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Cardiovascular Research 2000 47(2):234-243; doi:10.1016/S0008-6363(00)00113-9
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Mitral valve prolapse in the dog: a model of mitral valve prolapse in man

Henrik D. Pedersena,* and Jens Häggströmb

aDepartment of Anatomy and Physiology, Royal Veterinary and Agricultural University, Grønnegårdsvej 7, DK-1870 Frederiksberg C, Denmark
bDepartment of Animal Physiology, Swedish University of Agricultural Sciences, Uppsala, Sweden

* Corresponding author. Tel.: +45-35-282-526; fax: +45-35-282-525 hdp@kvl.dk

Received 21 January 2000; accepted 25 April 2000

KEYWORDS Aging; Epidemiology; Renin angiotensin system; Ultrasound; Valve (disease)

The first 150 words of the full text of this article appear below.


    1 Introduction
 
Mitral valve prolapse (MVP), i.e. abnormal systolic protrusion of mitral valve leaflets into the left atrium, is a common cause of severe mitral regurgitation (MR) requiring operation in people living in industrialized nations [1,2]. MVP has been reported to have many causes but in the majority of cases it is a primary condition (called primary MVP in this paper) characterized by a progressive myxomatous degeneration of the mitral valve leaflets and chordae tendineae [1–3]. The disease typically emerges in adolescence but complications such as severe MR usually do not occur until middleage or senescence [1–3]. An animal model with a shorter course of disease could be useful in several ways, for instance, by making it feasible to evaluate the effects of different drugs on disease progression. Despite this, no animal model of primary MVP has been described so far.

From pathological studies, it has long been known . . . [Full Text of this Article]


    2 Pathology
 

    3 Etiology and pathogenesis
 

    4 Epidemiology and natural history
 

    5 Auscultatory findings
 

    6 Two-dimensional echocardiography
 

    7 Possible associations with other conditions
 
7.1 Changes in the circulating renin–angiotensin system
7.2 Respiratory sinus arrhythmia
7.3 Hypomagnesemia
7.4 Platelet activation

    8 Concluding remarks
 

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