A histological study of the atria in patients with isolated rheumatic mitral regurgitation with and without atrial fibrillation.

BACKGROUND: There is a high incidence of atrial fibrillation (AF) in patients with isolated rheumatic mitral regurgitation (MR). The histopathologic changes in the atria of patients with isolated rheumatic MR with and without AF are unknown. OBJECTIVES: We aimed to determine the histological findings in patients with isolated severe rheumatic MR with and without AF. METHODS: Patients with severe isolated rheumatic MR undergoing valve replacement surgeries underwent endocardial biopsies from right atrial appendage, left atrial appendage, right free wall, left free wall, left posterior wall, and mitral valve. Group I consisted of patients in sinus rhythm (SR), and Group II included patients with AF. We analyzed and compared these 10 histological features in the biopsies of patients in Groups I and II. RESULTS: Of the 25 patients, 12 were in Group I and 13 in Group II. In Group I, patients had severe myocyte hypertrophy (60% vs. 18%, p = .04) that was significantly more in the right atrium (22.7% vs. 11.4%, p = .059). Interstitial adipose tissue deposition was more common in Group I (30% vs. 25%, p = .06). Interstitial fibrosis was evenly distributed at all sites without significant difference between the two groups. Group II patients had a higher prevalence and severity of vacuolar degeneration (91% vs. 60%, p = .09). CONCLUSIONS: Patients with isolated severe rheumatic MR and AF have more vacuolar degeneration in the atrial tissue. Patients with SR have myocyte hypertrophy and interstitial adipose tissue deposition. Interstitial fibrosis is uniformly distributed in patients in SR and AF.

Outcomes in congenital and childhood complete atrioventricular block: A meta-analysis.

BACKGROUND: The long-term outcomes of patients with congenital and childhood complete atrioventricular block (CCAVB/CAVB) after pacemaker implantation are unclear. METHODS: We performed a meta-analysis of all the studies of CCAVB. A systematic search of PubMed and CENTRAL databases from January 1, 1967 to January 31, 2020 was performed. The quality of studies included was critically appraised using the Newcastle-Ottawa scale, and outcome data were analyzed using the restricted maximum likelihood function. RESULTS: Twenty-nine studies were eligible for analysis, with a total of 1553 patients. The all-cause-mortality was 5.7% (95% confidence interval [CI]: 2.5%-9.9%), while pacing-induced cardiomyopathy (PICM) was seen in 3.8% (95% CI: 1.2-7.2). Diagnosis at birth (effect size [ES] [95%CI]: -2.23 [-0.36 to -0.10]; p < .001), presence of congenital heart disease (ES [95%CI]: -0.67 [0.41-0.93]; p < .001), younger age at pacemaker implantation (ES [95%CI]: -0.01 [-0.02 to -0.001]; p = .02), and duration of pacing (ES [95%CI]: -0.03 [-0.05 to -0.003]; p = .03), were associated with an higher mortality on binominal logistic regression. None of the parameters were significant on multivariate analysis. CONCLUSION: Pooled proportional mortality in patients with CCAVB and CAVB is 5.7% with an infrequent incidence of PICM (3.8%) in the paced patients with AVB suggesting that pacing in these patients is an effective management strategy with a low incidence of long-term side effects. Registry and randomized data can throw additional light regarding the natural history and appropriate management strategy in these patients.

A randomized study of yoga therapy for the prevention of recurrent reflex vasovagal syncope.

AIMS: Vasovagal syncope (VVS) is a common cardiovascular dysautonomic disorder that significantly impacts health and quality of life (QoL). Yoga has been shown to have a positive influence on cardiovascular autonomics. This study assessed the effectiveness of yoga therapy on the recurrence of VVS and QoL. METHODS AND RESULTS: We randomized subjects with recurrent reflex VVS (>3 episodes in the past 1 year) and positive head-up tilt test to guideline-directed therapy (Group 1) or yoga therapy (Group 2). Patients in Group 1 were advised guideline-directed treatment and Group 2 was taught yoga by a certified instructor. The primary endpoint was VVS recurrences and QoL. Between June 2015 and February 2017, 97 highly symptomatic VVS patients were randomized (Group 1: 47 and Group 2: 50). The mean age was 33.1 ± 16.6 years, male:female of 40:57, symptom duration of 17.1 ± 20.7 months, with a mean of 6.4 ± 6.1 syncope episodes. Over a follow-up of 14.3 ± 2.1 months Group 2 had significantly lower syncope burden compared with Group 1 at 3 (0.8 ± 0.9 vs. 1.8 ± 1.4, P < 0.001), 6 (1.0 ± 1.2 vs. 3.4 ± 3.0, P < 0.001), and at 12 months (1.1 ± 0.8 vs. 3.8 ± 3.2, P < 0.001). The Syncope functional score questionnaire was significantly lower in Group 2 compared with Group 1 at 3 (31.4 ± 7.2 vs. 64.1 ± 11.5, P < 0.001), 6 (26.4 ± 6.3 vs. 61.4 ± 10.7, P < 0.001), and 12 months (22.2 ± 4.7 vs. 68.3 ± 11.4, P < 0.001). CONCLUSION: For patients with recurrent VVS, guided yoga therapy is superior to conventional therapy in reducing symptom burden and improving QoL.

Safety and Efficacy of Ibutilide for Acute Pharmacological Cardioversion of Rheumatic Atrial Fibrillation.

INTRODUCTION: Ibutilide is indicated for acute cardioversion of nonvalvular atrial fibrillation (AF). However, its efficacy and safety in the pharmacological cardioversion of rheumatic AF are unknown. METHODS: Patients with mild-to-moderate rheumatic mitral valve (MV) disease with symptomatic, paroxysmal, or persistent AF were included in the analysis. Intravenous ibutilide was administered at doses tailored to body weight (0.5-2.0 mg) for over 10 min. The primary end point was efficacy, assessed as the rate of conversion of AF to sinus rhythm. The secondary end point was safety, including arrhythmic events and death within 24 h of drug initiation. RESULTS: From June 2016 to October 2018, 165 patients (94 with mitral stenosis, 23 with mitral regurgitation, 11 with mixed MV disease, and 37 with MV replacement) received ibutilide (mean dose 0.90 ± 0.54 mg). Ibutilide successfully converted AF to sinus rhythm in 127/165 (76.9%) patients, with a conversion time of 7.9 ± 4.1 min. The QTc increased from 419.9 ± 15.8 to 487.5 ± 34 ms after ibutilide administration (p < 0.001). The mean change in QTc after ibutilide administration (∆QTc) was 72.01 ± 36.03. There were no deaths, but 3 patients (1.8%) developed torsades de pointes (TdP) requiring defibrillation 55 ± 37 min after infusion. CONCLUSION: Ibutilide cardioverted 77% of rheumatic AF to sinus rhythm, indicating its potential as a clinically useful option for pharmacological cardioversion of rheumatic AF. TdP is a potentially serious adverse event that requires careful monitoring.

What are the atrioventricular delays in right ventricular apical and septal pacing for optimal hemodynamics in patients with normal left ventricular function?

INTRODUCTION: There is a surge of interest in alternate site pacing to prevent pacing-induced left ventricular dysfunction. However, little is known regarding the appropriate atrioventricular (AV) delay between right ventricular (RV) septal and RV apical pacing for optimal hemodynamic benefit. OBJECTIVES: To determine the programmed values of atrial sensed and atrial paced AV delays in basal RV septal and apical RV pacing that results in the maximum delivered stroke volume (SV). METHODS: We calculated the Doppler-derived SV at various sensed and paced AV delays in 50 patients with complete AV block implanted with a dual-chamber pacemaker (group A: 25 RV apical pacing; group B: 25 RV septal pacing). The hemodynamic difference in terms of the SV between sensed and paced AV delay, corresponding to the site of RV pacing was then compared for statistical significance. RESULTS: In group A, maximal SV was derived at a sensed AV delay of 123.2 ± 11 ms and paced AV delay of 129.2 ± 10 ms, and in group B, at a sensed AV delay of 123.6 ± 8 ms and paced AV delay of and 132.8 ± 7 ms. At these intervals, there was no difference in the SV between septal and apical RV pacing (P = .28 and .22, respectively). CONCLUSION: The atrial sensed and atrial paced AV delays for septal and apical RV pacing for optimal hemodynamics are similar. For optimal hemodynamics, the atrial paced AV delay is longer than the atrial sensed AV delay.

Electrocardiographic characteristics and mapping approach of ventricular arrhythmias originating from the left ventricular summit.

The left ventricular summit is the most common site of idiopathic epicardial ventricular tachycardia (VT). We report a case of a 48-yr-old lady who presented with VT of RBBB configuration, inferior axis and delayed initial activation. During electrophysiological study, local activation in the distal great cardiac vein (GCV) preceded surface QRS by 56 ms whereas mapping in the aortic sinuses and left ventricular outflow tract endocardially revealed late activation. Ablation in the distal GCV with an irrigated catheter successfully terminated the tachycardia. The 12­lead electrocardiogram is an invaluable tool for predicting the VT focus and planning the mapping strategy.

An unusual case of complete atrioventricular block causing Takotsubo syndrome.

Complete atrioventricular (AV) block in association with Takotsubo syndrome (TS) has been well recognized, but the cause and effect relationship has not been elucidated. We describe a 78-year-old female who presented with complete AV block but one week later developed new-onset, diffuse T-wave inversions, QT prolongation, and acceleration of junctional escape rate. Left ventriculogram revealed features typical of TS. One year after permanent pacemaker implantation, complete AV block persisted despite the reversal of wall motion defects implying that conduction abnormality was the trigger of TS rather than its consequence.

Long-term effects of cardiac resynchronization therapy on electrical remodeling in heart failure-A prospective study.

INTRODUCTION: Effects of cardiac resynchronization therapy (CRT) on arrhythmogenicity and sudden death have not been fully ascertained. CRT has been shown to increase transmural dispersion of repolarization (TDR) immediately on implantation, which may favorably remodel on long-term follow-up. However, such a hypothesis has not been prospectively evaluated. METHODS AND RESULTS: We included 35 consecutive patients who underwent CRT implantation between September 2013 and August 2014 (mean age 56.8 ± 11.09 years; 71.43% males). QT and Tpeak-Tend (Tp-e) intervals were measured during endocardial (RVendoP), epicardial (LVepiP), and biventricular pacing (BiVP) at CRT implantation and 1-year follow-up. Compared to RVendoP (130.41 ± 16.75 ms), Tp-e was significantly prolonged during BiVP (142.06 ± 21.98 ms; P < 0.001) and LVepiP (183.45 ± 27.87 ms; P < 0.001) at baseline. There was a significant decrease in Tp-e during BiVP on follow-up (117.93 ± 15.03 ms; P < 0.001). High responders had significantly lower Tp-e at 1 year compared to low responders (113.16 ± 14.3 ms vs 129.59 ± 9.75 ms, P  =  0.004). Tp-e at 1 year had strong negative correlation with reduction in LV end-systolic volumes (r  =  - 0.51; P  =  0.003). Seven patients with sustained ventricular arrhythmias during follow-up had significantly longer baseline Tp-e compared to those without arrhythmias (158.19 ± 17.59 ms vs 139.72 ± 20.94 ms, P  =  0.043). A baseline Tp-e value of ≥ 148 ms had a specificity of 75% and sensitivity of 71% to predict ventricular arrhythmias. CONCLUSIONS: Baseline TDR is greater during BiVP and LV epiP compared with RVendoP in patients with heart failure. However, BiVP causes a significant reduction in TDR reflective of reverse electrical remodeling on long-term follow-up.

Takotsubo syndrome presenting as syncope in a patient with permanent pacemaker.

Takotsubo syndrome is an acute reversible heart failure syndrome triggered by physical or emotional stress, especially in postmenopausal women. Herein, we describe a case of a 31-year-old pacemaker dependent lady who presented with syncope after she was bereaved of her father. Electrocardiogram at admission revealed ventricular paced rhythm at 60/min, prolonged QT interval and frequent runs of torsades de pointes. Transthoracic echocardiogram and left ventriculogram revealed findings typical of Takotsubo syndrome. QT prolongation and torsade de pointes in the context of fixed-rate ventricular pacing imply direct catecholamine toxicity on the ventricular myocardium independent of heart rate.

Narrow QRS Tachycardia with Transition: What Is the Mechanism?

A 50-year-old woman underwent radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead electrocardiogram was normal during sinus rhythm. The electrophysiological study showed normal atriohisian and hisioventricular intervals during sinus rhythm. Atrial burst pacing reproducibly induced two narrow QRS tachycardias. Figure 1 shows spontaneous switch of tachycardia 1 to tachycardia 2. What are the likely mechanisms of the tachycardia and the transition?

Narrow QRS Tachycardia in a Patient with Tachycardiomyopathy: What Is the Mechanism?

A 50-year-old female presented with incessant palpitation of 2 weeks duration. She was hemodynamically stable and there was no evidence of heart failure. A transthoracic echocardiogram showed mild left ventricular (LV) dysfunction with LV ejection fraction of 45%. Electrocardiogram (12 lead and rhythm strip) was taken during the palpitation. What is the mechanism?

Response of narrow QRS tachycardia to premature atrial extra. What is the mechanism?

A 60-year-old woman was referred for radiofrequency catheter ablation of narrow QRS tachycardia that was terminated with intravenous adenosine. Twelve-lead ECG showed no baseline preexcitation. Echocardiogram was essentially normal. The electrophysiological study showed a normal AH interval of 114 ms and HV interval of 48 ms during sinus rhythm. Anterograde study demonstrated no dual AV nodal physiology. Atrial pacing protocols easily and reproducibly induced narrow QRS tachycardia (Fig. 1A & 1B). Premature atrial extra (PAE) stimuli were delivered during the tachycardia (Fig. 2). What is the mechanism of the tachycardia?