BackgroundGalectin-3 (Gal-3) is an emerging biomarker in heart failure that is involved in fibrosis and inflammation. However, its potential value as a prognostic marker in atrial fibrillation (AF) is unknown. The aim of this study was to assess the impact of AF catheter ablation on Gal-3 and evaluate its prognostic impact for predicting rhythm outcome after catheter ablation.MethodsGal-3 was measured at baseline and after 6 months using specific ELISA. AF recurrences were defined as any atrial arrhythmia lasting longer than 30 sec within 6 months after ablation.ResultsIn 105 AF patients (65% males, age 62±9 years, 52% paroxysmal AF) undergoing catheter ablation, Gal-3 was measured at baseline and after 6 months and compared with an AF-free control cohort (n=14, 50 % males, age 58±11 years). Gal-3 was higher in AF patients compared with AF-free controls (7.8±2.9 vs. 5.8±1.8, ng/mL, p=0.013). However, on multivariable analysis, BMI (p=0.007) but not AF (p=0.068) was associated with Gal-3. In the AF cohort, on univariable analysis higher Gal-3 levels were associated with female gender (p=0.028), higher BMI (p=0.005) and both CHADS2 (p=0.008) and CHA2DS2-VASC (p=0.016) scores, however, on multivariable analysis only BMI remained significantly associated with baseline Gal-3 (p=0.016). Gal-3 was similar 6 months after AF catheter ablation and was not associated with sinus rhythm maintenance.ConclusionsAlthough galectin-3 levels are higher in AF patients, this is driven by cardiometabolic co-morbidities and not heart rhythm. Gal-3 is not useful for predicting rhythm outcome of catheter ablation.

Background The role of atrial arrhythmia inducibility as an endpoint of catheter ablation of atrial fibrillation (AF) has been a controversial subject in many studies. Our goal is to evaluate the significance of inducibility, the impact of multiple sites or protocols of stimulation or the change in inducibility status in a prospective study including patients with AF undergoing first catheter ablation. Methods We studied 170 consecutive patients with AF (62.9% paroxysmal) undergoing catheter ablation. All patients underwent two separate stimulation protocols before and after the ablation from the coronary sinus ostium and the left atrial appendage: burst pacing at 300, 250, 200 milliseconds (or until refractoriness) for 10 seconds and ramp decrementing from 300 to 200 milliseconds in increments of 10 milliseconds every three beats for 10 seconds. Inducibility was defined as any sustained AF or organized atrial tachycardia (AT) lasting >30 seconds. Results We had AF/AT inducibility in 55 patients at baseline compared to 36 following ablation. After a mean of 41, 3 months follow‐up, 115 patients were free of AF. Inducibility before or after the ablation or change in inducibility status did not influence AF recurrence. There were no significant differences regarding paroxysmal or persistent patients with AF. Conclusions Non‐inducibility of atrial arrhythmia or change in inducibility status following pulmonary vein (PV) isolation and substrate modification are not associated with long‐term freedom from recurrent arrhythmia. Therefore, the use of induction of an endpoint in AF ablation is limited.

Cardiac involvement is well known in a number of skeletomuscular diseases but not in facio-scapulohumeral muscular dystrophy (FSHD). We report on a 71 year old woman with progressive cardiac insufficiency in FSHD, which was also confirmed by molecular analysis in one of the two daughters affected by the disease. Autopsy of the deceased patient showed the typical changes in skeletal muscles including focal inflammatory infiltrates in the diaphragm and, in addition, cardiac muscular involvement. The histological changes resembled those seen in primary cardiomyopathy despite the normal muscle mass volume. Both clinically and morphologically, the cardiac disease was the cause of death in this patient with FSHD.

of Tatarstan, Russia (M.M.). *These authors contributed equally to this work.The online-only Data Supplement is available with this article at http://hyper.ahajournals.org/lookup/suppl

Introduction: Persistent systemic inflammation is considered to be predictive for future cardiovascular events. Here, in a patient with pyelonephritis of his failed renal allograft, consecutive coronary angiograms proved that coronary artery disease progressed within 3 weeks, when infection was uncontrolled. Patient concerns: A 52-year-old male type 2 diabetic with a failed renal allograft suffering from hematuria, leukocyturia, and chest pain at rest was hospitalized. Diagnoses: An acute coronary syndrome in presence of pyelonephritis was diagnosed. Besides pyelonephritis, the histological examination of the kidney transplant revealed signs of chronic rejection and the presence of a renal cell carcinoma in situ . Interventions: A percutaneous coronary intervention was performed, and an elective surgery for allograft removal was scheduled. However, within 5 weeks after discharge, two more surges of infection coincided with episodes of unstable angina. Outcomes: Once the renal allograft has been removed, systemic inflammation was contained. The patient was not re-hospitalized for acute-coronary syndrome within the next 12 months. Conclusion: Surges of systemic inflammation due to infection were paralleled by instability of coronary plaques as documented by repeat coronary angiograms.