Israel Medical Association Journal

Background: Catheter ablation (CA) is a well-established therapeutic option for patients with recurrent symptomatic atrial fibrillation (AF). Data on gender-related differences are limited with regard to baseline characteristics and long-term success rates of catheter ablation for AF.

Methods: We analyzed a cohort of 251 consecutive patients who underwent a first catheter ablation for AF in our institute during the period 2008 through 2015. All patients were followed by regular annual clinic visits, electrocardiograms, periodic 24–48 hour Holter monitoring, and loop recorders. The primary endpoint was first recurrence of AF during 1 year of follow-up.

Results: The cohort comprised 26% women (n=65), who were older (62.1 ± 9.6 vs. 54.4 ± 11.3 years, P < 0.01) and had a higher proportion of diabetes mellitus (23.1 vs. 5.4%, P < 0.001) than male patients. No other significant differences were evident. At 1 year follow-up, the cumulative survival free of AF was significantly higher in women compared with men (83% vs. 66%, respectively, log rank P value = 0.021). Subgroup analysis showed an interaction between female and small indexed left atrial diameter (LADi < 23 mm/m²).

Conclusions: Our findings suggest that women experience a significantly lower rate of AF recurrence post-CA compared with men. This gender-related advantage appears to be restricted to women without significant left atrial enlargement. It further implies that left atrial enlargement has a stronger negative impact on post-CA AF recurrence in females than in males. Due to the relatively small sample number of females further research is warranted to validate our conclusions.

Background: Pacemaker pocket early post-implantation inflammation (EPII) is defined as clinical signs of local erythema without any systemic signs of infection occurring early after implantation. Data on the best treatment regimen for apparent superficial EPII is scarce. 

Objectives: To investigate the prognostic value of medical treatment, rather than extraction surgery, in patients with EPII. 

Methods: Data from 6013 consecutive patients who underwent cardiac implantable electronic device (CIED) implantation or replacement from 2007–2015 were retrospectively analyzed; 40 (0.7%) presented with EPII. Our goal was the absence of major complications and to avoidance of extraction. 

Results: Patients with EPII were initially treated medically. Nineteen (47%) (group A) recovered with antibiotic treatment only. In the other 21 patients (53%) (group B), CIED extraction was performed. Group B had more major complications compared to group A (15 [71%] vs. 0 [0%], P < 0.001). The only significant difference in baseline characteristics was history of non-initial procedure. While 86% of group B patients had a previous non-initial procedure, only 53% of group A patients underwent previous replacement (P < 0.05). In multivariate analysis, previous non-initial procedure was the only predictor for need of extraction at 1 year, hazard ratio 3.5, 95% confidence interval 1.001–11.73, P < 0.05.

Conclusions: Conservative treatment in patients with EPII after non-initial procedure can lead to serious adverse events resulting in the need for extraction. Close follow-up and aggressive treatment should be considered early in the therapeutic course.

Background: Limited information exists about detailed clinical characteristics and management of the small subset of Brugada syndrome (BrS) patients who had an arrhythmic event (AE).

Objectives: To conduct the first nationwide survey focused on BrS patients with documented AE.

Methods: Israeli electrophysiology units participated if they had treated BrS patients who had cardiac arrest (CA) (lethal/aborted; group 1) or experienced appropriate therapy for tachyarrhythmias after prophylactic implantable cardioverter defibrillator (ICD) implantation (group 2).

Results: The cohort comprised 31 patients: 25 in group 1, 6 in group 2. Group 1: 96% male, mean CA age 38 years (range 13–84). Nine patients (36%) presented with arrhythmic storm and three had a lethal outcome; 17 (68%) had spontaneous type 1 Brugada electrocardiography (ECG). An electrophysiology study (EPS) was performed on 11 patients with inducible ventricular fibrillation (VF) in 10, which was prevented by quinidine in 9/10 patients. During follow-up (143 ± 119 months) eight patients experienced appropriate shocks, none while on quinidine. Group 2: all male, age 30–53 years; 4/6 patients had familial history of sudden death age < 50 years. Five patients had spontaneous type 1 Brugada ECG and four were asymptomatic at ICD implantation. EPS was performed in four patients with inducible VF in three. During long-term follow-up, five patients received ≥ 1 appropriate shocks, one had ATP for sustained VT (none taking quinidine). No AE recurred in patients subsequently treated with quinidine.

Conclusions: CA from BrS is apparently a rare occurrence on a national scale and no AE occurred in any patient treated with quinidine.

Background: Multiform fascicular tachycardia (FT) was recently described as a ventricular tachycardia (VT) that has a reentrant mechanism using multiple fascicular branches and produces alternate fascicular VT forms. Ablating the respective fascicle may cause a change in the reentrant circuit resulting in a change in morphology. Ablation of the septal fascicle is crucial for successful treatment.

Objectives: To describe four cases of FT in which ablation induced a change in QRS morphologies and aggravated clinical course.

Methods: Four out of 57 consecutive FT cases at three institutions were retrospectively analyzed and found to involve multiform FT. These cases underwent electrophysiological study, fascicular potential mapping, and electroanatomical mapping. All patients initially had FT with right bundle branch block (RBBB) and superior axis morphology.

Results: Radiofrequency catheter ablation (RFCA) targeting the distal left posterior fascicle (LPF) resulted in a second VT with an RBBB-inferior axis morphology that sometimes became faster and/or incessant and/or verapamil-refractory in characteristics. RFCA in the upper septum abolished the second VT with no complications and uneventful long-term follow-up.

Conclusions: The change in FT morphology during ablation may be associated with a change in clinical course when shifting from one route to another and may aggravate symptoms. Targeting of the proximal conduction system (such as bifurcation, LPF, left anterior fascicle, high septal/auxiliary pathway) may serve to solve this problem.

Background: Transvenous lead extraction can lead to tricuspid valve damage. 

Objectives: To assess the incidence, risk factors and clinical outcome of tricuspid regurgitation (TR) following lead extraction.

Methods: We prospectively collected data on patients who underwent lead extraction at the Sheba Medical Center prior to laser use (i.e., before 2012). Echocardiography results before and following the procedure were used to confirm TR worsening, defined as an echocardiographic increase of at least one TR grade. Various clinical and echocardiographic parameters were analyzed as risk factors for TR. Clinical and echocardiographic follow-up was conducted to assess the clinical significance outcome of extraction-induced TR.

Results: Of 152 patients who underwent lead extraction without laser before 2012, 86 (56%) (192 electrodes) had echocardiography results before and within one week following the procedure. New or worsening TR was discovered in 13 patients (15%). Use of mechanical tools and younger age at extraction were found on multivariate analysis to be factors for TR development (P = 0.04 and P = 0.03 respectively). Average follow-up was 22.25 ± 21.34 months (range 8–93). There were no significant differences in the incidence of right-sided heart failure (50% vs. 23%, P = 0.192) or hospitalizations due to heart failure exacerbations (37.5% vs. 11%, P = 0.110). No patient required tricuspid valve repair or replacement. Death rates were similar in the TR and non-TR groups (20% vs. 33%).

Conclusions: TR following lead extraction is not uncommon but does not seem to affect survival or outcomes such as need for valve surgery. Its long-term effects remain to be determined. 

 

Background: Hypertrophic cardiomyopathy (HCM) is a familial disease with autosomal dominant inheritance and age-dependent penetrance, caused primarily by mutations of sarcomere genes. Because the clinical variability of HCM is related to its genetic heterogeneity, genetic studies may improve the diagnosis and prognostic evaluation in HCM.

Objectives: To analyze the impact of genetic diagnosis on the clinical management of HCM.

Methods: Genetic studies were performed for either research or clinical reasons. Once the disease-causing mutation was identified, the management plan was reevaluated. Family members were invited to receive genetic counseling and encouraged to be tested for the mutation.

Results: Ten mutations in sarcomere protein genes were identified in 9 probands: 2 novel and 8 previously described. Advanced heart failure or sudden death in a young person prompted the genetic study in 8 of the 9 families. Of 98 relatives available for genotyping, only 53 (54%) agreed to be tested. The compliance was higher in families with sudden death and lower in what appeared to be sporadic HCM or elderly-onset disease. Among the healthy we identified 9 carriers and 19 non-carriers. In 6 individuals the test result resolved an uncertainty about "possible HCM." In several cases the genetic result was also used for family planning and played a role in decisions on cardioverter-defibrillator implantation.

Conclusions: Recurrence of a same mutation in different families created an opportunity to apply the information from the literature for risk stratification of individual patients. We suggest that the clinical context determine the indication for genetic testing and interpretation of the results.

background: many electrophysiologists recommend implantable cardioverter defibrillators for patients with Brugada syndrome who are cardiac arrest survivors or presumed at high risk of sudden death (patients with syncope or a familial history of sudden death or those with inducible ventricular fibrillation at electrophysiologic study).

objectives: To assess the efficacy and complications of ICD therapy in patients with Brugada syndrome.

Methods: The indications, efficacy and complications of ICD therapy in all patient with Brugada syndrome who underwent ICD implantation in 12 Israeli centers between 1994 and 2007 were analyzed.

Results: there were 59 patients (53 males, 89.8%) with a mean age of 44.1 years. At diagnosis 42 patients (71.2%) were symptomatic while 17 (28.8%) were asymptomatic. The indications for ICD implantation were: a history of cardiac arrest (n=11, 18.6%), syncope (n=31, 52.5%), inducible VF in symptomatic patients (n=14, 23.7%), and a family history of sudden death (n=3, 0.5%). The overall inducibility rates of VF were 89.2% and 93.3% among the symptomatic and a symptomatic patients, respectively (P=NS). During a follow-up of 4-160 (45+-35) months, all patients (except one who died from cancer) are alive. Five patients (8.4%), all with a history of cardiac arrest, had appropriate ICD discharge. Conversely, none of the patients without prior cardiac arrest had appropriate device therapy during 39+-30 month follow-up. Complications were encountered in 19 patients (32%). Inappropriate shocks occurred in 16 (27.1%) due to lead failure/dislodgment (n=5), T wave oversensing (n=2), device failure (n=1), sinus tachycardia (n=4), and supraventricular tachycardia (n=4). One patient suffered a pneumothorax and another a brachial plexus injury during the implant procedure. One patient suffered a late (2 months) perforation of the right ventricle by the implanted lead. Eleven patients (18.6%) required a reintervention either for infection (n=1) or lead problems (n=10). Eight patients (13.5%) required psychiatric assistance due to complications related to the ICD (mostly inappropriate shocks in 7 patients).

Conclusions: In this Israeli population with Brugada syndrome treated with ICD, appropriate device therapy was limited to cardiac arrest survivors while none of the other patients including those with syncope and/or inducible VF suffered an arrhythmic event. The overall complication rate was high.
 

Background: The appearance of pericarditis following insertion of a permanent pacemaker is not widely acknowledged in the literature.

Objectives: To describe our experience with pericarditis following 395 permanent pacemaker implantations over 2 years.

Methods: We retrospectively reviewed the medical records of 395 consecutive patients in whom new pacing systems or pacemaker leads had been implanted over a 2 year period. We searched the records for pericarditis that developed within 1 month after pacemaker implantation according to the ICD-9 code. The incidence, clinical picture, response to treatment and relationship to lead design and location were studied.

Results: Eight cases (2%) of pericarditis following implantation were detected. Clinical manifestations in all patients were similar to those of post-pericardiotomy syndrome and included chest pain (n=7), friction rub (n=1), fever (n=2), fatigue (n=2), pleural effusion (n=2), new atrial fibrillation (n=2), elevated erythrocyte sedimentation rate (n=4) and echcardiographic evidence of pericardial effusion (n=8). All affected patients had undergone active fixation (screw-in) lead implantation in the atrial position. The incidence of pericarditis with screw-in atrial leads was 3% compared to 0% in other cases (P < 0.05).

Conclusions: Pericarditis is not uncommon following pacemaker implantation with active fixation atrial leads. Special attention should be paid to identifying pericardial complications following pacemaker implantation, especially when anticoagulant therapy is resumed or initiated. The use of passive fixation leads is likely to reduce the incidence of pericarditis but this issue should be further investigated.