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The Journal of Thoracic and Cardiovascular Surgery, Vol 86, 479-489, Copyright © 1983 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
JA Spratt, CO Olsen, GS Tyson Jr, DD Glower Jr, JW Davis and JS Rankin
It has been suggested that mitral valve replacement for mitral
regurgitation can precipitate acute myocardial failure by increasing left
ventricular afterload. However, most studies of this problem have involved
anesthesia, acute surgical trauma, or ischemic cardioplegia, each of which
can influence myocardial function. The pure hemodynamic consequences of
mitral valve replacement were investigated by surgically instrumenting
eight dogs with ultrasonic transducers to measure left ventricular
diameter, electromagnetic flow probes to measure ascending aortic blood
flow, and micromanometers to measure left ventricular and pleural
pressures. At the time of implantation, an 8 mm stainless steel shunt was
inserted through the left ventricular myocardium at the base of the
anterior wall and sutured to the left atrial appendage, producing simulated
mitral regurgitation of 20% to 40% of total ventricular output. Balloon
occluders were placed around the left atrial shunt and both venae cavae.
One to 7 days after implantation, each dog was studied in the conscious
state, and data were recorded during acute occlusion of the shunt. After
shunt occlusion, left ventricular mean ejection pressure increased
significantly in all studies. Systolic wall tension also increased by an
average of 8%, diameter shortening decreased by 21%, and forward cardiac
output increased by 17%. Thus the higher afterload associated with
elimination of mitral regurgitation produced an acute fall in stroke
shortening and total left ventricular output. However, forward cardiac
output increased in all studies, implying improved pump efficiency and
overall cardiac performance. Thus the improvement in pump efficiency
associated with restoration of mitral valve competence uniformly increases
forward cardiac output despite an increased ventricular afterload and a
decreased total stroke volume. Although there may be differences between
this relatively acute model and chronic forms of mitral regurgitation
encountered clinically, these data suggest that forward cardiac output
should increase with correction of mitral regurgitation and that the
associated augmentation in afterload is probably not a major factor causing
low cardiac output after correction.
ARTICLES
Experimental mitral regurgitation. Physiological effects of correction on left ventricular dynamics
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