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The Variability of the Electrical Properties of the Pulmonary Veins

The demonstration by Haissaguerre and colleagues that ectopic activity arising in the proximal 2–4 cm of the proximal pulmonary veins (PVs) was the source of triggers for atrial fibrillation has ushered in a new era in the management of AF.1 Ablation of the ectopic foci within the veins, or isolation of the PVs, abolished atrial fibrillation. These observations have been confirmed in numerous clinical electrophysiology laboratories worldwide and ablation is now included as a treatment strategy in the most recent ACC/AHA/ESC guidelines for the management of atrial fibrillation.2 Many questions at the basic and clinical level are unresolved: what cell types are the basis of the ectopic activity, are the cells of a uniform type, what are the mechanism(s) of the ectopic activity, is there a difference in pharmacologic susceptibility between the various cell types, and what is the permanence of the ablative strategies? Answers to these questions may identify simple therapeutic strategies to abolish the ectopic foci. A number of investigators have attempted to answer these and other related questions. Identification of appropriate model systems to study AF is an immediate challenge. Availability of human tissue is restricted to autopsy material and is suitable for anatomic studies only. The rabbit, dog, and guinea pig are the principal sources of living tissue for electrophysiological studies. There are anatomic variations in the veins of these species. The anatomic complexity of multicellular tissue preparations makes them unsuitable for the study of the individual ionic currents. Single cells can be isolated from the PVs by enzymatic dissociation. However, the location of these cells along the course of the veins is usually unknown. The most relevant studies are those that study tissue or single cells from PVs that are isolated from hearts with atrial fibrillation or hearts that model atrial fibrillation, e.g., rapid atrial pacing or repetitive burst pacing. Few such studies have been performed. A simple anatomic question that is frequently overlooked is whether pulmonary venous tissue is the source of the ectopic activity. Available data suggest that the ectopic activity arises from the myocardial sleeves that surround the veins. These myocardial sleeves have been the subject of several detailed anatomic studies. Nathan and Eliakim examined the junction of the left atrium and pulmonary veins in 16 autopsy specimens.3 The myocardial sleeves around the proximal veins average 8–18 mm in length, and were longest