the mechanism by which the induction of VT is suppressed after procainamide administration remains to be determined. In the present study, the relationship between electrophysiological parameters and the noninducibility of VT was assessed during procainamide therapy with a special reference to the change of an excitable gap. Clinically documented monomorphic sustained VT was induced in 30 patients and, utilizing the phenomenon of transient entrainment, the zone of entrainment was measured as the difference between the cycle length of VT and the longest paced cycle length interrupting VT (block cycle length) which was determined as the paced cycle length decreased in steps of 10 ms, and used as an index of the excitable gap. The effective refractory period was measured at the pacing site and the paced QRS duration was used as an index of the global conduction time in the ventricle. The cycle length of VT, the block cycle length, and the width of the zone of entrainment were determined and compared between the responders and nonresponders. In 15 patients, these parameters were determined at the intermediate dose and related to subsequent noninducibility at the final dose. At the final doses of procainamide, VT was suppressed in 8 (26.7%) of 30 patients. However, the cycle length of VT, the block cycle length, and the width of the zone of entrainment were unable to predict the drug efficacy, i.e., noninducibility. The change in the effective refractory period at the pacing site or the width of the paced QRS duration was not different between the responders and nonresponders. Among the variables, only the width of the zone of entrainment showed a significant narrowing in the responders at the intermediate dose of procainamide, and it was smaller than that of the nonresponders. The significant narrowing of the width of the zone of entrainment was associated with the subsequent noninducibility of VT at the final dose. The present study showed that the baseline cycle length of VT, the block cycle length, the drug induced change of the effective refractory period, or the paced QRS duration was not a predictor of the noninducibility after procainamide administration. However, a significant narrowing of the width of the zone of entrainment at the intermediate dose was associated with the noninducibility of VT at the final dose.

RF catheter ablation was performed in 16 patients with nonreentrant idiopathic VT originating from the RVOT. All documented VT was monomorphic, but subtle morphological variation in the VT-QRS complex was observed in 10 (63%) of 16 patients. Through endocardial mapping, VT origin was determined within a narrow site (0.5 x 0.5 cm) in 4 of the 10 patients with the morphological variation. In the other 6 of 10 patients, the origin extended to an area of0.5 x 0.5 cm. In VT with morphological variation, the local electrogram at the site of VT origin also showed variation in morphology and activation sequence. For VT of narrow origin, RF application to the site eliminated the VT. However, in VT from a wide arrhythmogenic area, RF current had to be delivered to 3-7 distinct sites to cover the possible origin, and specific QRS configuration of VT and/or PVC was ablated at each of the earliest activation site. All but one VT were successfully ablated by RF current. Subtle morphological variation was frequent in this type of VT, and about half were associated with a wide arrhythmogenic area. Precise mapping and analysis of the efficacy of each RF application might be helpful to better understand the relationship between subtle changes of VT-QRS morphology and their origins.

Clinical implication of mechanical alternans is yet unclear. It may suggest the risk for sudden death in patients with chronic heart failure. Two cases with dilated cardiomyopathy showed mechanical alternans during diagnostic cardiac catheterization. They suddenly died due to ventricular fibrillation before the induction of beta-blocker therapy. Patients with mechanical alternans should be treated under intense monitoring until the induction of beta-blocker therapy.

A 74-year-old man with a history of partial gastrectomy presented with an electrocardiogram consistent with Brugada syndrome and marked meal related fluctuations in the ST segment. ST-segment elevation was prominently attenuated at 30 minutes and increased at 120 minutes after meals. Analysis of heart rate variability revealed a relationship between postprandial heightened parasympathetic activity and increase in Brugada-type ECG abnormality. A rapid postprandial increase in blood glucose may initially stimulate sympathetic nervous activity and secondarily increase parasympathetic tone. Food intake can be associated with fluctuations in ST-segment elevation in patients with the Brugada syndrome.

Background: Bepridil (a multiple channel blocker) may markedly prolong the QT interval and induce polymorphic ventricular tachyarrhythmias (VTA). We compared the transmural ventricular repolarization characteristics and inducibility of polymorphic VTA after administration of bepridil versus the pure IKr blocker, E-4031, each administered to five open-chest dogs. Methods: We used plunge needle electrode to record transmural left ventricular (LV) repolarization and activation-recovery interval (ARI) to estimate local repolarization. The correlation between paced cycle length and ARI was separately examined in the LV endocardium, mid-myocardium (Mid), and epicardium. Attempts to induce VTA were made during bradycardia and sympathetic stimulation. Results: Bepridil and E-4031 prolonged QT interval and ARI in all LV layers, though the magnitude of prolongation was greatest in Mid, increasing the transmural ARI dispersion, particularly during bradycardia. Compared with E-4031, bepridil caused mild, reverse use-dependent changes in ventricular repolarization, and less ARI dispersion than E-4031 during slow ventricular pacing. Both drugs increased ARImax and cycle length at 50% of ARImax, though the changes were smaller after bepridil than after E-4031 administration. Bradycardia after the administration of each drug induced no VTA; however, sympathetic stimulation induced sustained polymorphic VTA in two of five dogs treated with E-4031 versus no dog treated with bepridil. Conclusions: Unlike the pure Ikr blocker, E-4031, bepridil exhibited weak properties of reverse use-dependency and protected against sympathetic stimulation-induced VTA. It may be an effective supplemental treatment for recipients of implantable cardioverter defibrillator. (PACE 2010; 950–959)

CHINUSHI, M., et al.: Frequency and Output-Dependent Change in Conduction Over Slow Pathways in a Patient with Sustained Ventricular Tachycardia Unrelated to Coronary Artery Disease. In a patient with sustained ventricular tachycardia, we obtained two different paced QRS morphologies from a single pacing site. In one QRS morphology the stimulus to the QRS complex was long, 150 msec, and in the other it was 100 msec. At the paced cycle Iength of 600 msec and the stimulus output of 4 V, one QRS morphology with the stimulus to the onset of QRS activation (St-QRS) interval of 150 msec was observed. At the paced cycle length of 400 msec, the other QRS morphology with a St-QRS interval of 100 msec was observed alternately with the former. At the paced cycle length of 353 msec or 316 msec, the latter with a shorter St-QRS interval was exclusively observed. When the stimulus output was increased from 4 to 10 V, keeping with the paced cycle length at 400 msec, the St-QRS interval was shortened from 100 to 80 msec. For the two QRS morphologies with two St-QRS intervals, two slowly conducting pathways would be responsible. The site of the block in the faster pathway must be located at the proximity of the pacing site and the conduction at a shorter paced cycle length would be explained by “supernormal conduction.”

Two different monomorphic VTs were observed in two patients after a corrective operation for tetralogy of Fallot. The activation pattern of the wavefronts of the two VTs were different: in a counter-clockwise direction around the anatomical obstacle due to a ventriculotomy of the right ventricle in one VT; and in a clockwise direction around the same obstacle in the other VT. The different revolutions of the wavefronts could be the mechanism for the different morphologies of VT.

CHINUSHI, Y., et al.: Microdislodgment of Ventricular Pacing Lead Undetectable During Rapid Pacing One Year After Implantation.A 71-year-old woman had undergone valvular heart surgery in 1981, and implantation of a permanent ventricular pacemaker for ventricular pauses during atrial fibrillation in 2001. One year after pacemaker implantation, she complained of faintness. When pacing at 100 beats/min the pacemaker functioned properly. However, pacing and sensing failure was detected at a pacing rate of 60 beats/min. At rapid pacing rates, the lead tip was in closer contact with the endocardium, and its microdislodgment was undetectable. The symptoms have resolved since the lead was repositioned. (PACE 2003; 26:787–788)

CHINUSHI, M., et al.: QT Interval Prolongation and Torsades de Pointes Unmasked by Intracoronary Acetycholine Administration. Intracoronary acetylcholine administration, which was performed to exclude vasospasms, unmasked an abnormal QT interval prolongation and initiated torsades de pointes in a patient with normal QT interval at rest.