RUPTURE OF THE LEFT-VENTRICLE AFTER MITRA L-VALVE REPLACEMENT - PATHOLOGICAL-ANATOMICAL FINDINGS

Citation
C. Kuhnen et al., RUPTURE OF THE LEFT-VENTRICLE AFTER MITRA L-VALVE REPLACEMENT - PATHOLOGICAL-ANATOMICAL FINDINGS, Der Pathologe, 18(3), 1997, pp. 238-242
Citations number
17
Categorie Soggetti
Pathology
Journal title
ISSN journal
01728113
Volume
18
Issue
3
Year of publication
1997
Pages
238 - 242
Database
ISI
SICI code
0172-8113(1997)18:3<238:ROTLAM>2.0.ZU;2-U
Abstract
The rupture of the free left ventricular wall is considered a serious complication following mitral valve replacement. We report about 3 cas es characterized by similar pathologic-anatomical findings within the region of the left ventricle after mitral valve replacement. Following resection of the original and pathologically altered mitral valve and implantation of a prothesis, rupture of the left ventricular wall occ urred in short time intervalls ranging from 1 to 12 h postoperatively. All cases represented a transverse midventricular disruption located between the mitral valve anulus and the resected papillary muscles. Th e histologic findings included necrotic, damaged myocardial structures with considerable bleeding to the interstitium. Inflammatory infiltra tion could be detected within the myocardial defects. Abnormal patholo gic findings of the coronary arteries or intraoperative lesions could be excluded by thorough autoptic studies. Because of central localizat ion of the ventricular disruption between the mitral valve anulus and the papillary muscles a direct traumatic myocardial injury caused by m itral valve protheses is to be excluded. When taking into account seve ral reports from literature in combination with our described findings in autopsy, a loss of contractile integrity of the left ventricle fol lowing resection of mitral valve apparatus, especially the chordae ten dinaea, should be considered as primary cause for this type of ventric ular rupture. This destabilization will lead to a regionally stressed myocardial ''stretching'' which finally results in rupture of the left ventricular free wall. The described pathogenetic concept seemingly r epresents the decisive mechanism of this transverse midventricular dis ruption in all 3 cases. To prevent such post-operative complications, only very limited resection of the mitral valve apparatus should be pe rformed to maintain parts of the chordae tendineae.