title: Role of the left atrium in adaptation of the heart to chronic mitral regurgitation in conscious dogs.
abstract: The manner in which the left atrium adapts to chronic mitral regurgitation and the role of the adapted left atrium as a modulator of excessive central blood volume were analyzed in seven conscious dogs, instrumented with high-fidelity pressure transducers and ultrasonic dimension gauges for measurement of left atrial and left ventricular pressure and cavity size. After obtaining data in a control situation, mitral regurgitation was produced by transventricular chordal sectioning. Heart rate was matched by right atrial pacing. In the "early" stage (7-14 days), left ventricular end-diastolic and mean left atrial pressures increased from 6 to 16 mm Hg and from 4 to 12 mm Hg, respectively. Both left ventricular end-diastolic segment length and left atrial diameter prior to atrial contraction increased by 7%. In the "late" stage (20-35 days), despite significant decreases in left ventricular filling pressure (11 mm Hg) and left atrial pressure (8 mm Hg), there was a continuous increase in left ventricular end-diastolic dimension (10%) and atrial end-diastolic diameter (10%). After the onset of mitral regurgitation, the left atrium performed greater work with a more enlarged cavity. Left atrial chamber stiffness was progressively decreased. These changes were associated with progressive increase in the left atrial diameter at zero stress, and there was a significant increase in the diameter of the left atrial myocyte. These results indicate that during chronic mitral regurgitation, the left atrium enlarges in size and mass, with a more potent booster action. The left atrial chamber becomes more compliant. Thus, the enlarged left atrium appears to exert an important compensatory mechanism in the case of excessive central blood volume by buffering pressure rise in the atrium and by providing an adequate ventricular filling volume.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Kihara
authors.forename: S
authors.initials: S
authors.lastname: Sasayama
authors.forename: S
authors.initials: S
authors.lastname: Miyazaki
authors.forename: T
authors.initials: T
authors.lastname: Onodera
authors.forename: T
authors.initials: T
authors.lastname: Susawa
authors.forename: Y
authors.initials: Y
authors.lastname: Nakamura
authors.forename: H
authors.initials: H
authors.lastname: Fujiwara
authors.forename: C
authors.initials: C
authors.lastname: Kawai
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001810:Blood Volume; D003243:Consciousness; D004285:Dogs; D005260:Female; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology*; D006984:Hypertrophy; D008297:Male; D008944:Mitral Valve Insufficiency / Q000503:physiopathology*; D009200:Myocardial Contraction