Bundle Branch Block Configuration Research Articles

Clinical and Electrophysiological Characteristics of Ventricular Tachycardias From the Basal Septum in Structural Heart Disease.

This study describes the clinical and electrophysiological characteristics of basal-septal ventricular tachycardias (VTs) in patients with structural heart disease (SHD). The basal septum is a common source of VT in patients with SHD. Data from 312 consecutive patients with SHD undergoing catheter ablation of ventricular arrhythmias were reviewed. Thirty-three basal-septal VTs in 31 patients (mean age 67.4 ± 14.2 years, mean left ventricular ejection fraction [LVEF] 42% ± 15%) were identified. Patients with VTs with left ventricular basal-septal breakthrough were more likely to have ischemic cardiomyopathy and lower LVEF; patients with right ventricular basal-septal VT were more likely to have sarcoidosis or right ventricular cardiomyopathy of unknown significance, with higher LVEF. Atrioventricular block was present in 45% of patients and intraventricular block including persistent biventricular pacing in 77%. Unipolar scar was larger than bipolar scar (area 18.8% ± 19.4% vs 12.7% ± 14.6%; P< 0.001). VTs with right bundle branch block configuration and S wave in lead V6 with positive V3/V4 polarity consistently indicated left ventricular basal-septal breakthrough. Inferior limb-lead discordance with right bundle branch block configuration and "reverse pattern break in lead V2" were identified in left ventricular basal inferior-septal origin in 3 patients. VT noninducibility was achieved in 55%, and VT recurred in 42% of patients after a single procedure, but VT burden was significantly reduced after ablation (59 episodes before vs 2 episodes after ablation; P=0.02). Basal-septal VTs in patients with SHD have a distinct clinical, electrocardiographic, and electrophysiological profile depending on the breakthrough site, accompanied by a deep intramural septal substrate that limits procedural success after catheter ablation.

Successful termination of ventricular tachycardia with intrinsic anti-tachycardia pacing

Intrinsic anti-tachycardia pacing (iATP) is a novel automated ATP algorithm that employs post-pacing interval (PPI) to design the next ATP sequence based on an analysis of the prior failed ATP sequence. A patient with hypertrophic cardiomyopathy received an implantable cardioverter-defibrillator (ICD) (Cobalt™ XT DR, Medtronic, Minneapolis, MN, USA) following an episode of syncope due to macro-reentrant ventricular tachycardia (VT) (right bundle branch block configuration, cycle length [CL] 280 ms). The VF zone was set to VTCL <300 ms and iATP therapy was prescribed before and during capacitor charging. The iATP was initiated when VT recurred 3 months later. The first attempt with an assumption of 150 ms propagation time from the pacing site to the VT circuit (9 pulses) could not reset the VT, leaving a PPI of 650 ms. A subsequent attempt involving 20 pulses with an assumption of 250 ms propagation time terminated the VT. Failure to reach the circuit is a major cause of unsuccessful ATP. In this regard, iATP is expected to have theoretical advantages over empirical and traditional ATP therapies. To the best of our knowledge, this is the first intracardiac electrogram illustrating how automated precision ATP terminates VT in a clinical setting.

Two P waves followed by 1 QRS complex: What is the mechanism?

A 71-year-old man with a history of inferior myocardial infarction was referred to the hospital for management of subarachnoid hemorrhage. The baseline 12-lead electrocardiogram showed sinus rhythm with a left bundle branch block configuration as well as 2:1 atrioventricular (AV) block (Figure 1A). After several hours, the electrocardiogram exhibited a slower rhythm with a right bundle branch block pattern following 2 narrow P waves (red arrows, Figure 1B). The slow ectopic rhythm converted to sinus rhythm after a spontaneous premature ventricular complex (PVC).

Incidence of outflow tract ventricular tachycardia long after surgical aortic valve replacement.

BackgroundThe peri‐outflow tract region could be the origin of ventricular tachycardia (VT) after aortic valve replacement (AVR). However, the clinical characteristics of outflow tract ventricular tachycardias (OTVTs) after AVR are yet to be clarified. This study investigated the incidence, risk factors, and clinical characteristics of patients with OTVTs after AVR.MethodsWe retrospectively analyzed the clinical course of 120 patients who had undergone surgical AVR (SAVR) between April 1980 and October 2018. The patients had no ischemic or diagnosed cardiomyopathies other than primary aortic valve diseases.ResultsSix patients (5.0%) developed OTVTs after SAVR. The average onset was at 10.8 ± 5.7 years after SAVR. All cases of VT arose from the inferior axis and included left and right bundle branch block configuration. Two patients who underwent cardiac magnetic resonance imaging (MRI) had late gadolinium enhancement (LGE) in the midlayer of the left ventricle basal anteroseptal wall. Patients with periaortic VTs had significantly larger left ventricular (LV) diameter at systole, lower LV ejection fraction, higher positive rates of signal‐averaged electrocardiogram (SAECG), and nonsustained VTs on Holter monitoring. On ablation, local fragmented potentials with low voltage zones were observed in accordance with the LGE distribution. Multiple VTs originating from the periaortic region were provoked in the sessions.ConclusionsAcute OTVT was found in 5% of patients after SAVR. Arrhythmia risk stratification by SAECG, Holter ECG, and cardiac MRI should be considered for a long period in patients after SAVR.

QRS complex axis deviation changing in catheter ablation of left fascicular ventricular tachycardia.

The mechanisms of the QRS complex axis deviation changing of idiopathic left fascicular ventricular tachycardia (FVT) during or after radiofrequency catheter ablation were investigated in this study, which were still not well defined. In the index procedure, FVTs characterized by right bundle branch block configuration and left-axis deviation (LAD-FVT) were ablated at the VT exit site guided by the earliest ventricular activation with fused presystolic Purkinje potential (PP) in 234 consecutive patients. A new type of FVT characterized by right-axis deviation (RAD-FVT) was identified after successful elimination of the LAD-FVT in 12 patients, including 9 patients during the index procedure and 3 patients during follow-up. The QRS duration of RAD-FVT was shorter than that of LAD-FVT (115.3 ± 15.2 vs. 125.3 ± 16.4 ms, P = 0.006). The RAD-FVTs showed an earliest ventricle activation site localized at anterior fascicle area in 11 patients and anterior-median fascicle area in 1. However, the earliest PP during the RAD-FVT was still identified within the posterior fascicular network. Elimination of the RAD-FVTs was successfully achieved by applying radiofrequency current at a more proximal site within the left posterior fascicular network guided by the earliest PP. After a mean of 1.6 ± 0.8 ablation procedures and median follow-up of 132 (range 19-216) months since the last procedure, no recurrence was observed in any patients. The axis deviation changing of QRS complex in FVT may be attributed to the different exit sites of the reentry.

The yield of long-term electrocardiographic recordings in refractory focal epilepsy.

ObjectiveTo determine the incidence of clinically relevant arrhythmias in refractory focal epilepsy and to assess the potential of postictal arrhythmias as risk markers for sudden unexpected death in epilepsy (SUDEP).MethodsWe recruited people with refractory focal epilepsy without signs of ictal asystole and who had at least one focal seizure per month and implanted a loop recorder with 2‐year follow‐up. The devices automatically record arrhythmias. Subjects and caregivers were instructed to make additional peri‐ictal recordings. Clinically relevant arrhythmias were defined as asystole ≥ 6 seconds; atrial fibrillation < 55 beats per minute (bpm), or > 200 bpm and duration > 30 seconds; persistent sinus bradycardia < 40 bpm while awake; and second‐ or third‐degree atrioventricular block and ventricular tachycardia/fibrillation. We performed 12‐lead electrocardiography (ECG) and tilt table testing to identify non–seizure‐related causes of asystole.ResultsWe included 49 people and accumulated 1060 months of monitoring. A total of 16 474 seizures were reported, of which 4679 were captured on ECG. No clinically relevant arrhythmias were identified. Three people had a total of 18 short‐lasting (<6 seconds) periods of asystole, resulting in an incidence of 2.91 events per 1000 patient‐months. None of these coincided with a reported seizure; one was explained by micturition syncope. Other non–clinically relevant arrhythmias included paroxysmal atrial fibrillation (n = 2), supraventricular tachycardia (n = 1), and sinus tachycardia with a right bundle branch block configuration (n = 1).SignificanceWe found no clinically relevant arrhythmias in people with refractory focal epilepsy during long‐term follow‐up. The absence of postictal arrhythmias does not support the use of loop recorders in people at high SUDEP risk.

Long-Term Effect of Different Optimizing Methods for Cardiac Resynchronization Therapy in Patients with Heart Failure: A Randomized and Controlled Pilot Study

Aim: During cardiac resynchronization therapy (CRT), optimized programming of the atrioventricular (AV) delay and ventricular-to-ventricular (VV) interval can lead to improved hemodynamics, symptomatic response, and left ventricular systolic function. Currently, however, there is no recommendation for the best optimization method. This study aimed to compare the long-term clinical outcomes of 4 different CRT optimization methods. Methods: One hundred and twenty-four consecutive CRT patients with severe heart failure and left bundle-branch block configuration were randomly assigned into four groups to undergo AV/VV delay optimization through echocardiogram (ECHO; n = 30), electrocardiogram (ECG; n = 32), QuickOpt algorithm (n = 28), and nominal AV/VV (n = 36) groups. Patients were followed up and underwent examinations, including New York Heart Association (NYHA) cardiac functional classification, 6-min walking distance (6MWD), and echocardiography, at 6, 12, 24, 36, and 48 months, respectively. The patients’ survival and clinical outcomes were compared among the four groups. Results: Kaplan-Meier survival analyses showed that the median survival was the same in the 4 groups: ECHO, 43 months; ECG, 44 months; QuickOpt, 44 months, and nominal, 41 months. At the 6-month follow-up, the reduction in left ventricular end diastolic diameter (LVEDD) was significantly less in the nominal group (–1.91 ± 2.58 mm) than that in the other three groups (ECHO: –3.70 ± 2.78 mm, p = 0.012; ECG: –3.53 ± 3.14 mm, p = 0.020; QuickOpt: –3.46 ± 2.65 mm, p = 0.032); 6MWD was significantly shorter in the nominal group (87.88 ± 34.76 m) than that in the other three groups (ECHO: 120.63 ± 56.93 m, p = 0.006; ECG: 114.97 ± 54.95 m, p = 0.020; QuickOpt: 114.57 ± 35.41 m, p = 0.027). Left ventricular ejection fraction (LVEF) significantly increased in ECHO (7.23 ± 2.76%, p = 0.010), ECG (8.50 ± 3.17%, p < 0.001), and QuickOpt (8.39 ± 2.90%, p < 0.001) compared with the nominal group (5.35 ± 2.59%). There were no significant differences among the groups in the aforementioned parameters at 24, 36, and 48 months, respectively. Conclusion: While LVEDD, LVEF, 6MWD, and NYHA were significantly improved in ECHO, ECG, and QuickOpt at 6 months, there were no significant improvements in any of the groups at 12, 24, and 48 months. These findings suggested that the long-term effect of the four CRT methods for heart failure was not significantly different.

Ischemic ventricular tachycardia from below the posteromedial papillary muscle, a particular entity: Substrate characterization and challenges for catheter ablation

In patients with ischemic ventricular tachycardia (VT), substrate may be "protected" by the posteromedial papillary muscle (PMPM), explaining failure of endocardial-only ablation. We sought to characterize the arrhythmogenic substrate and ablation approach in patients with ischemic VT mapped to the inferior left ventricle in which endocardial ablation failed because of inaccessible substrate underlying the PMPM. We included 10 patients with recurrent ischemic VT, evidence of inferior scar, and failed endocardial ablation. In all patients, epicardial mapping was performed via a percutaneous (n = 9) or surgical (n = 1) approach, and VT elimination was achieved by ablation opposite to the PMPM. Clinical characteristics, electrocardiographic characteristics, and procedural data were analyzed. In all patients, intracardiac echocardiography showed hyperechoic scar below the PMPM, and 5 exhibited a pattern characterized by subendocardial basal scar that became intramural and epicardial at distal segments. In 4 patients, VT remained inducible despite endocardial scar isolation, manifested by the absence of electrograms, dissociated potentials, and/or exit block. Eleven inducible VTs were mapped to the epicardium underlying the PMPM: 8 had a right bundle branch block configuration with variable transition, while 3 exhibited left bundle branch block with negative concordance. An inferior QS pattern was present in 10 of 11 VTs. Noninducibility was achieved in 8 patients, and 7 patients remained arrhythmia-free after a mean follow-up of 27 ± 23 months. In patients with inferior ischemic scar, VT may arise from the area underneath the PMPM, limiting endocardial ablation. Intracardiac echocardiography accurately defines the substrate distribution, and an epicardial approach may eliminate VT. A pattern of "basal-endocardial/apical-epicardial" ischemic involvement is described.

Electrocardiography changes and their significance during treatment of patients with intermediate-high and high-risk pulmonary embolism.

Electrocardiography (ECG) signs, typical or acute pulmonary embolism, and their changes can be used for the prediction of clinical and haemodynamic outcomes. To study the predictive value of the resolution of admission ECG signs in higher risk pulmonary embolism patients for 30-day survival and for the decrease in right ventricular systolic pressure. We analysed the 12-lead ECGs at admission and daily for the first 5 days after hospitalisation in 110 intermediate-high and high-risk pulmonary embolism patients admitted to the intensive care unit of a single tertiary centre. The predictive value of the resolution of four ECG signs were analysed for 30-day survival and for the changes in right ventricular systolic pressure during hospitalisation: S-wave in the first standard lead, right bundle branch block pattern, S-wave in the aVL lead and negative T-waves in precordial leads. ECG recordings showed the existence of S-wave in the I lead in 71 (64.5%), S-wave in the aVL in 77 (70%), right bundle branch block pattern in 30 (27.3%) and negative T-waves in 66 (60%) patients. All-cause 30-day in-hospital mortality was 13.6%. Among the ECG signs, only the presence of right bundle branch block at admission was significantly associated with 30-day all-cause mortality (hazard ratio (HR) adjusted for age, gender and right ventricular systolic pressure at admission was 7.7, 95% confidence interval (CI) 2.1-27.9; P=0.002). The resolution of three ECG signs during the first 5 days of hospitalisation, S-wave in the I lead (HR 26.4, 95% CI 3.1-226.6; P=0.003), S-wave in the aVL (HR 21.5, 95% CI 2.6-175.3; P=0.004) and right bundle branch block configuration (HR 5.2, 95% CI 1.3-20.8; P=0.020) were associated with 30-day survival. The intermediate-high and high-risk pulmonary embolism patients with S-wave resolution in lead aVL had 0.0% and 7.1% 30-day all-cause mortality, respectively. The patients with resolution of the S-wave in the first lead and in aVL as well as right bundle branch block had more pronounced changes in right ventricular systolic pressure at discharge (27±13 vs. 13±15 mmHg; P=0.011 for S-wave in I lead resolution, 27±12 vs. 15±17 mmHg; P=0.004 for S-wave in aVL resolution and 23±14 vs. 9±14 mmHg; P=0.040 for right bundle branch block resolution) than patients without resolution. Resolution of S-waves and right bundle branch block in ECG correlates with lower all-cause 30-day mortality in intermediate-high and high-risk pulmonary embolism patients. Resolution of S-waves in the first lead and in aVL and right bundle branch block correlates with a decrease of right ventricular systolic pressure.

Cardiac resynchronization therapy response in heart failure patients with different subtypes of true left bundle branch block

Left bundle branch block (LBBB) configuration has been described as a predictor of response to cardiac resynchronization therapy (CRT). We investigated whether different subtypes of true LBBB configuration could help select patients with better response and clinical outcome. This retrospective study included 198 consecutive LBBB patients implanted with a CRT. True LBBB was defined using the Strauss and the Predict study criteria. Echocardiographic response was evaluated by the reduction in left ventricular end-systolic volume (LVESV) and the increase in left ventricular ejection fraction (LVEF). Clinical response was defined as an improvement in one category of the NYHA functional class. Patients with true LBBB had a greater improvement in both LVESV reduction (median = - 27.6%, interquartile range = [- 4.9, - 50.1]) and LVEF increase (median 10.8 ± 10) than those with non-true LBBB (- 19.7%, [16.7, - 48.0]) p = 0.04 and 5.1 ± 10, p = 0.03, respectively. No differences were exhibited between true LBBB Strauss group (- 26.7%, [- 11.0, - 46.9]) and true LBBB Predict group (- 26.6%, [- 15.9, - 39.4]). There were no statistically significant differences in the percentage of patients with clinical response, assessed by NYHA improvement, among all groups. In the Cox model for death, age, ischemic etiology, and ΔLVESV were independent predictors of mortality. True LBBB (Strauss + Predict) patients had a trend towards lower mortality than non-true LBBB [HR = 0.55, 95% CI = (0.22-1.15)], p = 0.08. In the Cox model for HF hospitalization, age, sex male, prior LVEF, and ΔLVESV were independent predictors. True LBBB (Strauss + Predict) patients had a significantly lower risk of developing HF hospitalization than those with non-true LBBB [0.45 (0.21-0.90)], p = 0.029. Patients with true LBBB, either Strauss or Predict criteria, had greater echocardiographic response and lower incidence of HF hospitalization than non-true LBBB when implanted with CRT.

Right Bundle Branch Block-Like Pattern During Uncomplicated Right Ventricular Pacing and the Effect of Pacing Site

Right bundle branch block (RBBB) configuration is an unexpected finding during right ventricular (RV) pacing that raises the suspicion of inadvertent left ventricular lead positioning. The aim of this study was to evaluate the prevalence of paced RBBB pattern in relation to RV lead location. This is a secondary analysis of a prospective, multicenter study, which randomized implantable cardioverter defibrillator recipients to an apical versus midseptal defibrillator lead positioning. A 12-lead electrocardiogram was recorded during intrinsic rhythm and RV pacing. Paced RBBB-like pattern was defined as positive (>0.05mV) net amplitude of QRS complex in leads V1 and/or V2. In total, 226 patients (65.6 ± 12.0years, 20.8% women, 53.1% apical site) were included in the study. The prevalence of paced RBBB pattern in the total population was 15.5%. A significantly lower percentage of patients in the midseptal group demonstrated RBBB-type configuration during RV pacing compared with the apical group (1.9% vs 27.5%, p <0.001). Baseline RBBB, prolonged QRS duration during intrinsic rhythm, and reduced ejection fraction were not associated with increased likelihood of paced RBBB. In the subgroup of patients with RBBB type during pacing, 91.4% of patients had a paced QRS axis from-30° to-90°, whereas 100% of patients displayed a negative QRS vector at lead V3. In conclusion, RBBB configuration is encountered in a considerable percentage of device recipients during uncomplicated RV pacing. Midseptal lead positioning is associated with significantly lower likelihood of paced RBBB pattern compared with apical location.

Upgrading and replacement in CRT devices: experience counts.

Cardiac resynchronisation therapy has proven to be highly effective in patients with heart failure and an asynchronous contraction pattern of the left ventricle, due to late activation of the posterolateral wall with left bundle branch block configuration on the ECG of more than 150 ms [1]. In pacemaker patients with a high percentage of right ventricular pacing, pacing-induced left ventricular (LV) dysfunction can appear. This newly developing heart failure is most probably the result of pacing-induced LV asynchrony. These patients with pacing-induced heart failure and ICD patients with heart failure who develop a wide QRS complex during follow-up account for the majority of patients who are eligible for an upgrade to a CRT device. In an European survey, up to 25 % of CRT implants were upgrading procedures [2]. The REPLACE registry demonstrated a high percentage of complications in upgrade and revision procedures in 434 CRT patients from 71 centres. It was not stated how many centres actually contributed to this total number of CRT upgrades [3]. Their conclusion ‘pacemaker and implantable cardioverter-defibrillator generator replacements are associated with a notable complication risk, particularly those with lead additions’ made cardiologists somewhat cautious and even reluctant to perform a therapeutic upgrade to CRT. These REPLACE data support careful decision making before device replacement when managing device advisories and when considering upgrades to more complex systems, concluded the authors [3]. And indeed, an upgrade procedure can be complicated and is in need of an experienced skilled operator or at least her or his direct supervision during the procedure. As experience is a major factor in reducing complications during and after device implantation [4], it is reasonable that experience is an even stronger denominator in complicated procedures as primary CRT implants and CRT upgrades. In this issue, the retrospective data of upgrading procedures to CRT devices were compared with the complications in primary CRT implants during the same period [5]. These retrospective data originate from one tertiary centre with a high patient load. Only three experienced operators performed the majority of procedures or supervised them. A: Total number of individual implants of 165 (62 %), including 82 upgrade procedures. Thirty assists of which 16 assists in an upgrade procedure. B: Total number of individual implants of 30 (11 %), including 13 upgrade procedures. Six assists of which 4 assists in an upgrade procedure. C: Total number of individual implants of 18 (7 %), including 9 upgrade procedures. Three assists of which 0 assists in an upgrade procedure. Though these data are retrospective, the complication rate is considerably lower when compared with the literature [3]. The most determining factor in the difference of complication rate is most likely skill, which comes from experience and cooperation during these complicated procedures. It was not investigated whether the determining factor was cooperation or experience or its combination.

Verapamil-Sensitive Upper Septal Idiopathic Left Ventricular Tachycardia: Prevalence, Mechanism, and Electrophysiological Characteristics

ObjectivesThis study sought to demonstrate the prevalence, mechanism, and electrocardiographic and electrophysiological characteristics of upper septal idiopathic left fascicular ventricular tachycardia (US-ILVT). BackgroundILVT is classified into left anterior and posterior types with no clear data about US-ILVT. MethodsAmong 193 ILVT patients, we identified 12 patients (6.2%; age 41 ± 22 years, 7 men) with US-ILVT. ResultsOf 12 patients with US-ILVT, 6 patients (50%) had previous history of radiofrequency catheter ablation for common ILVT. Sustained VT (cycle length: 349 ± 53 ms) was seen in all patients with a QRS interval slightly wider (104 ± 18 ms) than that during sinus rhythm (90 ± 19 ms). The VT exhibited an identical QRS configuration as sinus rhythm in 6 (50%) and incomplete right bundle branch block configuration in another 6. His-ventricular interval during VT was always shorter than that during sinus rhythm (27 ± 5 ms vs. 47 ± 10 ms). Purkinje potentials were activated in a reverse direction to that of common ILVT; namely, the diastolic potential (P1) was activated retrogradely but the pre-systolic potential (P2) was activated antegradely. At the left upper-middle ventricular septum, P1 potential was recorded during VT, preceding the QRS by 54 ± 20 ms. Radiofrequency catheter ablation at that site eliminated the VT with no recurrence during a 58 ± 35 months of follow-up. ConclusionsUS-ILVT is an identifiable VT that shares common criteria with ILVT and has a narrow QRS interval. Some US-ILVT cases appeared after common ILVT ablation. It is a reverse type of common ILVT (orthodromic form) with baseline morphological abnormalities that might provide a potential substrate for such VT.

Changes in QRS morphology during atrial fibrillation: What is the mechanism?

Case presentation The electrocardiogram shown in Figure 1 has been recorded from a 58-year-old man suffering from hypertension, thyrotoxicosis, and permanent atrial fibrillation. He was on propranolol, methimazole, and warfarin. The tracing (lead V1) shows atrial fibrillation with an average ventricular rate of 90 beats/min. The QRS complex morphology is variable: most beats show a left bundle branch block (LBBB) configuration, but in some complexes a right bundle branch block (RBBB) pattern or a normal morphology is evident. What is the mechanism underlying such a marked QRS variability?

A case of arrhythmogenic right ventricular cardiomyopathy in a 70-year-old patient.

A 70-year-old man was admitted because of syncope and dyspnea. Two months before admission, exertional dyspnea occurred with syncope. Ventricular tachycardia with a monomorphic left bundle-branch block configuration was detected. An echocardiographic examination showed severe dilatation and diffuse, severe hypokinesis of the right ventricle, with thrombus formation in the right ventricular apex. Based on the clinical picture, the patient was diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC). This case emphasizes the need for early identification of RV abnormalities in patients with ARVC to determine appropriate therapy.

Programmed versus Effective VV Delay during CRT Optimization: When What You See Is Not What You Get

In cardiac resynchronization therapy (CRT) devices, the interventricular (VV) delay denotes the time interval between left (LV) and right ventricular (RV) pacing. This study aimed to determine the proportion of patients in whom the effective VV delay (VVeff , delay between LV and RV depolarization, being induced either by pacing or intrinsic conduction) is different from the programmed VV delay during a standard VV delay optimization procedure. Thirty-three patients with heart failure and left bundle branch block configuration without total atrioventricular (AV) block receiving CRT were prospectively included. VVeff was calculated from intrinsic AV intervals, programmed optimal AV delay, and programming system. Intrinsic AV intervals were measured on intracardiac electrograms. The optimal AV and VV delays were determined by highest increase in maximum rate of LV pressure rise (dP/dtmax ). VV delays of 20-80 ms LV and RV preactivation were tested. Calculated maximum possible VVeff was shorter than 80 ms LV preactivation in up to 46% of patients and shorter than 40 ms LV preactivation in up to 3% of the patients. These proportions were 6% and 0% during 80 and 40 ms RV preactivation, respectively. In CRT patients with left bundle branch block without total AV block, the effective VV delay is shorter than the programmed VV delay during a standard optimization procedure in approximately half of the patients and this phenomenon is encountered predominantly during LV preactivation by 40 ms or more. Calculation of the individual maximum VVeff in advance can shorten the VV delay optimization procedure.

Delayed-Onset Complete Atrioventricular Block in a Patient with Murine Typhus Myocarditis

Murine typhus is a flea-borne infectious disease caused by Rickettsia typhi, of which myocarditis is a rare complication in the acute disseminating phase. A 62-year-old female presented with a fever and was diagnosed with murine typhus. She was treated with doxycycline and discharged after complete resolution of the fever. However, recurrent presyncope and exertional dyspnea developed 6-8 weeks later. Complete atrioventricular (AV) block with a wide QRS escape rhythm and a left bundle branch block configuration was documented. Subacute myocarditis was diagnosed based on persistent cardiac troponin-I elevation and typical cardiac magnetic resonance imaging findings. A permanent pacemaker was implanted for symptomatic complete AV block. Few reports of myocarditis in murine typhus have been published. We report a case of murine typhus myocarditis complicated by complete AV block in the late convalescence phase. (Korean J Med 2013;84:723-727)

Successful Catheter Ablation of Bidirectional Ventricular Premature Contractions Triggering Ventricular Fibrillation in Catecholaminergic Polymorphic Ventricular Tachycardia With RyR2 Mutation

The subject of this report is a 38-year-old woman who often experienced syncope since childhood. Syncope occurred >10 times a year and was associated with convulsion during exercise and emotionally exciting situations. The patient's 13-year-old daughter had also experienced frequent episodes of syncope and developed ventricular fibrillation (VF) during treadmill exercise testing that was successfully defibrillated with electric shock. Witnessing this situation, the patient also lost consciousness, with documented VF that was converted to sinus rhythm by cardiopulmonary resuscitation without electric defibrillation. Both the patient and her daughter were admitted to our hospital. We performed echocardiography, coronary angiography, and cardiac CT, the results of which revealed no structural heart disease. Resting 12-lead ECG did not indicate any abnormalities, including long-QT syndrome or Brugada syndrome. A signal-averaged ECG revealed no late potentials. Treadmill exercise testing easily induced bigeminal ventricular premature contractions (VPCs) with a right bundle branch block configuration and inferior axis (Figure 1A), and the exercise was terminated because of intolerable symptoms. Catecholamine stress test was started with administration of continuous intravenous infusion of epinephrine in a stepwise manner from 0.025 μg/kg per minute.1 During epinephrine infusion at a rate of 0.1 μg/kg per minute, multifocal VPCs (VPC #1, right bundle branch block configuration and superior axis; VPC #2, right bundle branch block configuration and inferior axis [the same VPC configuration as that induced during the treadmill exercise testing]; and VPC #3, left bundle branch block configuration and inferior axis) appeared, and VPC #1 following VPC #2 subsequently induced VF (Figure 1B). Figure 1. A , Twelve-lead ECG recording during treadmill exercise testing. Bigeminal ventricular premature contractions (VPCs) appeared during the second stage of the Bruce protocol. VPC morphology …

Radiofrequency Catheter Ablation for Unifocal Premature Ventricular Complexes Triggering Recurrent Ventricular Fibrillations in a Young Man Without Structural Heart Disease

A 17-year-old man was referred for aborted sudden cardiac death. Ventricular fibrillation (VF) was recorded by automated external defibrillator. Post-resuscitation electrocardiograms showed frequent monomorphic premature ventricular complexes (PVCs), with left bundle branch block configuration and inferior axis. Cardiac arrest due to VF recurred twice within the initial 42 hours. Rhythm monitoring revealed multiple episodes of sustained VF triggered by a triplet of monomorphic PVCs having similar morphology with isolated PVCs. Comprehensive cardiologic workup revealed no structural heart disease and ion-channelopathies. With the impression of idiopathic VF triggered by unifocal PVCs of right ventricular outflow tract (RVOT) origin, radiofrequency catheter ablation was performed to prevent frequent VF recurrence before implantable cardioverter-defibrillator (ICD) implantation. After successful ablation of the origin of unifocal PVCs at anterolateral wall of RVOT, the burden of PVCs decreased remarkably and VF did not recur. The patient was discharged after ICD implantation.

Usefulness of the 12-lead electrocardiogram in the follow-up of patients with cardiac resynchronization devices. Part II

The interval from the pacemaker stimulus to the onset of the earliest paced QRS complex (latency) may be prolonged during left ventricular (LV) pacing. Marked latency is more common with LV than right ventricular (RV) pacing because of indirect stimulation through a coronary vein and higher incidence of LV pathology including scars. During simultaneous biventricular (BiV) pacing a prolonged latency interval may give rise to an ECG dominated by the pattern of RV pacing with a left bundle branch block configuration and commonly a QS complex in lead V1. With marked latency programming the V-V interval (LV before RV) often restore the dominant R wave in lead V1 representing the visible contribution of the LV to overall myocardial depolarization. When faced with a negative QRS complex in lead V1 during simultaneous BiV pacing especially in setting of a relatively short PR interval, the most likely diagnosis is ventricular fusion with the intrinsic rhythm. Fusion may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate BiV capture. The diagnosis of fusion depends on temporary reprogramming a very short atrio-ventricular delay or an asynchronous BiV pacing mode. Sequential programming of various interventricular (V-V) delays may bring out a diagnostic dominant QRS complex in lead V1 that was previously negative with simultaneous LV and RV apical pacing even in the absence of an obvious latency problem. The emergence of a dominant R wave by V-V programming strongly indicates that the LV lead captures the LV from the posterior or the posterolateral coronary vein and therefore rules out pacing from the middle or anterior coronary vein. In some cardiac resynchronization systems LV pacing is achieved with the tip electrode of the LV lead as the cathode and the proximal electrode of the bipolar RV as the anode. This arrangement creates a common anode for both RV and LV pacing. RV anodal capture can occur at a high LV output during BiV pacing when it may cause slight ECG changes. During LV only pacing (RV channel turned off) RV anodal pacing may also occur in a more obvious form so that the ECG looks precisely like that during BiV pacing. RV anodal stimulation may complicate threshold testing and ECG interpretation and should not be misinterpreted as pacemaker malfunction. Programming the V-V interval (LV before RV) in the setting of RV anodal stimulation cancels the V-V timing to zero.