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Functional mitral stenosis in patients with massive mitral annular calcification
Insights
Severe mitral annular calcification can cause mitral diastolic obstruction without leaflet stenosis, primarily affecting diastolic relaxation. This condition can lead to significant mitral regurgitation and left ventricular dilation in patients.
Area of Science:
- Cardiology
- Cardiac Surgery
- Valvular Heart Disease
Background:
- Mitral annular calcification (MAC) is often associated with mitral insufficiency, particularly in elderly females.
- Previous descriptions focused on MAC causing mitral insufficiency, but its role in diastolic obstruction without leaflet stenosis was less clear.
Purpose of the Study:
- To investigate mitral diastolic obstruction in patients with mitral annular calcification without mitral leaflet stenosis.
- To determine the clinical and pathological features of this condition.
Main Methods:
- Retrospective study of six patients (3 male, 3 female, aged 43-77) with MAC and mitral diastolic obstruction.
- Analysis of catheterization data for diastolic gradients, surgical findings, and pathological examination.
- Review of clinical outcomes including valve replacement and left ventricular function.
Main Results:
- All six patients exhibited significant holodiastolic mitral gradients (mean 16 mm Hg) due to MAC.
- No evidence of mitral leaflet retraction, thickening, or commissural fusion was found.
- Three patients had severe mitral insufficiency, with causes including prolapsing leaflets and ruptured chordae tendineae.
- Left ventricular dilation was observed in three patients, associated with mitral regurgitation or mixed aortic valve disease.
Conclusions:
- Severe mitral annular calcification can independently cause significant mitral diastolic obstruction by impairing diastolic relaxation.
- This obstruction can coexist with or lead to mitral insufficiency and left ventricular dysfunction.
- Understanding MAC's impact on diastolic function is crucial for managing valvular heart disease.
Abstract:
Mitral insufficiency with mitral annular calcification occurring predominantly in elderly females has been described. We studied six patients with mitral diastolic obstruction associated with mitral annular calcification without stenosis of the mitral leaflets. Three were males and three were females, aged 43-77 years. All had significant diastolic gradients across the mitral valve (mean gradient 16 mm Hg) recorded at catheterization. Two patients had aortic and three had mitral valve replacement. No patient had retraction of the mitral leaflets, diffuse thickening or fusion of the commissures at surgery or pathologic examination. Three patients had severe mitral insufficiency, one associated with voluminous prolapsing mitral leaflets and one as a result of ruptured chordae tendineae. The left ventricle was dilated in three patients, two with mitral regurgitation and one with mixed aortic valve disease. Active mitral annular motion is a normal event and is necessary for normal valvular function; severe calcification of the ring interferes with its normal diastolic relaxation and this alone may explain the holodiastolic mitral gradient found in these patients.