© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Comparison of mitral valve prolapse in dogs and humans
Division of Cardiology, Department of Medicine The George Washington University, Medical Center, Washington, DC, USA
Received 10 October 2000; accepted 10 October 2000
To the Editor:
I read with great interest the comprehensive review on mitral valve prolapse in the dog by Pedersen and Häggström [1]. Although I have had a longstanding interest in mitral valve prolapse in humans and knew that mitral valve prolapse is the commonest cardiac disease in the dog [2] as in humans [3], I have never examined a dog with mitral valve prolapse. However, I was greatly impressed by the similarities between mitral valve prolapse in the dog and in the human, as were convincingly presented by Pedersen and Häggström [1].
Sudden cardiac death is a recognized, though relatively rare (only 106 cases reported up to 1989 [4]), complication of mitral valve prolapse in humans [5]. It was interesting to speculate on the mechanism of sudden cardiac death in mitral valve prolapse. Pedersen and Häggström cited the work of Falk and Jönsson [6] who found nonatherogenic dysplasia of the intramural coronary arteries in dogs that died suddenly. Although similar finding was reported in humans with mitral valve prolapse [7,8], its significance in contributing to sudden cardiac death is unclear. Evidence to date suggests that the predominant mechanism of sudden cardiac death in mitral valve prolapse is fatal ventricular arrhythmias [9]. Therefore, it would be extremely difficult for a pathological study to prove or disprove conclusively the causal relation between mitral valve prolapse and sudden cardiac death which is a physiological event [10].
A recent report from the Mayo Clinic [11] seemed to indicate that the incidence of sudden cardiac death in mitral valve prolapse has been underestimated and that sudden cardiac death occurred only in patients with mitral valve prolapse and significant mitral regurgitation. This author and other investigators from the literature [12] have encountered patients with mitral valve prolapse who died suddenly even though the degree of their mitral regurgitation was mild. The mode of sudden cardiac death in mitral valve prolapse is presumably ventricular tachyarrhythmias deteriorating into ventricular fibrillation.
The mechanism of ventricular tachyarrhythmias in mitral valve prolapse is multifactorial [4]:
- 1. abnormal tension on the papillary muscle and adjacent myocardium from the prolapsing mitral leaflet(s);
- 2. endocardial friction lesions produced by contact between the tense chordae tendineae attached to the prolapsing mitral leaflet(s) and left ventricular endocardium;
- 3. diastolic dumping of the floppy mitral leaflets;
- 4. coronary embolism from deposits of fibrin and platelets on the fissures of the redundant leaflets and in the angle between the prolapsing posterior leaflet and the left atrial wall;
- 5. coronary vasospasm;
- 6. associated cardiomyopathy;
- 7. adrenergic hyperactivity [13,14];
- 8. increased QT dispersion [15,16];
- 9. hypomagnesemia [17].
- 2. endocardial friction lesions produced by contact between the tense chordae tendineae attached to the prolapsing mitral leaflet(s) and left ventricular endocardium;
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