The effects on atrial electrophysiology and structure of surgically induced right atrial enlargement in dogs.

Abstract

We evaluated the relationship between susceptibility to arrhythmias caused by right atrial (RA) enlargement and alterations in transmembrane potentials and ultrastructure. RA enlargement was produced in eight dogs (TI) by excising the septal cusp of the tricuspid valve through a right atriotomy and constricting the pulmonary artery. This procedure resulted in RA dilation and hypertrophy. Four sham-operated dogs (S) also were studied. Neither TI nor S dogs developed spontaneous atrial arrhythmias. Atrial overdrive (OD) and premature stimulation (PS) were used to initiate and terminate arrhythmias. At 2 weeks and for 20 to 30 weeks after surgical preparation, TI dogs were more susceptible to arrhythmias than S dogs. The duration of arrhythmias exceeded 10 minutes more often in TI dogs than in S dogs. Sixty-one percent of all arrhythmias in the TI dogs had rates of 320-450 impulses/min, and electrogram and ECG characteristics of atrial flutter (type II rhythm), whereas no S dogs developed rhythms with these slower rates. The type II rhythms were persistent, 30% lasting longer than 30 minutes, while 22% lasted more than 60 minutes. Transmembrane potentials recorded in vitro from the RA free wall of TI dogs, and responses to norepinephrine and acetylcholine were not different from control. Histological and ultrastructural studies on TI atria showed hypertrophy of fibers and some increase in connective tissue between cells. These results suggests that altered susceptibility to long-lasting arrhythmias need not be associated with significant abnormalities of cellular electrophysiology.