Myxomatous mitral valve disease

image of Myxomatous mitral valve disease
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Myxomatous mitral valve disease (MMVD) of the atrioventricular (AV) valves is characterized by the accumulation of glycosaminoglycans (myxamtous proliferation) and fibrosis of the valve leaflets and tendinous chordae. The condition has been given many names, including endocardiosis, chronic degenerative valvular disease, chronic valvular disease, chronic valvular fibrosis and acquired mitral or tricuspid regurgitation or insufficiency. The valvular degeneration leads to insufficient coaption of the valve leaflet, valvular regurgitation and, in some animals, eventually to congestive heart failure (CHF). The condition most commonly involves the mitral valve with or without involvement of the tricuspid valve. Isolated tricuspid myxomatous degeneration occurs but is less common. Likewise, myxomatous changes occur infrequently on the semilunar valves (especially the aortic) but are rarely of clinical importance. The chapter looks at Aetiology; Epidemiology and inheritance; Pathophysiology; Clinical signs; Diagnostic approach; Treatment; and Prognosis.

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Image of 21.1
21.1 Post-mortem specimen of a dog with end-stage MMVD. The mitral valve leaflets appear thickened and contracted when observed from the atrial side. The thickening consists of nodules on the free edges of the leaflets and thickening of the chordae tendineae, and the left ventricle and atrium are dilated. Chordal rupture, particularly of lesser-order chordae, is a common finding but not apparent in this image. Jet lesions are present on the atrial wall, which occur when regurgitant jets of blood from the left ventricle strike the atrial wall.
Image of 21.3
21.3 Phonocardiogram (PCG) from a Cavalier King Charles Spaniel with a moderate intensity murmur due to MMVD. The recording is displayed in two modes: the upper mode shows synchronous PCG and ECG traces; and the lower mode shows a time–frequency graph where different frequencies are displayed according to intensity, with high-intensity frequencies in red and low-intensity frequencies in blue. The two PCG tracings are timed with respect to each other. Note that the murmur is composed of sound with a frequency up to 1400 Hz, but the most intense part of the murmur is composed of low-frequency components (<400 Hz), which gives the murmur a harsh character. M = Murmur; S1 = First heart sound; S2 = Second heart sound.
Image of 21.4
21.4 Right parasternal long-axis views of the left atrium (LA) and left ventricle (LV) during systole in: a normal dog; a dog with mild mitral valve prolapse and MMVD. a dog with severe mitral valve prolapse and MMVD. In (c) the mitral valve appears thickened in diastole (arrowheads); and prolapse is evident in (b) and (d) as systolic displacement of both leafl ets to the atrial side of the mitral annulus (arrowheads). Colour Doppler echocardiography in (d) shows valvular regurgitation during systole. Mitral regurgitation is usually, but not always, best captured in a left apical four-chamber view because of better alignment with the blood flow. Flow velocity of the regurgitant jet (e) is often measured in the same view because of the same reason, and flow velocity in a typical case is often approximately 5.5–6 m/s unless there is significant systolic dysfunction, when the flow velocity is lower, or there is poor alignment. Appearance of the LA in a right parasternal short-axis view at the aortic valve level in: a normal dog; and a dog with a severely enlarged LA. Complications to the disease include rupture of multiple major chordae tendineae causing: a “flail” mitral valve leaflet (arrowheads); and the development of intracardiac blood clots (arrowhead). RA = Right atrium; RV = Right ventricle.
Image of 21.5
21.5 Left lateral recumbent views of a dog with MMVD and mitral regurgitation. The dog was asymptomatic, and the radiograph shows a normal cardiac silhouette and vascular perfusion. Radiograph of the same dog 2 years later. The dog was still asymptomatic, but the intensity of the murmur had increased. Left atrial and left ventricular enlargement are evident, with elevation and slight compression of the left mainstem bronchus, but the vascular markings are within normal limits. 1 year later the dog had developed respiratory distress and had suffered episodes of syncope. In addition to the findings in (b), there is more obvious cardiomegaly, compression of the left mainstem bronchus and evidence of pulmonary congestion and interstitial oedema. (Courtesy of K. Hansson.)
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