Safety and Efficiency of Cephalic Vein Puncture by Modified Seldinger Technique Compared to Subclavian Vein Puncture for Cardiac Implantable Electronic Devices.

INTRODUCTION: The establishment of venous access is one of the driving factors for complications during implantation of pacemakers and defibrillators (cardiac implantable electronic devices [CIED]). Recently, a novel approach of accessing the cephalic vein for CIED by cephalic vein puncture (CVP) using a modified Seldinger technique has been described, promising high success rates and simplified handling with steeper learning curves. In this single-center registry, we analyzed the safety and efficiency of CVP to SVP access after defining CVP as the primary access route in our center. METHODS: A total of 229 consecutive patients receiving a CIED were included in the registry. Sixty-one patients were implanted by primary or bail-out SVP; 168 patients received primary cephalic preparation and CVP was performed when possible, using a hydrophilic transradial sheath. RESULTS: Implantation of at least one lead via CVP was successful in 151 of 168 patients (90%), and implantation of all leads was possible in 122 of 168 patients (72.6%). Total implantation times and fluoroscopy times and doses did not differ between CVP and SVP implantations. Pneumothorax occurred in 0/122 patients implanted via CVP alone, but 8/107 (7.5%) patients received at least one lead via SVP. CONCLUSION: Our data confirms high success rates of the CVP for CIED implantation. Moreover, this method can be used without significantly prolonging the total procedure time or applying fluoroscopy dose compared to the highly efficient SVP while showing lower overall complication rates.

Esophageal safety in CLOSE-guided 50 W high-power-short-duration pulmonary vein isolation: The PREHEAT-PVI-registry.

INTRODUCTION: Pulmonary vein isolation (PVI) using high-power-short-duration (HPSD) radiofrequency ablation (RF) is emerging as the standard of care for treatment of atrial fibrillation (AF). While procedural short-term to midterm efficacy and efficiency are very promising, this registry aims to investigate esopahgeal safety using an optimized ablation approach. METHODS: In a single-center experience, 388 consecutive standardized first-time AF ablation were performed using a CLOSE-guided-fixed-50 W-circumferential PVI and substrate modification without intraprocedural esophageal temperature measurement. Three hundred patients underwent postprocedural esophageal endoscopy to diagnose and grade endoscopically detected esophageal lesions (EDEL) and were included in the analysis. RESULTS: EDEL were detected in 35 of 300 patients (11.6%), 25 of 35 were low-grade Kansas-city-classification (KCC) 1 lesions with fast healing tendencies. Six patients suffered KCC 2a lesions, 4 patients had KCC 2b lesions (1.3% of all patients). No esophageal perforation or fistula formation was observed. Patient baseline characteristics, especially patients age, gender, and body mass index did not influence EDEL incidence. Additional posterior box isolation did not increase the incidence of EDEL. In patients diagnosed with EDEL, mean catheter contact force during posterior wall ablation was higher (11.9 ± 1.8 vs. 14.7 ± 3 g, p < .001), mean RF duration was shorter (11.9 ± 1 vs. 10.7 ± 1.2 s, p < .001), while achieved ablation index was not different between groups (434 ± 4.9 vs. 433 ± 9.5, n.s.). CONCLUSION: Incidence of EDEL after CLOSE-guided-50 W-HPSD PVI is lower compared to historical cohorts using standard-power RF settings. Catheter contact force during posterior HPSD ablation should not exceed 15 g.

Left ventricular clefts - incidental finding or pathologic sign of Wilson's disease?

BACKGROUND: Wilson's disease is an inherited autosomal recessive multi-systemic disorder characterized by reduced excretion and consequently excessive accumulation of copper in different organs, such as the heart. RESULTS: In a prospective controlled trial, which is the largest to date, we evaluated 61 patients with Wilson's disease, age- and sex-matched to 61 healthy patients, for cardiac manifestation using cardiac magnetic resonance imaging. Patients were under stable disease and had no signs of heart failure at the time of examination. We detected a left ventricular cleft, an invagination penetrating more than 50% wall thickness of the adjoining compact myocardium in diastole, in 20% of the patients (12 out of 61) compared to 5% among control patients (3 out of 61, p = 0.013). No correlation between the incidence of cleft and a certain genotype of Wilson's disease was found. All described cases were incidental findings and none of the patients showed other signs of cardiac involvement. CONCLUSIONS: To conclude, the results of this study suggests that the increased occurrence of left ventricular clefts is due to Wilson's disease. Large studies with a long observation period are needed for further evaluation.

Cardiac and autonomic function in patients with Wilson's disease.

BACKGROUND: The clinical effect of copper accumulation on the heart of patients suffering from Wilson's disease (WD) is not completely understood. We aimed to determine if patients with WD show signs of cardiac involvement, structural heart disease or autonomic dysfunction. In this prospective trial, we studied 61 patients (mean age 44.3 ± 15.2 years, 51% males) with WD and compared them to 61 age- and gender-matched healthy controls. All subjects underwent clinical examination, blood tests, echocardiography and 24 h electrocardiographic (ECG) recording. RESULTS: Left- and right ventricular systolic function did not differ significantly between WD patients and controls. However, 5 of the 61 patients had a reduced left ventricular ejection fraction (LVEF). Furthermore, diastolic dysfunction was more prevalent in WD patients (9 of 61 vs. 0 of 61, p = 0.001). The severity of WD based on the Unified Wilson's Disease Rating Scale was significantly correlated to NT-pro BNP (r = 0.34, P = 0.013). Patients with an exacerbation of WD in medical history had higher troponin levels compared to those without (11.3 ± 4.7 vs 4.6 ± 1.2). The autonomic function assessed by triangular index (TI) and SDNN-index was significantly reduced in WD patients compared to controls in most in almost every age category (p-value TI and SDNN: age 20-29, p < 0.001 and 0.05; age 30-39, p < 0.01 and not significant (ns); age 40-49, p < 0,01 and 0.001; age 50-59, p = ns and < 0.001, age 60-70, p < 0.05 and ns). CONCLUSION: Our data demonstrate that cardiac involvement and autonomic dysfunction in WD is possible, however the underlying cause is still not known. We suggest that patients with signs and symptoms of structural heart disease should be examined by a cardiologist in addition to the interdisciplinary treatment team of WD.