Time for primary review 31 days. 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 that most dogs develop myxomatous mitral valve disease with age and that this disease is very similar macroscopically as well as microscopically to primary MVP in humans [4,5]. Traditionally, however, the canine disease has been given names other than MVP, including endocardiosis and chronic valvular disease. Recently, a number of studies, including many based on well-defined echocardiographic criteria for the diagnosis of MVP, have increased our understanding of this disease in the dog. The purpose of this article is to compare the knowledge which has been accumulated about myxomatous mitral valve disease/MVP in the dog with knowledge of primary MVP in humans. Pathologically, primary MVP in humans is very similar to canine myxomatous mitral valve disease [4,5]. In both species, the principal macroscopic findings are enlarged, thickened leaflets, interchordal hooding and elongated chordae tendineae (Fig. 1A, B) [4–9]. In addition, affected … * Corresponding author. Tel.: +45-35-282-526; fax: +45-35-282-525 hdp{at}kvl.dk