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Figure 13-77: (Plate 64) A. Mitral regurgitation. Left: apical three-chamber plane. Right: same plane with color Doppler imaging. A large jet of mitral regurgitation (arrow) is present. AO = aorta; LA = left atrium; LV = left ventricle. B. Parasternal long-axis view from a patient with angiographically proved severe mitral regurgitation. The color Doppler jet in this case is directed posteriorly and eccentric (black arrows). The jet hugs the wall of the left atrium (LA) and wraps around all the way to the aortic root (white arrows). LV = left ventricle.

TEE is also useful for assessment of MR, as the close proximity of the probe and its higher-frequency interrogating beam permit imaging of regurgitant jets in greater detail than TTE.313-315 Eccentric jets and mitral valvular anatomy are well visualized (&> Fig. 13-78A and B, Plate 65), and rightward bulging of the interatrial septum with severe MR is also sometimes apparent. As the regurgitant jets often appear larger with TEE than with TTE, one must avoid overestimation of MR severity.!54 TEE often yields Doppler interrogation of the pulmonary veins that is superior to TTE, and several recent studies have shown that systolic reversal of flow into the pulmonary veins is a reliable sign of severe MR152'315a'315b Fig. 13-79).

Another color Doppler method of flow quantitation involves measurement of the zone of flow convergence proximal to the regurgitant orifice (or the proximal isovelocity surface area, referred to as PISA).316-319 The mechanism for this phenomenon is derived from the hydrodynamic principle that blood flow accelerates before passing through a small orifice under high pressure. If this increase in flow velocity exceeds the Nyquist limit, color aliasing occurs and the velocity aliasing border is equal to the Nyquist limit Fig. 13-31 and Fig. 13-8CL4 and

B; Plate 66). If one assumes that the aliasing border conforms to the geometry of a hemisphere around the mitral orifice, then the instantaneous flow rate of blood through the orifice can be calculated as:

where r is the radius of the hemisphere shell (distance from alias border to orifice) and Vr is the velocity of blood at distance r (the Nyquist limit velocity).316 If the maximal calculated flow rate is divided by the peak regurgitant flow velocity (measured with CW Doppler), the regurgitant orifice area is then obtained.320 The product of regurgitant orifice area and integrated velocity of the MR jet by CW yields regurgitant volume.

The PISA method avoids the variables associated with jet size and the assumptions and technical limitations of volumetric calculations. Numerous studies have shown a correlation between both flow rate and regurgitant orifice area calculated by PISA and the severity of MR assessed by standard methods.316,320 In addition, flow convergence calculations have been applied to other valvular lesions, including AR and MS321'322 Fig. 13-81, Plate 67), ventricular septal defect,323 and prosthetic heart valves.324 The proximal flow convergence assumes a hemispheric geometry for the PISA signal and that the plane of the mitral leaflets is flat, two sources of potential error.325 Despite these limitations, the method holds considerable promise for the clinical evaluation of valvular regurgitation.

Mitral Valve Prolapse

As is true of so many aspects of mitral valve prolapse (MVP),326 the echocardiographic findings in this disorder have been controversial for many years.327 Recent insights into the anatomy of the mitral annulus and the significance of abnormal leaflet structure have established a central role for echocardiography in the diagnosis and prognosis of MVP.328 The classic echocardiographic findings in overt MVP syndrome consists of mid- to late-systolic bulging of one or both mitral leaflets across the plane of the mitral valve annulus into the LA (&H0; Fig. 13-82^4 to C).329 The leaflets are often observed to be structurally abnormal, with thickening, elongation, and hooding.330 Mid- to late-systolic MR is sometimes present, often eccentric, and generally directed away from the prolapsing leaflet.326 The chordae tendineae may be thickened and elongated, the aortic root may be dilated, and the tricuspid valve leaflets may prolapse as well. LV function is usually normal, although the LA and LV may be enlarged if MR is significant. The greater temporal resolution of M-mode over 2D echocardiography often yields striking evidence of abrupt midsystolic posterior/superior motion of the mitral valve leaflets in prolapse patients33! Fig. 13-82Q. Although such M-mode findings, which resemble a question mark on its side, are specific for mitral valve prolapse, patients with classic MVP occasionally may demonstrate diagnostic findings only with 2D imaging (Chap. 58).

Although the diagnosis of classic, fully expressed MVP is straightforward by echocardiography, identification of mild prolapse is more difficult, and no absolute diagnostic criteria currently exist.329 This is largely related to the absence of any "gold standard" with which to validate findings, including auscultation, angiography, and even pathology.326 For prolapse to be present, the mitral valve leaflets must cross the plane of the mitral valve annulus after initial systolic coaptation. Recent studies have established that the mitral valve annulus is not flat but rather saddle-shaped.332 The annulus reaches its nadir in the apical four-chamber view, and even normally coapting mitral valve leaflets may appear to prolapse in this projection. Therefore, current criteria require that MVP be diagnosed only when one or both of the mitral leaflets clearly bulge past the plane of the mitral valve annulus in the parasternal long-axis view.328 Unfortunately, the degree to which the mitral leaflets must break the plane of the annulus is unclear. The greater the portion of the mitral valve leaflets entering the LA, the more likely the existence of signs and symptoms related to this disorder; a peak distance behind the annulus of 2 mm almost invariably establishes the presence of MVP.329 The diagnosis of mild MVP may be assisted by examination of the structure of the leaflets and chordae tendineae, since it has been demonstrated that patients with redundant or thickening valve leaflets (greater than 5 mm in midleaflet) are at increased risk of complications, including severe MR and infective endocarditis333 (Chap. 73).

Torn Chordae Tendineae

Rupture of chordae tendineae may occur spontaneously or in conjunction with MVP or endocarditis. This can result in a flail mitral leaflet and severe MR. Although TTE often detects these lesions, TEE is especially sensitive and accurate and often demonstrates free motion of the leaflet and ruptured chord into the LA even when the TTE is equivocal (&H0; Fig. 13-83^4 and B).334 As with MVP, the MR jet in this condition is usually eccentric and directed away from the affected leaflet, often "hugging" the adjacent left atrial wall (Coanda effect). Therefore, the jet's cross-sectional area may be misleadingly small. The findings of mitral valvular anatomy on TEE may also be helpful in predicting the feasibility and success of valve repair surgery.335

In the setting of ischemic heart disease, both LV enlargement and papillary muscle dysfunction (from infarction or transient ischemia) may cause MR.336 Both the MR and the contractile abnormality responsible for it are usually well visualized by 2D echocardiography. In rare cases, papillary muscle rupture (partial or complete) occurs in the postinfarction period.337 Rapid echocardiographic diagnosis often requires TEE and may be lifesaving in these cases.334

Mitral Annular Calcification

The finding of mitral annular calcification (MAC) is fairly common in adults and occurs more frequently with advancing age. Although ultrasound cannot discern histology, calcification typically appears as thickened, extremely high-intensity ("bright") signals Fig. 13-84). The posterior portion of the mitral annulus is affected much more commonly than the anterior segment, and calcification often extends into the posterior mitral leaflet, sometimes restricting its motion.338-340 The abnormality, best visualized in the parasternal long- and short-axis views, is seen as a bright calcific density at the junction of the posterior mitral leaflet and the annulus. In the short-axis view, the posterior band of calcification often appears crescentic. Rarely, the calcification is extensive enough to cause marked valvular thickening and clinically significant mitral stenosis.339 MAC has also been implicated as a source of cardiogenic embolization.344

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