A starting point for structure function relationships in the canine pulmonary veins

See article by Verheule et al. [6] (pages 727–738) in this issue. The recent demonstration of the effectiveness of catheter ablation of the pulmonary veins as a curative treatment for paroxysmal atrial fibrillation (AF) has prompted efforts to examine in detail the sleeves of atrial myocardium encasing their left atrial ends [1]. Multi-electrode catheter mapping of spontaneous episodes of AF in patients show that the majority (>90%) of paroxysms begin with earliest activation at the ostium or within the pulmonary veins [2]. Consistent initiation of paroxysms of AF from tissue in this region reinforces the probability of distinctive structural or functional characteristics being responsible for such anatomical localization. Activation mapping within the confines of the pulmonary veins is limited by their diameter (about 15–17 mm), complex branching structure as well as the limitations of access through a transseptal puncture. A preformed loop shaped multi-electrode catheter positioned orthogonal to the venous long axis, at the relevant ostium or within the vein, provides a slice of circumferential activation [3], while the integration of an additional longitudinal mapping ability e.g. with a basket catheter provides the maximal currently and clinically possible mapping coverage of the vein. Nevertheless, this leaves unmapped territory in the first order branches. Though decremental conduction, spontaneous activity as well as exit block have been documented within the veins or at their junction with the left atrium using the above catheters [2,4], there is limited detail about the electrophysiology of this region. A recent report described basket catheter mapping of a tachycardia originating in the superior vena cava—a thoracic vein with a structure similar to the pulmonary veins [5]. Activation compatible with a physically small circus movement reentry circuit (based on nonuniform anisotropy) was found to be confined to the myocardial sleeve of the superior vena cava with intermittent conduction to the right atrium. During both tachycardia as well as programmed stimulation in sinus rhythm, evidence of marked slow conduction was found; notably, conduction was faster in the long axis of the vein as compared to perpendicularly. In contrast to such abnormal impulse conduction, the first beat(s) of the initiation of a paroxysm of AF displays characteristics compatible with triggered activity though abnormal automaticity cannot be ruled out. These abnormal impulses likely trigger a reentrant arrhythmia, that spreads to involve the atria. Thus, a combination of arrhythmia mechanisms is very likely responsible for AF. The myocardial fiber arrangement, their coupling by means of gap junctions and the intervening fibrous tissue certainly affect the milieu for reentry by affecting the wavelength of the tissue. Whether they similarly affect or promote abnormal impulse generation is not clear though some degree of protection or isolation from normal currents of surrounding cells is felt to be necessary for abnormal automaticity.