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Modes of failure of Hancock and Carpentier-Edwards (C-E) porcine bioprosthetic valves placed in the mitral position are not completely understood. We reviewed transesophageal echocardiographic (n = 19) and pathologic features of failed Hancock (n = 22) and C-E (n = 8) porcine mitral valves in 30 patients (mean age 70 +/- 13 years). Age at implantation (59 +/- 14 vs 58 +/-14 years, p = 0.9), time to implanted valve degeneration (13 +/- 5 vs 11 +/- 2 years, p = 0.3), and size of bioprosthesis (30 +/- 2 vs 31 +/- 2 mm, p = 0.14) of the implanted Hancock and C-E valves were similar. Anterior leaflet was flail in 15 versus flail posterior leaflet in 5 patients (p = 0.0004). Eccentric posterior mitral regurgitation jet was present in 12, eccentric anterior jet in 2, central jet in 2, and paravalvular jet in 3 patients. Stenosis of bioprosthesis was present in 1 1 Hancock versus 1 C-E valve (p = 0.06). Stent creep at any stent post was present in 14 Hancock versus no C-E valve (p = 0.0013). Large commissural dehiscence was present in 5 C-E versus 1 Hancock valve (p = 0.0006). Ring margin perforation was the most common perforation in Hancock valves (p

Recent data suggest that posterior leaflet repair alone corrects mitral regurgitation in patients with bileaflet prolapse and normal anterior chordae. The purpose of this study was to use echocardiography to define the anatomic differences between posterior and bileaflet prolapse and to determine if posterior leaflet repair alone leads to correction of bileaflet prolapse. We studied patients who underwent quadrangular resection of the posterior mitral valve leaflet to treat bileaflet prolapse (group I, n = 20) or isolated posterior leaflet prolapse (group II, n = 20). Echocardiographic characteristics were compared before and after the procedure. There were no differences in the left ventricular end-diastolic or end-systolic dimensions or function between the 2 groups. However, anterior leaflet length was greater in patients with bileaflet prolapse (3.3 +/- 0.6 cm vs 2.6 +/- 0.4 cm, p = 0.003). In group I, posterior leaflet repair changed anterior leaflet displacement from -0.8 +/- 0.2 to 0.5 +/- 0.4 cm (p0.001) and posterior leaflet displacement from -0.8 +/- 0.3 cm below to 0.5 +/- 0.4 cm (p0.001) in front of the mitral annular plane. In group II, anterior leaflet displacement was unchanged from 0.2 +/- 0.1 to 0.3 +/- 0.2 cm (p = 0.22), whereas posterior leaflet displacement changed from -0.7 +/- 0.2 to 0.4 +/- 0.2 cm (p0.001). Thus, patients with bileaflet prolapse and no ruptured chords have excessive anterior leaflet length. In such patients, posterior leaflet repair alone corrects anterior and posterior leaflet prolapse.

To elucidate predisposing factors for severe mitral regurgitation (MR) in idiopathic mitral valve prolapse (MVP), 124 MVP patients were classified into the following categories: 55 with isolated clicks (click group), 35 with a late-systolic murmur (late-SM group), and 34 with a holosystolic murmur (holo-SM group). Their clinical and echocardiographic findings were compared with those of 26 patients with spontaneous chordal rupture (rupture group). In 22 patients in the click group, 24 in the late-SM group, and 22 in the holo-SM group, follow-up studies were performed for a mean of 4.5 years (range 1 to 13.5). The mean age was youngest in the click group and oldest in the rupture group. The click and late-SM groups showed a female predominance, but the holo-SM and rupture groups showed a male predominance. There was no difference in the incidence of systemic hypertension among the 4 groups. Most patients in the click and late-SM groups had anterior leaflet prolapse. In the holo-SM and rupture groups, however, the incidence of posterior leaflet involvement was significantly increased. The incidence of thickened mitral valve increased in order of the click (8%), late-SM (21%), holo-SM (38%), and rupture (50%) groups. Six patients in the holo-SM group developed chordal rupture with severe MR during the follow-up period. In the click and late-SM groups, however, there were no complications and no development into a holo-SM. Thus, aging, male sex, posterior leaflet prolapse, thickened mitral valve, and holo-SM were round to be important predisposing factors for severe MR in idiopathic MVP.

Study of 16 normal and 33 flail mitral valves provides evidence of the active participation of chordae tendineae in mitral valve opening. The normal valves have straight chordae at all phases of opening. During isovolumic relaxation and progressive opening phases, the smooth configuration of the mid-anterior mitral leaflet is broken by a sharp outward “tenting.” This tenting is localized at chordal insertions, reflecting significant tension at these points. Flail mitral valves allow comparison of opening motion between mitral segments with normal chordal attachment and flail segments without chordal support. Posterior flail leaflets demonstrate delay in initiation of opening motion relative to the normal anterior leaflet. The most dramatic examples of this delay reveal a maximal opening excursion of the anterior leaflet before the flail posterior leaflet initiates opening motion. The untethered free margins of opening flail anterior leaflets produce the appearance of the flail segment trailing the body of the anterior leaflet with a sharp break in leaflet contour between the supported and unsupported segments. These configurational expressions of mitral valve opening are inconsistent with a passive hemogenic mechanism. They support an active myogenic process mediated through direct traction on the valve by the chordae tendineae.

Twenty pathologic specimens of heart, each with a cleft in the anterior leaflet of the mitral valve not associated with septal defects of persistent common atrioventricular canal (isolated cleft of the mitral valve), were studied. In 9 cases, there were either no associated anomalies or ones not of functional significance. In each of the other 11 cases there were other significant associated cardiac anomalies, including ventricular septal defect and d-transposition of the great arteries. Functional consequences of the mitral anomaly were mitral insufficiency, subaortic stenosis, or both. Mitral insufficiency was related principally to the width of the cleft. Subaortic stenosis, when present, was due to the position of insertion of accessory chordae in the ventricular septum in a position under the commissure, between the left and right aortic cusps or under the right aortic cusp.

The mechanism of severe mitral regurgitation (MR) due to active rheumatic carditis is ill defined. This study involved 73 patients, aged 7 to 27 years (mean 13), with severe MR and active rheumatic carditis who were subjected to surgery. Sixty-one were studied retrospectively (group 1) and 12 prospectively (group 2). Active rheumatic carditis was diagnosed according to the modified Jones' criteria, morphologic appearances of the heart at operation and histology of the valve. All patients had preoperative 2-dimensional echocardiographic and intraoperative assessment of the mitral valve apparatus. The presence of mitral valve prolapse--defined as failure of leaflet edge coaptation resulting in systolic displacement of the free edge of the involved leaflet toward the left atrium--was determined in all patients. Mitral anular diameter and maximal systolic chordal length were measured at 2-dimensional echocardiography in group 2 patients and compared to values obtained from matched control subjects. Anular and chordal dimensions in 6 of the group 2 patients were correlated with precise measurements obtained at surgery. Mitral valve prolapse involving the anterior leaflet was detected on echocardiography and confirmed at surgery in 69 patients (94%). Mitral anular dilatation was observed at operation in 70 patients (96%). Maximal anular diameter was significantly greater (p less than 0.0001) than in matched control subjects (37 +/- 4 vs 23 +/- 2 mm). The mean anular dimension measured at surgery (36 +/- 3 mm) was similar to that obtained by echocardiography and individual values using the 2 methods correlated well (r = 0.93). Chordal elongation was observed in 66 patients at operation (90%).(ABSTRACT TRUNCATED AT 250 WORDS)

An echocardiographic measurement of the minimal separation between the anterior mitral valve leaflet at its E point and the Interventricular septum was evaluated as an index of left ventricular function. Mitral-septal separation was found to be easily measured, reproducible and independent of patient position or heart rate changes of up to 32 beats/min. In a group of 30 normal subjects, E point-septal separation was absent in 25 and minimal (less than 4 mm) in the remaining 5. The relation of this variable to biplane angiographic ejection fraction was examined in 125 patients with a variety of cardiac diseases. After the 15 patients with mitral stenosis and aortic insufficiency (conditions that affect anterior leaflet motion) were excluded, a strong negative correlation ( r = −0.87, P r = −0.86, P

The axial angiograms of 20 patients with an atrioventricular (A-V) canal defect were carefully examined and compared with anatomic observations made at operation. A common A-V valve was present in 15 patients and two separate valves in 5. The atrial septal defect, the anatomy of the ventricular septum and the morphology and functional status of the A-V valves were well demonstrated. There was consistent angiographic deformation of the normally straight contour extending from the noncoronary aortic cusp to the crux cordis observed in the four chamber and elongated right anterior oblique projections of the left ventricular angiogram of each patient. This deformity is caused by the deficiency or absence of the A-V septum and is the best angiographic sign of the malformation. The differentiation of two separate valves from a common A-V valve was uniformly made. When a common A-V valve was present, three of the five leaflets were usually identified but distinction of the free floating from the tethered anterior leaflet was not always possible. It is concluded that axial techniques provide more complete angiographic definition of the anatomic abnormalities of A-V canal defects than are demonstrated from frontal and lateral views.

A new physical sign, a systolic thrill over the middle thoracic part of the vertebral column and just to the left of it, is described in patients with mitral valve incompetence secondary to a flail anterior mitral leaflet. This systolic thrill was noted in 7 patients, 6 of whom had ruptured chordae tendineae of the anterior mitral leaflet; the seventh patient had marked elongation of the chordae tendineae to the anterior mitral leaflet which gave rise to a similar pathophysiologic disturbance.

With use of simultaneously recorded echocardiograms and phonocardiograms the relation of the first heart sound to mitral valve closure was studied in 34 normal subjects. Only those cardiac cycles that showed unbroken anterior leaflet echos with clearly defined initial points of systolic coaptation with the posterior leaflet (C points) were measured. The intervals analyzed were the Q-C interval (Q wave of the electrocardiogram to C point) and the Q-S1 interval (Q wave to first high frequency or "mitral" component of the first heart sound). The mean value for the Q-C interval was 44.2 msec ± 2.4 (standard error of the mean), and the mean value for the Q-S1 interval was 63.2 msec ± 1.8. The paired t test showed these values to be significantly different ( P r = −0.61, P r = −0.36, P This study shows that in human subjects the mitral component of the first heart sound is not coincident with the initial coaptation of the mitral valve leaflets; some later event or events are responsible for generation of the first heart sound.

The first documented case is reported of mitral valve malformation of the Ebstein type in the absence of corrected transposition. In this case, the ring of the inferior leaflet of the mitral valve was displaced downward into the left ventricle, dividing the latter into a proximal atrialized and a distal effective ventricular chamber. The anterior leaflet was not displaced. The chordae tendineae of both leaflets were thickened. The papillary muscles were hypertrophied and abnormal in architecture. The outflow tract of the effective left ventricle was shortened. The valve leaflets were thickened, and the mitral valve was probably insufficient.

The typical textbook description of Ebstein's anomaly of the heart usually singles out and emphasizes the downward displacement of septal and posterior leaflets of the tricuspid valve. An anatomic reappraisal of this uncommon anomaly suggests that other structural abnormalities of import should be equally stressed. Among the 15 well preserved autopsy specimens in this series, enlargement of the right atrioventricular (A-V) junction and malalignment of the giant and sometimes muscularized anterior leaflet of the tricuspid valve were consistently found. In addition, massive aneurysmal dilation of the right ventricle was present in almost two thirds (9 of 15) of the hearts. Our observations raise the possibility that abnormal embryonic development of the right A-V junction may be the primary event that leads to malformation of the tricuspid valve apparatus.

Echocardiography was performed in 10 consecutive patients who had a clinically normally functioning porcine aortic bioprosthesis in the mitral position. Strong well defined echoes were recorded from the anterior and posterior aspects of the xenograft stent. The maximal separation of the anterior and posterior stent echoes approximated the diameter of the stent at its base. The maximal excursion of the anterior stent was 5 to 10 mm (mean 7.5) with a mean systolic slope of 15 to 35 mm/sec (mean 22.2) and diastolic slope of 11 to 59 mm/sec (mean 21.5). In all 10 patients it was possible to record an anterior xenograft leaflet with anterior movement at the onset of diastole and posterior movement at the onset of systole and with appropriately steep (more than 200 mm/sec) slopes. The diastolic (E-F) slope of the anterior leaflet in 9 of the 10 patients ranged from 9 to 38 mm/sec (mean 19). In 6 of the 10 patients a posterior xenograft leaflet with a movement pattern symmetric with that of the anterior leaflet was recorded. In two patients, the central aortic leaflet was recorded with little diastolic displacement. These two patients also had mild aortic regurgitation, which was associated with diastolic shudder of the the xenograft leaflets. Echocardiography was also performed in one patient who was later shown to have a 10 cm3 thrombus on the ventricular surface of a xenograft valve. The echocardiogram in this patient revealed the following abnormalities: (1) excessive anterior stent movement and systolic slope suggesting paravalvular leak in the presence of abnormal cinefluoroscopic valve tilt, and (2) multiple dense nonhomogeneous echoes between the anterior and posterior aspects of the valve stent, with an early diastolic clear space behind the anterior stent and abnormal echoes behind the posterior stent during systole. Echocardiography therefore appears to be useful in evaluating the porcine aortic bioprosthesis in the mitral position.

To examine problems in echocardiographic diagnosis of mitral valve prolapse, multiple crystal cross-sectional echocardiography and single crystal recordings derived from the multiple crystal array were used to study 45 clinically normal children aged 3 to 15 years (Group A), 26 children aged 2 to 10 years with known mitral valve prolapse (Group B), 12 children with a catheterization-proved large left to right shunt at the ventricular level (Group C) and 8 children with catheterization-proved left ventricular outflow tract obstruction (Group D). Children in Groups A and B were not studied hemodynamically. Children in Groups C and D had no evidence of mitral valve prolapse on angiography and were studied echocardiographically to determine the effect of changes in ventricular shape on the patterns of mitral valve motion. In the real time cross-sectional studies, normal patients demonstrated a spectrum of mitral valve motion in which the bodies of the anterior and posterior leaflets became slightly horizontal with systolic ejection. The mitral apparatus assumed a curvilinear funnel shape. Arching of the leaflets into a horizontal configuration was more striking in the presence of either left ventricular dilatation in left to right shunt or involvement of the anterior mitral anulus in subaortic stenosis (two patients) and was associated with false positive M mode tracings suggesting mitral valve prolapse. This latter configuration was easily differentiated from the superior motion of the body of the leaflets in true prolapse. Studies of single crystal M mode recordings derived from the cross-sectional array in known locations from six normal patients revealed M mode patterns of pseudoprolapse in tracings derived from the leaflet body and patterns of normal motion at the free edge. In contrast, superior-posterior prolapse visualized in cross-sectional studies in patients with the click-murmur syndrome was associated with abnormal M mode recordings from all parts of the leaflet, including the free edge, although the abnormalities were most striking in tracings derived from the leaflet body. The M mode echocardiographic findings of mitral valve prolapse in both normal patients and patients with the click-murmur syndrome were dependent upon transducer angulation and the portion of the valve examined. The critical differentiation of the spectrum of normal valve motion from prolapse requires careful evaluation of echoes from the free edge of the leaflet where the posterior and anterior leaflet echoes coapt in early systole.

The detection of mitral stenosis has been a classic application of echocardiography. The technique utilizes the recording of an echo from the anterior leaflet of the mitral valve. A reduced diastolic slope is the principal criterion for the diagnosis of mitral stenosis. Several investigators have noted that a similar pattern of mitral valve motion can occur in patients without mitral stenosis. This study shows how the recording of the posterior leaflet of the mitral valve can help alleviate this confusion. Anterior and posterior mitral valve echograms were obtained in normal subjects, patients with mitral stenosis proved at cardiac catheterization, and patients with abnormal anterior mitral valve motion but no evidence of mitral stenosis at catheterization. The results demonstrate that in normal persons the posterior and anterior leaflets move in virtually opposite directions. In patients with true mitral stenosis the leaflets move in essentially the same direction but to a different degree. In patients with an abnormal diastolic mitral valve motion, possibly due to reduced rates of left ventricular filling, the posterior leaflet moves in a direction opposite to that of the anterior leaflet. Thus, this study can clearly distinguish these patients from those with true mitral stenosis.

Bacterial endocarditis was observed in a 77 year old white woman with acute myocardial infarction complicated by rupture of the interventricular septum. Margins of the septal perforation as well as the anterior leaflet of the mitral valve were involved. The association of these lesions has not previously been reported.

More than 2 decades ago the auscultatory features of a late systolic murmur and non-ejection systolic click were shown to originate at the mitral va1ve.i Left ventricular cineangiocardiography confirmed that late systolic murmurs were indicative of mild mitral regurgitation and demonstrated “massive dilatation,” “aneurysmal protrusion,” “billowing” or “ballooning” of the posterior mitral leaflet.2g3 Later studies showed that the anterior leaflet was also involved. In 1966, Criley et al4 clarified the cineangiocardiographic appearances and introduced the term prolapse. Mitral valve prolapse (MVP) is now a widely used term regardless of whether the valve anomaly is anatomically mild, echocardiographically demonstrable, functionally normal or clinically silent. This has contributed to the general confusion, and it is now crucial for the terms billowing, floppy, prolapse and flail to be defined. Such definitions should be based essentially on the functional anatomic, or pathologic, characteristics of the mitral valve mechanism. Auscultatory, echocardiographic, cineangiocardiographic and other clinical features should then be correlated with the probable functional anatomy. It is, after all, the functional anatomy of the mitral valve mechanism that we attempt to assess by all invasive or noninvasive investigations. We recently expressed the view5 that the concept propounded by the French cardiac surgeon, Alain Carpentier, defines the essential differences between prolapse and billowing. In this context Carpentier restricts the use of the term prolapse to failure of the leaflet edges to appose normally. Such partial loss of apposition may occur with or without abnormal billowing of the bellies of the leaflets, and mitral regurgitation, albeit mild or even minimal, will inevitably result. This concept of prolapse implies that the valve function is abnormal which is, in fact, both appropriate and correct. Any cardiac valve, provided there is not a hole or a cleft in a leaflet, remains competent while there is sustained coaptation of the leaflet edges. Prevention of apposition may occur if 1 or more leaflets are fibrosed or retracted. If leaflets are normal in size or larger, failure of sustained apposition will result in prolapse. Based on Carpentier’s understanding of MVP, we consider that the following terms, which reflect normal and abnormal mitral valve functional anatomy, should clarify much of the current confusion. The normal mitral leaflets billow slightly, after closure, into the left atria1 cavity (Fig. 1A). Exaggeration