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[Heart rupture after mitral valve replacement. Pathologic-anatomic findings]
C Kuhnen1, C Fakir, A Laczkovics
1Institut für Pathologie der Berufsgenossenschaftlichen Kliniken Bergmannsheil, Ruhr-Universität, Bochum.
Insights
Left ventricular free wall rupture is a severe complication after mitral valve replacement. Preserving mitral valve apparatus, particularly chordae tendineae, can prevent this rupture by maintaining left ventricular integrity.
Area of Science:
- Cardiovascular Surgery
- Cardiac Pathology
- Surgical Complications
Background:
- Mitral valve replacement is a common procedure, but carries risks.
- Rupture of the left ventricular free wall is a rare yet serious complication.
- Understanding the mechanism is crucial for prevention.
Observation:
- Three cases of transverse midventricular disruption post-mitral valve replacement are presented.
- Rupture occurred 1-12 hours after prosthesis implantation.
- Histology revealed necrotic myocardium with interstitial bleeding and inflammation.
Findings:
- Ventricular rupture was located between the mitral valve annulus and resected papillary muscles.
- Coronary artery abnormalities and intraoperative lesions were excluded.
- Loss of left ventricular contractile integrity after mitral valve apparatus resection, especially chordae tendineae, is the primary cause.
Implications:
- This loss of integrity leads to regional myocardial stretching and subsequent rupture.
- Limited resection of the mitral valve apparatus, preserving chordae tendineae, is recommended.
- This approach may prevent devastating post-operative left ventricular free wall ruptures.
Abstract:
The rupture of the free left ventricular wall is considered a serious complication following mitral valve replacement. We report about 3 cases 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 prosthesis, rupture of the left ventricular wall occurred in short time intervals 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. The histologic findings included necrotic, damaged myocardial structures with considerable bleeding to the interstitium. Inflammatory infiltration could be detected within the myocardial defects. Abnormal pathologic findings of the coronary arteries or intraoperative lesions could be excluded by thorough autoptic studies. Because of central localization of the ventricular disruption between the mitral valve anulus and the papillary muscles a direct traumatic myocardial injury caused by mitral valve orotheses is to be excluded. When taking into account several reports from literature in combination with our described findings, in autopsy, a loss of contractile integrity of the left ventricle following resection of mitral valve apparatus, especially the chordae tendinaea, should be considered as primary cause for this type of ventricular rupture. This destabilization will lead to a regionally stressec myocardial "stretching" which finally results in rupture of the left ventricular free wall. The described pathogenetic concept seemingly represents the decisive mechanism of this transverse midventricular disruption in all 3 cases. To prevent such post-operative complications, only very limited resection of the mitral valve apparatus should be performed to maintain parts of the chordae tendineae.