Feasibility Of Temporary Biventricular Pacing In Patients With Reduced Left Ventricular Function After Coronary Artery Bypass Grafting

Background and Methods: Biventricular pacing improves hemodynamics after weaning from cardiopulmonary bypass in patients with severely reduced left ventricular (LV) function undergoing coronary artery bypass grafting (CABG). We examined the feasibility of temporary biventricular pacing for 96 hours postoperatively. Unipolar epicardial wires were placed on the roof of the right atrium (RA), the right ventricular (RV) outflow tract, and the LV free lateral wall and connected to an external pacing device in 51 patients (mean LV ejection fraction 35 ± 4%). Pacing and sensing thresholds, lead survival and incidence of pacemaker dysfunction were determined.
Results: Atrial and RV pacing thresholds increased significantly by the 4th postoperative day, from 1.6 ± 0.2 to 2.5 ± 0.3 V at 0.5 ms (P = 0.03) at the RA, 1.4 ± 0.3 V to 2.7 ± 0.4 mV (P = 0.01) at the RV, and 1.9 ± 0.6 V to 2.9 ± 0.7 mV (P = 0.3) at the LV, while sensing thresholds decreased from 2.0 ± 0.2 to 1.7 ± 0.2 mV (P = 0.18) at the RA, 7.2 ± 0.8 to 5.1 ± 0.7 mV (P = 0.05) at the RV, and 9.4 ± 1.3 to 5.5 ± 1.1 mV (P = 0.02) at the LV. The cumulative overall incidence of lead failure was 24% by the 4th postoperative day, and was similar at the RV and LV. We observed no ventricular proarrhythmia due to pacing or temporary pacemaker malfunction.
Conclusions: Biventricular pacing after CABG using a standard external pacing system was feasible and safe.     

Time course of effects of cardiac resynchronization therapy in chronic heart failure: benefits in patients with preserved exercise capacity

Objectives: To assess in patients with chronic heart failure the effect of cardiac resynchronization therapy (CRT) over 12 months' follow-up the time course of the changes in functional and neurohormonal indices and to identify responders to CRT.
Methods: Eighty-nine patients (74.1 ± 1 years, left ventricular ejection fraction [LVEF] < 35%), QRS complex duration >150 ms, in stable New York Heart Association (NYHA) class III or IV on optimal medical treatment were prospectively randomized either in a control (n = 45) or CRT (n = 44) group and underwent clinical evaluation, cardiopulmonary exercise testing (CPET), 2D-Echo, heart rate variability (HRV), carotid baroreflex (BRS), and BNP assessments before and at 6- and 12-month follow-up.
Results: In the CRT group, improvement of cardiac indices and BNP concentration were evident at medium term (over 6 months) follow-up, and these changes persisted on a longer term (12 months) (all P < 0.05). Instead CPET indices and NYHA class improved after 12 months associated with restoration of HRV and BRS (all P < 0.05). We identified 26 responders to CRT according to changes in LVEF and diameters. Responders presented less depressed hemodynamic (LVEF 25 ± 1.0 vs 22 ± 0.1%), functional (peak VO₂ 10.2 ± 0.2 vs 6.9 ± 0.3 ml/kg/min), and neurohormonal indices (HRV 203.6 ± 15.7 vs 147.6 ± 10.ms, BRS 4.9 ± 0.2 vs 3.6 ± 0.3 ms/mmHg) (all P < 0.05). In the multivariate analysis, peak VO₂ was the strongest predictor of responders.
Conclusions: Improvement in functional status is associated with restoration of neurohormonal reflex control at medium term. Less depressed functional status (peak VO₂) was the strongest predictor of responders to CRT.     

Abnormal Atrioventricular Node Conduction and Atrioventricular Nodal Reentrant Tachycardia in Patients Older Versus Younger Than 65 Years of Age

Study Objective: We examined the possible role of atrioventricular node (AVN) conduction abnormalities as a cause of AVN reentrant tachycardia (RT) in patients >65 years of age.
Study Population: Slow pathway radiofrequency catheter ablation (RFCA) was performed in 104 patients. Patients in group 1 (n = 14) were >65 years of age and had AV conduction abnormalities associated with structural heart disease. Patients in group 2 (n = 90) were <65 years of age and had lone AVNRT.
Results: Patients in group 1 versus group 2 (66% vs. 46% men) had a first episode of tachycardia at an older age than in group 2 (68 ± 16.8 vs 32.5 ± 18.8 years, P = 0.007). The history of arrhythmia was shorter in group 1 (5.4 ± 3.8 vs 17.5 ± 14, P = 0.05) and was associated with a higher proportion of patients with underlying heart disease than in group 2 (79% vs 3%, P < 0.001). The electrophysiological measurements were significantly shorter in group 2: atrial-His interval (74 ± 17 vs 144 ± 44 ms, P = 0.005), His-ventricular (HV) interval (41 ± 5 vs 57 ± 7 ms, P = 0.001), Wenckebach cycle length (329 ± 38 vs 436 ± 90 ms, P = 0.001), slow pathway effective refractory period (268 ± 7 vs 344 ± 94 ms, P = 0.005), and tachycardia cycle length (332 ± 53 vs 426 ± 56 ms, P = 0.001). The ventriculoatrial block cycle length was similar in both groups. The immediate procedural success rate was 100% in both groups, and no complication was observed in either group. One patient in group 2 had recurrence of AVNRT. One patient with a 98-ms HV interval underwent permanent VVI pacemaker implantation before RFCA procedure.
Conclusion: In patients undergoing RFCA for AVNRT at >65 years of age had a shorter history of tachycardia-related symptoms than patients with lone AVNRT. The longer AVN conduction intervals and refractory period might explain the late development of AVNRT in group 1.     

Segmental Wall Motion Abnormality Analyzed by Equilibrium Radionuclide Angiography and Improvement in Ventricular Function by Cardiac Resynchronization Therapy

Introduction: The purpose of this study was to determine the impact of the left ventricular (LV) segmental wall motion abnormalities detected by equilibrium radionuclide angiography (ERNA) on the improvement in LV and right ventricular (RV) function during biventricular (BIV) stimulation .
Results: We studied 28 patients in NYHA functional classes III or IV and QRS duration >150 ms on resting electrocardiogram. ERNA was performed before and during BIV stimulation at a 6-month follow-up. A significant shortening of QRS duration was observed during BIV stimulation (165 ± 5 ms before vs 133 ± 6 ms during, P < 0.01). Wall motion abnormalities (WMA) were observed in 16 patients (10 with nonischemic cardiomyopathies). In this group, LV and RV ejection fractions (EF) did not increase during BIV stimulation (LVEF = 22 ± 2% vs 20 ± 1.6%, ns; RVEF = 34 ± 3% vs 37 ± 3.8%, ns). Significant increases in RVEF (23 ± 3.2 %→ 38 ± 2.9%, P = 0.001) and LVEF (20 ± 2.5 %→ 30 ± 3%, P = 0.01) were observed in the group of patients without segmental WMA and with global hypokinesia (GH). In this group, a significant decrease in the dispersion in the phase of RV contraction was observed (SD = 39 ± 5 vs 26 ± 2 ms; P < 0.01). WMA predicted an increase in LVEF, in contrast to a baseline 6-minute-walk test, maximal oxygen consumption and LVEF, or amount of QRS shortening.
Conclusions: BIV stimulation increased in LV and RV EF in patients with ventricular dyssynchrony in absence of segmental WMA. ERNA was reliable in the selection of candidates for CRT.     

The Effects of Trimetazidine on P-Wave Duration and Dispersion in Heart Failure Patients

Background: P-wave duration and dispersion (PWD) have been shown to be noninvasive predictors for development of atrial fibrillation. Thus, it may be possible to attenuate atrial fibrillation risk through normalization of P-wave duration and dispersion. Trimetazidine, a metabolic modulator, has been reported to improve cardiac function in heart failure (HF) patients.
Methods: Thirty-six HF patients being treated with angiotensin inhibitors, carvedilol, spironolactone, and furosemide were prescribed trimetazidine, 20 mg three times a day. Electrocardiographic and echocardiographic examinations were obtained before and 6 months after addition of trimetazidine in HF patients and 36 healthy control group patients having normal echocardiographic examination.
Results: Maximum P-wave duration (Pmax) (106.7 ± 15.8 vs. 91.7 ± 12.7 ms) and PWD (57.2 ± 15.4 vs. 37.9 ± 16.7 ms) were significantly longer in HF patients compared to the control group. There were significant correlations of Pmax and PWD with left atrial diameter (r = 0.508, P = < 0.001 and r = 0.315, P = 0.029), left ventricular ejection fraction (LVEF) (r = 0.401, p = 0.005 and r = 0.396, P = 0.005), deceleration time (r = 0.296, P = 0.032 and r = 0.312, P = 0.035), and isovolumetric relaxation time (r = 0.265, P = 0.038 and r = 0.322, P = 0.015). There were significant improvements in LVEF (32.7 ± 6.5% to 37.2 ± 5.5%, P = 0.036), left atrial diameter (41.5 ± 6.7 to 40.3 ± 6.1 mm, P < 0.001), and Pmax (106.7 ± 15.8 to 102.2 ± 11.5 ms, P = 0.006) and PWD (57.2 ± 15.4 to 48.9 ± 10.1 ms, P < 0.001) during follow-up.
Conclusions: Trimetazidine added to optimal medical therapy in HF may improve Pmax and PWD in association with improved left ventricular function. Longer-term and larger studies are necessary to evaluate whether these findings may have clinical implications on prevention of atrial fibrillation.     

Local Repolarization Abnormalities Induced by Transcatheter Radiofrequency Ablation in Pigs

Radiofrequency (RF) ablation alters action potential repolarization of myocardial cells and, theoretically, tbis should induce ST-T segment changes in the ECG. Since these ECG abnormalities have been rarely reported in patients submitted to RF ablation we assess the ability of the procedure to caase ST-T segment changes in local electrograms. Epicardial ECG mapping was performed in 17 anesthetized open chest pigs submitted to endocardial (n = 9) or to epicardial (n = 8) unipolar radiofrequency ablation (500 kHz, 20 W for 5-10 s). To characterize the cellular electrophysiological alterations induced by RE ablation transmembrane action potentials were recorded at various distances from the ablation lesion; these were compared with seven control pigs. Endocardial RE ablation induced a transient (< 5 min) change of 6.1 ± 2.4 m V in T wave amplitude (baseline: 12.8 ± 5.6 mV, P < O.OOl) in 141 out of 269 epicardial electrodes. T wave changes were associated with shortening in local activation time (20.1 ± 2.3 ms at baseline vs 18.5 ± 2.5 ms at 60 s after ablation, P = 0.03). RE current caused persistent ST segment elevation at the center of the ablation lesion with no transmural expansion. Intracellular potentials along a 2-6-mm wide myocardial band bordering the RE lesion showed lower amplitude (101 ± 7.0 mV vs 71 ± 23 mV, P < 0.01) and shorter duration (254 ± 44 ms vs 156 ± 29 ms, P < 0.01) than control hearts. The center of the ablation lesion was electrically anexcitable. We concluded that RF ablation alters cellular electrophysiology in small areas surrounding the ablation lesion and this causes short-lasting transmural changes in T wave amplitude and nontransmural ST segment elevation.     

The Dynamic Behavior of the Diastolic Slope of Monophasic Action Potential Can be Related to the Occurrence and Maintenance of Delayed Afterdepolarization Dependent Arrhythmias

We have described the value of the diastolic slope of the MAP recording at the end of a pacing train as a qualifying marker for the induction of delayed afterdepolarization (DAD) dependent arrhythmias. In the present study (1) the behavior of the slope at different time points during a pacing train was quantified and related to the arrhythmogenic outcome (group A) and (2) termination of DAD dependent VT was related to changes in the slope steepness (group B). In dogs with chronic complete AV block, a MAP was recorded during (1) ventricular pacing, before and after ouabain administration (group A) and (2) 6 spontaneous and 6 lidocaine induced VT terminations (group B). During control (group A), the slope at the end of pacing train was 5 ± 3 mV/s (mean ± SD), independent of the pacing duration. During ouabain, this increased to 20 ± 15 mV/s (P < 0.05), varying with the duration of pacing. The slope was steeper after pacing for 4 seconds, compared to 20 seconds (26 ± 12 mV/s vs 16 ± 13 mV/s, P < 0.05) which corresponded with more frequent VT induction. In spontaneously terminating VTs (group B), CL increased from 353 ± 54 ms at the start to 434 ± 78 ms (P < 0.05) before VT termination. This corresponded with a decreasing steepness of the slope from 19 ± 10 mV/s to 6 ± 5 mV/s (P < 0.05). In lidocaine induced VT termination, the CL and the steepness of the slope showed an identical behavior. There is a dynamic variation in the steepness of the diastolic slope during pacing, which depends on the duration of pacing and predicts arrhythmogenic outcome. Furthermore, a decrease in steepness of the slope during DAD dependent VT can be used to predict VT termination.     

QT Duration and Dispersion in Patients with Anomalous Origins of Coronary Arteries

Background: Coronary artery anomalies have been reported to show various symptoms ranging from chest pain and dyspnea to cardio-respiratory arrest and sudden death. In this study, we attempted to assess the changes in QT interval duration and dispersion in anomalous origins of coronary arteries (AOCA).
Methods: Nineteen AOCA patients (mean age: 52 ± 11 years) and 30 healthy control subjects (mean age: 50 ± 12 years) were included in the study. Minimum and maximum corrected QT intervals, and corrected QT dispersion were calculated. The two groups were compared in terms of QT dispersion and QT duration.
Results: There was no difference between the two groups in terms of baseline demographic characteristics. Maximum corrected QT intervals (QTc max), minimum corrected QT intervals (QTc min), and corrected QT dispersion were higher in AOCA patients than controls (452 ± 38 vs 411 ± 25 ms [P = 0.0001], 402 ± 31 vs 383 ± 28 ms [P = 0.048], and 51 ± 30 vs 28 ± 12 ms [P = 0.001], respectively).
Conclusion: In the patients with anomalous origins of coronary arteries, QT dispersion that is an indicator of sudden cardiac death and arrhythmias frequency increased. QTc max, QTc min, and corrected QT dispersion are higher in patients with anomalous origin of the coronary artery than in control subjects.     

Intracardiac echocardiography-guided his bundle pacing and atrioventricular nodal ablation

Background: His bundle pacing (HBP) results in rapid synchronous ventricular activation, but has been associated with long procedure times and compromised pacing and sensing performance. This study sought to reduce procedure time and radiation exposure, and improve electrical performance through more accurate lead placement.
Methods: Intracardiac echocardiography (ICE) was used to guide ablation and lead implantation at the His bundle, right atrial appendage (RAA), and right ventricular apex (RVA), and to assess cardiac function. Custom bipolar screw-in leads with steerable delivery sheaths and an ablation catheter were navigated using ICE (local detailed imaging) and fluoroscopy (global imaging) in anesthetized closed-chest canines (N = 6).
Results: HBP (N = 1) or His + ventricular septal pacing (N = 5) was achieved in all canines. The QRS width was 59.7 ± 5.3 ms for canines in sinus rhythm (SR) and 82.8 ± 16.6 ms for canines with HBP (P = 0.0086). The QRS width for RVA pacing was 106.3 ± 18.4 ms (P = 0.042 vs HBP; P = 0.00013 vs SR). HBP thresholds were 3.0 ± 1.0 volts at 0.5 ms (N = 5 due to a late exit block in one canine). The average procedure duration for His lead placement was 40 ± 28 minutes (range of 3–81 minutes) and the total procedural X-ray exposure was 12 ± 12 minutes (range of 2–30 minutes). Hemodynamic performance was similar for HBP and RAA pacing.
Conclusions: Feasibility of ICE guidance for His pacing and precision ablation of the atrioventricular (AV) node has been shown. This anatomic approach improved accuracy, limited X-ray exposure, and might allow His pacing in patients with preexisting AV nodal block.     

Atrial Synchronous Ventricular Pacing with a Single Lead: Reliability of Atrial Sensing During Physical Activities, and Long-term Stability of Atrial Sensing

A VDD pacing system with bipolar single-pass leads, were implanted in 36 consecutive patients (average age 72 ± 2years) with high degree atrioventricular block and normal sinus node function. At implant the atrial signal amplitude was 2.6 ± 0.2mV measured by a pacing system analyser (PSA), 1.8 ± 0.1mV measured peak-to-peak from the telemetered calibrated electrogram, and 1.3 ± 0.1mV measured from the sensing threshold. At one month follow-up the peak-to-peak amplitudes (mV) of the telemetered atrial electrograms were not significantly different measured continuously during resting supine with quiet breathing (1.4 ± 0.1), sitting (1.6 ± 0.2). standing (1.5 ± 0.1), arm swinging (1.4 ± 0.2), hyperventilation (1.3 ± 0.1), Vaisalva manoeuvre (1.4 ± 0.1), and treadmill exercise (1.9 ± 0.6). The telemetered atrial electrogram amplitude and the atrial sensing threshold varied between 1.2 ± 0.09mV and 1.8 ± 0.1mV, and between 0.95 ± 0.07mV and 1.3 ± 0.01mV, respectively at 0.5, 1, 3, 6 and 12 months follow-up, but the changes were statistically nonsignificant. The Event Summary showed sensing of 98% to 99% of the atrial events at the different follow-up periods.     

环磷酰胺致小鼠心脏功能损伤超声评价及其与血清外泌体miRNA的相关性

目的分析环磷酰胺心脏毒性小鼠模型血清外泌体miRNA的改变,为更准确的评估环磷酰胺导致心脏功能损伤的程度提供新方法。 方法选用7~8周龄的C57BL/6小鼠,随机分为对照组和环磷酰胺组2组。环磷酰胺组小鼠给予环磷酰胺100 mg /（kg?周）,根据临床化疗方案,连续腹腔注射2周后,休息1周,再连续注射2周,共5周;对照组小鼠腹腔注射等量0.9%氯化钠溶液。第5周进行小鼠心脏超声检查,测量或计算左心室射血分数（LVEF）、短轴缩短率（FS）、左心室等容舒张期时间（IVRT）及Tei指数,同时行血清外泌体候选miRNA的q-PCR检测。采用t检验比较环磷酰胺组与对照组小鼠LVEF、FS、IVRT、Tei指数、血清外泌体miRNA表达量。 结果与对照组小鼠比较,环磷酰胺组小鼠LVEF、FS均降低［0.62±0.05 vs 0.72±0.06,（28.00±3.10）% vs （35.10±4.95）%］,且差异均有统计学意义（t=3.591,P=0.003;t=3.453,P=0.004）;Tei指数、IVRT均升高［0.71±0.17 vs 0.59±0.14,（27.42±8.42）ms vs （23.40±6.70）ms］,但差异无统计学意义。与对照组小鼠比较,环磷酰胺组小鼠血清外泌体中miR-133a-3p、miR-146a-5p表达增高（1.931±1.460 vs 0.072±0.077,1.895±1.059 vs 0.790±0.296）,且差异均有统计学意义（t=4.072,P=0.001;t=3.168,P=0.006）;miR-30c-5p、miR-99a-5p表达差异无统计学意义（0.870±0.327 vs 0.530±0.670,0.404±0.134 vs 0.714±0.404）。 结论C57BL/6小鼠腹腔注射环磷酰胺能够引起心脏功能明显损伤,心脏功能受损小鼠血清外泌体中miR-133a-3p和miR-146a-5p表达增高,使其有望成为诊断环磷酰胺心脏功能受损新的血清标志物。     

Comparison of Bipolar Atrial Electrogram Amplitude in Sinus Rhythm, Atrial Fibrillation, and Atrial Flutter

Automatic mode switching pacemakers revert to non-atrial tracking modes in response to sensed atrial tachyarrhythmias. It is unclear how atrial electrogram amplitudes in sinus rhythm compare to those during atrial tachyarrhythmias. In this study, peak-to-peak bipolar atrial electrogram amplitudes were measured during sinus rhythm and either atrial fibrillation or atrial flutter in 69 patients. The mean atrial electrogram amplitudes were 1,59 ± 1.36 m V during sinus rhythm and 0.77 ± 0,58 mV during atrial fibrillation (P < 0.0001) for 25 patients with atrial fibrillation and 1.81 ± 2.07 mV during sinus and 1.5 ± 1.81 mV(P < 0.0001) for 44 patients with atrial flutter. The mean electrogram amplitudes during both atrial fibrillation and flutter correlated significantly with amplitudes during sinus rhythm (R = 0.79, R = 0.94. respectively, both P < 0,0001). The coefficient of variance of individual electrogram amplitudes was greater in atrial fibrillation than sinus (P < 0.0001). By comparing 20th percentile electrogram amplitudes in atrial fibrillation and flutter to mean sinus amplitudes, intermittent very low electrogram amplitudes (< 0.3 mV) were more likely during atrial fibrillation and flutter if the mean sinus electrogram amplitudes were < 1.5 mV and < 0.5 mV, respectively (P < 0.01). Eightieth percentile electrogram amplitude values in atrial fibrillation and flutter were equally likely to exceed mean sinus amplitude values in respective patients, in conclusion, mean atrial electrogram amplitudes during atrial fibrillation and flutter are less than but correlated to sinus rhythm electrogram amplitudes. Very low amplitude individual electrograms during these atrial arrhythmias are associated with low mean sinus rhythm electrogram amplitudes. These findings may have implications for the programming of permanent dual chamber pacemakers in patients with paroxysmal atrial fibrillation and flutter.     

Relationship Between Global Myocardial Index and Automatic Left Ventricular Border Detection Pattern to Identify Biventricular Pacing Candidates

Objective of the Study: to evaluate the relation between global myocardial index (GMI) and the pattern of left ventricular (LV) volume curves variation, using automatic border detection (ABD), and their role in assessing LV asynchrony.
Methods: We studied 52 patients (mean age = 55 ± 17 years) with dilated cardiomyopathy. QRS duration (QRSd) and GMI were measured. Currently accepted TDI and M-mode parameters were used to indicate LV dyssynchrony. On-line continuous LV volume changes were recorded using ABD. Ejection time (ET ABD) was measured from the ABD wave-forms as time interval between maximal and minimal volume variation during LV electromechanical systole. We derived the ejection time index (ETiABD) as the ratio between ET ABD and RR interval (ETiABD = ET/RR).
Results: 31 patients had a QRSd >120 ms and 21 patients had a QRSd <120 ms. Ventricular dyssynchrony was observed in 39 patients (29 patients had a QRSd > 120 ms). GMI was significantly higher in patients with, than in patients without ventricular dyssynchrony (1.06 ± 0.18 vs 0.73 ± 0.13, P = 0.0001), while ETABD was significantly smaller (233 ± 39 ms vs 321 ± 28 ms, P = 0.0001). The corresponding difference for ETiABD was 26.9 ± 6.8% vs 6.3 ± 4%, P < 0.0001. By simple regression analysis an inverse linear correlation was observed between GMI and ETiABD (r²=–0.51, P < 0.0001). The pattern of ABD waveforms showed increased isovolumic contraction and relaxation times in patients with LV asynchrony, similar to the GMI pattern.
Conclusions: Regional delays in ventricular activation cause uncoordinated and prolonged ventricular contractions, with lengthening of the isovolumic contraction and relaxation times and shortening of the time available for filling and ejection. GMI explores these parameters and together with ABD might be useful to identify patients with ventricular asynchrony.     

Abnormal Nocturnal Heart Rate Variability and QT Dynamics in Patients with Brugada Syndrome

Background: In Brugada syndrome (BSY), most of the ventricular arrhythmic events are nocturnal, suggesting an influence of the autonomic nervous system.
Methods: In 46 patients (mean age = 41 ± 14 years, 43 men) with electrocardiograms (ECG) consistent with BSY and structurally normal hearts, we measured heart rate variability (HRV) and QT dynamics (QT/RR slopes) on 24-hour ambulatory ECG. Type 1 BSY-ECG was spontaneous in 23 (50%) and induced in 23 patients.
Results: History of syncope was present in 23 patients (50%). Programmed ventricular stimulation induced ventricular tachyarrhythmias (VTA) in 13 patients (28%). A single patient developed ventricular tachycardia during a mean follow-up of 34 months. Compared to a control group matched for age and sex, HRV was decreased over 24 hours and during nighttime in patients with BSY (SDNN 122 ± 44 vs 93 ± 36 ms, P = 0.0008 and SDANN 88 ± 39 vs 54 ± 24 ms, P < 0.0001). QTend /RR slopes were decreased over 24 hours in patients with BSY (0.159 ± 0.05 vs 0.127 ± 0.05, P = 0.003) and particularly at night (0.123 ± 0.04 vs 0.089 ± 0.04, P = 0.0001). QTend /RR slopes were significantly decreased during nighttime in patients with spontaneous versus provoked BSY-ECG patterns. By contrast, HRV and QT/RR slopes were similar in symptomatic and asymptomatic patients, whether VTA were induced or not.
Conclusions: Patients with a BSY-ECG pattern had lower HRV and QT/RR slopes than control subjects during nighttime. High-risk patients with spontaneous BSY-ECG patterns had the lowest nocturnal QTend/RR slopes. These unique repolarization dynamics might be related to the frequent nocturnal occurrence of VTA in BSY.     

Atrial Electromechanical Sequence and Contraction Synchrony during Single- and Multisite Atrial Pacing in Patients with Brady-Tachycardia Syndrome

Objectives: Investigation of which atrial pacing modality provides atrial synchrony and the most physiological atrial contraction pattern in patients with brady-tachycardia syndrome.
Methods: Fifteen healthy subjects and 57 patients with sinus node dysfunction, atrial fibrillation recurrences, and prolonged P-wave on the electrocardiogram treated with multisite atrial (MSA) pacing were studied. One atrial lead was implanted in the coronary sinus (CS) ostium area, the other at the right atrial appendage (RAA): RAA+CS group (28 patients), or Bachmann's bundle (BB) region: BB+CS group (29). Sinus rhythm (SR) and CS, RAA, BB, RAA+CS, and BB+CS pacing modalities were evaluated. Electromechanical delay (EMD) in atrial walls was assessed by tissue Doppler echocardiography. Interatrial (ΔinterA), intra-right (ΔRA), and intra-left (ΔLA) atrial dyssynchrony were calculated.
Results: During SR, in the study group versus controls, important ΔinterA: 55 ± 23 versus 22 ± 11 ms (P < 0.01) and ΔLA: 47 ± 21 versus 21 ± 6 ms (P < 0.001) were present. Single-site BB and both MSA pacing modes restored ΔinterA and ΔLA (ΔinterA: 24 ± 16, 20 ± 13 and 14 ± 9 ms, ΔLA: 28 ± 18, 28 ± 13 and 20 ± 10 ms during BB, RAA+CS and BB+CS pacing, respectively). CS pacing prolonged lateral RA EMD, while RAA pacing LA walls EMD, which resulted in ΔinterA persistence. CS pacing induced ΔRA (50 ± 23 vs 16 ± 8 ms, P < 0.0001 vs controls). Atrial contraction sequence during BB pacing resembled that observed in controls.
Conclusions: (1) Single-site BB and both MSA pacing modes restored atrial synchrony. (2) Single-site RAA and CS ostium pacing retained interatrial dyssynchrony; moreover, CS pacing created RA dyssynchrony. (3) Single-site BB pacing provided physiological atrial contraction sequence.     

Brugada-Like Changes in the Peripheral Leads during Diagnostic Ajmaline Test in Patients with Suspected Brugada Syndrome

Background: Although cases of Brugada-type electrocardiographic (ECG) pattern in peripheral (limb) leads have been reported ("atypical" Brugada syndrome [BS]), their incidence in patients investigated for BS is unknown.
Methods: We retrospectively analyzed an ECG database collected during ajmaline test in 143 patients (89 men) with suspected BS. In 42 patients, 12-lead ECGs were recorded, whereas in 101 patients, leads V1–V3 from the third intercostal space were also recorded. The presence of types 1, 2, and 3 Brugada pattern in each limb and precordial lead was noted and the PR, QRS, and QTc intervals were calculated.
Results: There were 114 (79.7%) negative and 29 (20.3%) positive tests. Type 1 pattern developed in ≥1 limb lead in six patients (4.2%) (3/29 with positive tests, 10.3%); all of them were male, symptomatic, and/or with family history of BS or sudden cardiac death. Their pre- and posttest QRS were significantly longer compared with the rest with positive (n = 26) or negative (n = 111) test (pretest: 129 ± 31 ms vs 101 ± 11 ms and 97 ± 12 ms, P < 0.001; posttest: 175 ± 44 ms vs 134 ± 14 ms and 131 ± 19 ms, P < 0.001). The posttest QTc was longer in patients with peripheral changes compared with the rest (507 ± 47 ms vs 453 ± 22 ms and 447 ± 24 ms, P < 0.001). The pretest QTc and pre- and posttest heart rate and PR intervals were not significantly different between the three groups.
Conclusions: Type 1 Brugada pattern in the peripheral leads was observed in 4.2% of patients during ajmaline test (10.3% of positive tests) and was associated with longer QRS and greater QTc prolongation compared with the rest of the patients.     

Right Atrial Appendage Versus Bachmann's Bundle Stimulation: A Two-Year Comparative Study of Electrical Parameters in Myotonic Dystrophy Type-1 Patients

Aim: We performed a two-year follow-up comparative study of long-term electrical parameters between the right atrial appendage (RAA) and Bachmann's Bundle (BB) stimulation in myotonic dystrophy type 1 (MD1) patients.
Methods: Twenty-five MD1 patients (18 men; age: 54 ± 13 years) with no difference in the electrical parameters between the RAA site and the BB region at implantation were randomized into two groups: in group I (13 patients; age: 52 ± 14 years; four women) the atrial lead was placed in the RAA and in group II (12 patients, age: 56 ± 12 years, three women) the lead was placed in the BB region. Measurements of electrical parameters were recorded at follow-up intervals of 6 weeks and then 12 and 24 months postimplant.
Results: There was no statistically significant different in P-wave amplitude, pacing threshold, and impedance values between the two groups at 6 weeks. At 24 months follow-up, the intrinsic P-wave amplitude was 2.05 ± 1.45 mV in the RAA group versus 3.28 ± 1.09 mV in the BB group (P < 0.05); the pacing threshold was 1.85 ± 1.8 V in the RAA group versus 0.50 ± 0.39 V in the BB group (P = 0.03); there were no differences in the atrial impedance between the two groups during the follow-up period.
Conclusions: In a direct two-year follow-up comparison between the RAA and BB atrial pacing sites, we showed a statistically significant increased pacing threshold and decreased intrinsic P-wave amplitude during RAA stimulation in MD1 patients.     

P-Wave Duration and Dispersion in Patients with Metabolic Syndrome

Background: Metabolic syndrome (MS) has been reported to be associated with an increased risk of atrial fibrillation (AF). The aim of this study was to investigate P-wave dispersion (PWD) in patients with MS.
Methods: The study population included 66 patients with MS (21 men, 45 women; mean age, 49.7 ± 9.1 years) and 63 control subjects without MS (26 men, 37 women; mean age, 47.0 ± 10.6 years). The diagnosis of MS was based on the National Cholesterol Education Program Adult Treatment Panel III criteria. A 12-lead electrocardiogram was recorded for each subject. The difference between maximum and minimum P-wave duration was calculated and defined as PWD. An echocardiographic examination was also performed for each subject.
Results: Maximum P-wave duration and PWD were found to be significantly higher in patients with MS compared with the control subjects (Maximum P-wave duration: 113.5 ± 9.7 ms vs 101.0 ± 8.1 ms, PWD: 37.8 ± 7.6 vs 23.3 ± 5.9, respectively, P < 0.001 for both). However, there was no statistically significant difference between two groups regarding minimum P-wave duration (75.6 ± 6.9 ms vs 77.6 ± 7.8 ms, respectively, P = 0.18). In addition, PWD was positively correlated with age, body mass index, waist circumference, systolic and diastolic blood pressure, triglyceride level, deceleration time, isovolumetric relaxation time and negatively correlated with high-density lipoprotein cholesterol level and early-to-late diastolic velocity ratio .
Conclusion: We have shown that patients with MS have higher PWD, indicating increased risk for AF, compared to the control subjects without MS.     

Cavotricuspid Isthmus Ablation with Large-Tip Gold Alloy Versus Platinum-Iridium-Tip Electrode Catheters

Background: Gold has excellent electrical conductive properties and creates deeper and wider lesions than platinum-iridium during radiofrequency (RF) ablation in vitro . We tested the maximum voltage-guided technique (MVGT) of cavotricuspid isthmus (CTI) ablation using two 8-mm tip catheters containing gold (group G) or platinum-iridium (group PI).
Methods: We enrolled 31 patients who underwent CTI ablation. In group G (n = 15) CTI ablation was performed with a gold-tip ablation catheter, while in group PI (n = 16) a platinum-iridium tip was used. Ablation was guided by CTI potentials with the highest amplitude until achievement of bidirectional block (BIB). If BIB was not achieved after 10 RF applications, RF was delivered via a 3.5-mm irrigated-tip catheter. Success rate, procedure duration, duration of fluoroscopic exposure, and number of RF applications were measured.
Results: BIB was achieved in all patients in group G, while in group PI an irrigated tip was used in four patients (0% vs 25%, P < 0.001). These four patients required a total of 21 additional RF applications (5.25 ± 2.22). Procedure time (56.4 ± 12 vs 73.1 ± 15 minutes P < 0.05) and fluoroscopic explosure (4.9 ± 2.3 vs 7.1 ± 3.8 minutes, P < 0.01) were shorter in group G than in group PI. Mean number of RF applications was lower (4.6 ± 1.9 vs 6.6 ± 3.1 P < 0.001) and total RF duration shorter (280 ± 117 vs 480 ± 310 seconds) in group G than in group PI. No difference was observed in the number of recurrences at a 6 month-follow up (1 in group G vs 1 in group PI).
Conclusion: Using the MVGT of CTI ablation, gold-tip catheters were associated with shorter procedural and fluoroscopic times, and fewer RF applications.     

Baroreflex Sensitivity and Heart Rate Variability in Coronary Disease Compared to Dilated Cardiomyopathy

This study was designed to compare baroreceptor sensitivity and heart rate variability as measures of cardiac autonomic tone in patients with coronary disease (CAD, n = 49) and idiopathic dilated Cardiomyopathy (IDC, n = 130). Time domain heart rate variability, including SDNN, SDANN, and pNN50, was determined during 24-hour Holter ECG. Baroreflex sensitivity was analyzed nonivasively using the phenylephrine method. Baroreflex sensitivity and heart rate variability were comparable between patients with CAD versus IDC (baroreflex sensitivity: 6.1 ± 3 vs 6.9 ± 5 ms/mmHg; SDNN: 97 ± 40 vs 114 ± 41 ms; SDANN: 83 ± 33 vs 99 ± 41 ms; pNNSO: 3.9 ± 4 vs 9.6 ± 13 ms, P = NS for all comparisons). Likewise, a subgroup analysis of patients with a left ventricular ejection fraction (LVEF) ≤ 30% showed no significant difference in baroreceptor sensitivity and heart rate variability between IDC and CAD patients. Patients with CAD and an LVEF > 30% had a decreased heart rate variability but not a decreased baroreflex sensitivity compared to patients with IDC and LVEF > 30 % (baroreflex sensitivity: 6.4 ± 4 vs 8.3 ± 6 ms/mmHg, P = NS; SDNN: 98 ± 19 vs 128 ± 42 ms, P < 0.05; SDANN: 86 ± 21 vs 112 ± 43 ms, P < 0.05; pNN50: 4.2 ± 3 vs 12.3 ± 8 ms, P < 0.05). Patients with a markedly depressed LVEF show comparable alterations in cardiac autonomic tone whether they have CAD or IDC. Patients with CAD and preserved LV function, however, have a decreased heart rate variability compared to patients with IDC and preserved LV function. The prognostic significance of these findings will be determined prospectively in a large patient cohort at our institution.