Aims To evaluate the effectiveness and safety of cryoballoon ablation (CBA) compared with radiofrequency ablation (RFA) for symptomatic paroxysmal or drug-refractory persistent atrial fibrillation (AF). Methods and results Prospective cluster cohort study in experienced CBA and RFA centres. Primary endpoint was ‘atrial arrhythmia recurrence’, secondary endpoints were as follows: procedural results, safety, and clinical course. A total of 4189 patients were included: CBA 2329 (55.6%) and RFA 1860 (44.4%). Cryoballoon ablation population was younger, with fewer comorbidities. Procedure time was longer in the RFA group (P = 0.01). Radiation exposure was 2487 (CBA) and 1792 cGycm2 (RFA) (P < 0.001). Follow-up duration was 441 (CBA) and 511 days (RFA) (P < 0.0001). Primary endpoint occurred in 30.7% (CBA) and 39.4% patients (RFA) [adjusted hazard ratio (adjHR) 0.85, 95% confidence interval (CI) 0.70–1.04; P = 0.12). In paroxysmal AF, CBA resulted in a lower risk of recurrence (adjHR 0.80, 95% CI 0.64–0.99; P = 0.047). In persistent AF, the primary outcome was not different between groups. Major adverse cardiovascular and cerebrovascular event rates were 1.0% (CBA) and 2.8% (RFA) (adjHR 0.53, 95% CI 0.26–1.10; P = 0.088). Re-ablations (adjHR 0.46, 95% CI 0.34–0.61; P < 0.0001) and adverse events during follow-up (adjHR 0.64, 95% CI 0.48–0.88; P = 0.005) were less common after CBA. Higher rehospitalization rates with RFA were caused by re-ablations. Conclusions The primary endpoint did not differ between CBA and RFA. Cryoballoon ablation was completed rapidly; the radiation exposure was greater. Rehospitalization due to re-ablations and adverse events during follow-up were observed significantly less frequently after CBA than after RFA. Subgroup analysis suggested a lower risk of recurrence after CBA in paroxysmal AF. Trial Registration ClinicalTrials.gov (NCT01360008), https://clinicaltrials.gov/ct2/show/NCT01360008.

LAA closure with the LAmbre device shows encouraging results for stroke prevention.

This paper suggests a new approach for cardiac source localization of origin of arrhythmias using only the 12-lead ECG by means of CNN, and may have important applications for future real-time monitoring and localizing origins of cardiac arrhythmias guiding ablation treatment.

Fatty acid-binding protein 3 (FABP3), a low-molecular-weight protein, participates in lipid transportation, storage, signaling transduction, oxidation, and transcription regulation. Here, we investigated the expression and function of FABP3 in ischemic heart diseases and explored the mechanisms by which FABP3 affected remodeling after myocardial infarction (MI). We showed that ischemic or hypoxic conditions upregulated FABP3 expression in vivo and in vitro. Notably, overexpression of FABP3 induced more myocyte apoptosis in the infarction and border areas and aggravated cardiac dysfunction, with lower left ventricular ejection fraction. Meanwhile, overexpression of FABP3 drastically promoted death and apoptosis of neonatal rat ventricular cardiomyocytes under hypoxia. Furthermore, deficiency of FABP3 exerted protective effects against ischemic heart injuries by decreasing cardiac myocyte apoptosis and heart remodeling after MI. We found that overexpression of FABP3 upregulated the phosphorylation of MAPK signaling pathway and decreased phosphorylated Akt levels, which may account for the augmentation of apoptosis and remodeling after MI. To the best of our knowledge, this is the first study to demonstrate that deficiency of FABP3 would protect cardiac myocytes from apoptosis and alleviate cardiac remodeling after MI, suggesting FABP3 as a potential target to preserve cardiac function after MI. NEW & NOTEWORTHY It is an undisputable fact that myocyte apoptosis plays a crucial role in cardiac remodeling and the development of heart failure after myocardial infarction. Here, fatty acid-binding protein 3 deficiency improved myocardial structural remodeling and function by decreasing cell apoptosis and regulating MAPK signaling pathways. We suppose that fatty acid-binding protein 3 may be regarded as a potential intervention approach to preserve cardiomyocytes during myocardial infarction.