No abstract

No abstract

The definition of atrial fibrillation (AF) as a functional electrical disorder does not reflect the significant underlying structural abnormalities. Atrial and Pulmonary Vein (PV) muscle sleeve microstructural remodeling is present, and establishes a vulnerable substrate for AF maintenance. In spite of an incomplete understanding of the anatomo-functional basis for AF, current evidence demonstrates that this arrhythmia usually requires a trigger for initiation and a vulnerable electrophysiological and/or anatomical substrate for maintenance. It is still unclear whether the trigger mechanisms include focal enhanced automaticity, triggered activity and/or micro re-entry from myocardial tissue. Initiation of AF can be favored by both parasympathetic and sympathetic stimulation, which also seem to play a role in maintaining AF. Finally, evolving clinical evidence demonstrates that inflammation is associated with new-onset and recurrent AF through a mechanism that possibly involves cellular degeneration, apoptosis, and subsequent atrial fibrosis.

The architectural arrangement of cardiomyocytes aggregated together within the ventricular walls remains controversial. Two models currently attract clinical attention, with neither model standing rigorous anatomical scrutiny. The first is based on the notion that ventricular mass can be unraveled consistently to produce a unique myocardial band. The second model was initially based on the notion that cardiomyocytes were bundled together in uniform fashion, with fibrous shelves interposed in transmural fashion. This concept was subsequently modified to accept the fact that the fibrous matrix supporting the cardiomyocytes within the ventricular walls does not form transmural sheets. Current observations demonstrate that not all cardiomyocytes are aggregated together in tangential fashion. A significant netting component is aligned in obliquely intruding and transversal fashion. The interaction between the tangential and transversal chains of cardiomyocytes with the fibrous matrix produces antagonistic forces, with both unloading and auxotonic forces necessary to explain normal and abnormal cardiodynamics. This article is part of a JCTR special issue on Cardiac Anatomy.

AimsTo establish a temporal safety window for cryoablation at minimal temperatures and to assess the electrophysiological and histological changes as a function of the application duration.Methods and resultsTwenty mini-pigs underwent AV nodal cryoablation at −80°C without prior cryomapping. The duration of the cryoapplication following atrioventricular block (AVB) was randomized to 0, 10, 20, 40, or 60 s. Atrioventricular block was obtained in all animals after a median of 3 (1–8 interquartile range) applications. One week later, AV nodal conduction fully recovered in animals with application duration <10 s, whereas persistent AVB incidence increased as a function of time in animals with longer applications duration. Cryoablation application duration following AVB was the only independent predictor of persistent AVB (OR, 1.116; 95% CI, 1.013–1.229; P = 0.026). There was no difference in lesion location or size between animals with vs. those without persistent AVB at 1 week. However, animals randomized to longer application duration demonstrated higher degree of cell destruction and fibrotic content.ConclusionIn this closed-chest pig model, there was a relation between cryoapplication duration following AVB at −80°C and recovery of conduction. A safety window of at least 10 s was observed in all cases.