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. 2000 Aug;11(8):888-94.
doi: 10.1111/j.1540-8167.2000.tb00068.x.

Left atrial myocardial extension onto pulmonary veins in humans: anatomic observations relevant for atrial arrhythmias

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Left atrial myocardial extension onto pulmonary veins in humans: anatomic observations relevant for atrial arrhythmias

T Saito et al. J Cardiovasc Electrophysiol. 2000 Aug.

Abstract

Introduction: Electrophysiologic studies have shown that spontaneous initiation of atrial fibrillation (AF) by ectopic beats may originate from within pulmonary veins. The extensions of left atrial myocardium are considered to play a role, but there is little detailed anatomic information available, particularly in humans.

Methods and results: Thirty-nine human autopsy hearts were studied; 22 with AF and 17 without atrial arrhythmias. The muscle fiber arrangement of the left atrial wall and pulmonary veins was dissected. In 18 hearts, myocardial sleeves were studied microscopically; in five hearts, three-dimensional reconstruction of the fiber arrangement in the myocardial sleeves was performed. Of 99 pulmonary veins examined, 96 contained a myocardial sleeve. The length of the sleeves was largest in the superior pulmonary veins (P < 0.01). There were no statistically significant differences between uniform and nonuniform muscle fiber arrangements. Microscopic evaluation revealed myocardial sleeves positioned on the adventitial side of the pulmonary vein, separated from the muscular media by a fibrofatty tissue plane. The most distal zone of the myocardial sleeves showed increasing fibrosis with encapsulation of small groups of myocardial cells and eventually with total disappearance of atrophic cells within fibrous tissue. Node-like structures were not encountered. There was no relationship with presence or absence of AF.

Conclusion: The observation that the peripheral zones of myocardial sleeves are associated with increasing connective tissue deposition between myocardial muscle groups suggests a degenerative change that, from the histologic viewpoint, fits with progressive ischemia. These changes could provide a basis for microreentry and, hence, for atrial arrhythmias.

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