Background-Although arterial hypertension and left ventricular hypertrophy are considered good epidemiological indicators of the risk of atrial fibrillation (AF) in patients, the link between elevated afterload and AF remains unclear. We investigated atrial remodeling and the substrate for arrhythmia in a surgical model of elevated afterload in rats. Methods and Results-Male Wistar rats (aged 3-4 weeks) were anesthetized and subjected to either partial stenosis of the ascending aorta (AoB) or sham operation (Sham). Experiments were performed on excised hearts 8, 14, and 20 weeks after surgery. Unipolar electrograms were recorded from the left atrial epicardial surface of perfused hearts using a 5ϫ5 electrode array. Cryosections of left atrial tissue were retained for histological and immunocytochemical analyses.

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AIMTo describe the long-term follow-up of patients with complex congenital heart disease who underwent subcutaneous implantable cardiac defibrillator (S-ICD), focusing on local complications, appropriate and inappropriate shocks.METHODSPatients with complex congenital heart disease underwent S-ICD implant in two centers with the conventional technique. Data at follow-up were retrieved from clinical notes and institutional database.RESULTSEight patients were implanted in two centres between 2010 and 2016. Median age at implant was 37.5 years (range 13-57). All patients who were deemed suitable for S-ICD implant passed the pre-procedural screening. Three patients were previously implanted with a anti-bradycardia device, one of whom with CRT. In one patient the device was explanted due to local infection. During the total median follow-up of 874 d, one patient had an appropriate and one inappropriate shock triggered by fast atrial tachycardia. None of the patients had inappropriate shocks secondary to T wave oversensing or electrical interference with anti- bradycardia devices.CONCLUSIONS-ICD appears to be effective and safe in patients with complex congenital heart disease.

Investigations into the functional modulation of the cardiac Na+–Ca2+ exchanger (NCX) by acute β-adrenoceptor/PKA stimulation have produced conflicting results. Here, we investigated (i) whether or not β-adrenoceptor activation/PKA stimulation activates current in rabbit cardiac myocytes under NCX-‘selective’ conditions and (ii) if so, whether a PKA-activated Cl−-current may contribute to the apparent modulation of NCX current (INCX). Whole-cell voltage-clamp experiments were conducted at 37 °C on rabbit ventricular and atrial myocytes. The β-adrenoceptor-activated currents both in NCX-‘selective’ and Cl−-selective recording conditions were found to be sensitive to 10 mM Ni2+. In contrast, the PKA-activated Cl− current was not sensitive to Ni2+, when it was activated downstream to the β-adrenoceptors using 10 μM forskolin (an adenylyl cyclase activator). When 10 μM forskolin was applied under NCX-selective recording conditions, the Ni2+-sensitive current did not differ between control and forskolin. These findings suggest that in rabbit myocytes: (a) a PKA-activated Cl− current contributes to the Ni2+-sensitive current activated via β-adrenoceptor stimulation under recording conditions previously considered selective for INCX; (b) downstream activation of PKA does not augment Ni2+-sensitive INCX, when this is measured under conditions where the Ni2+-sensitive PKA-activated Cl− current is not present.

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Highlights► We report the block of the β-adrenoceptor-activated cardiac CFTR Cl− current by Ni2+. ► Extracellular Ni2+ inhibits the current activated by β1-adrenoceptors in a concentration-dependent manner. ► The action of Ni2+ is insensitive to β2-blockade. ► Ni2+ does not affect the β-adrenoceptor-activated current from the intracellular side. ► The data are consistent with an action of Ni2+ at the β1-adrenoceptor from the external side.