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Mitral Regurgitation After Partial Left Ventriculectomy As the Cause of Ventricular Redilatation
Author(s) -
Kawaguchi Akira T.,
Bocchino Lise O.,
Shimura Shin'ichiro,
Karamanoukian Hratch L.,
Koide Shirosaku,
Batista Randas J. V.
Publication year - 2001
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.2001.tb00492.x
Subject(s) - medicine , mitral regurgitation , cardiology , volume overload , etiology , cardiomyopathy , heart failure , heart disease , dilated cardiomyopathy , hemodynamics , surgery
A bstractBackground : It remains unclear whether ventricular redilatation after partial left ventriculectomy (PLV) is due to underlying pathology or to continued volume overload amenable to surgery. Methods : Among patients undergoing PLV, 32 had Doppler echocardiography preoperatively, immediately after surgery (> 1 week), early after surgery (1–3 months), and late after surgery (8–14 months). Patients were divided into groups with mitral regurgitation (MR; MR+, n = 16) and without postoperative MR (MR‐, n = 16) and were compared for ventricular size, performance, and survival. Results : After initial surgical reduction, left ventricular dimension on average gradually increased back to the preoperative level in subgroups of patients with valvular disease and cardiomyopathy and in all patients combined. Most patients showed drastically reduced left ventricular dimension early after PLV. In MR+ patients, dimension increased back to the preoperative level within 3 months after surgery, whereas the MR‐ group maintained reduced dimension throughout the first year in all patients combined and in a subgroup of patients with cardiomyopathy. Occurrence of significant MR after PLV appeared to be related to severity of fibrosis in excised myocardium but not to severity of preexisting MR, etiology, or performance of mitral valvuloplasty. Conclusions : Early postoperative MR, residual or new, appeared to play an important role in dictating early hemodynamics and late outcome in patients undergoing PLV. Results suggest an aggressive simultaneous approach to abolish MR. Causative role of myocardial fibrosis remains unclear and needs further study.

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