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The mitral valve area in mitral stenosis was determined from Doppler velocity recordings and by cross-sectional echocardiography. There was good agreement (r = 0.93) between the two methods in 18 adult patients with mitral stenosis. The results confirm that the non-invasive continuous wave Doppler ultrasound technique is of diagnostic value in the assessment of mitral stenosis.
The increase of coronary artery size in myocardial hypertrophy represents an adaptive mechanism to keep coronary blood flow normal. The relationship between coronary cross-sectional area and left ventricular muscle mass was determined angiographically in 10 patients with severe mitral regurgitation before and 28 +/- 15 months after successful mitral valve surgery. 10 subjects with atypical chest pain without coronary artery disease served as controls (C). Left ventricular muscle mass was increased preoperatively in mitral regurgitation (257 g vs C = 129 g; p < 0.001) and decreased postoperatively (205 g; p < 0.01 vs preop. and vs C). The cross-sectional area of the left coronary (= left anterior descending+left circumflex) artery was augmented preoperatively (26.5 vs C = 14.0 mm2; p < 0.001) and decreased postoperatively (22.9 mm2; p < 0.05 vs preop. and vs C). The cross-sectional area of the left coronary artery per 100 g LV muscle mass was not different in the three groups. The cross-sectional area of the right coronary artery was also increased before surgery (12.7 vs C = 8.8 mm2; p < 0.05) and decreased postoperatively (11.3 mm2; p < 0.05 vs preop. ns vs C). Our data show that in mitral regurgitation the size of the left coronary artery increases proportionally to the increase in left ventricular muscle mass. Also, the right coronary artery shows slight enlargement which is probably due to the pressure overload of the right ventricle. After surgery there is regression but not normalization of the size of the coronary arteries.
A prospective evaluation of 333 consecutive patients undergoing isolated mitral valve replacement between 1982 and 1985 was performed to identify the predictors of survival and valve failure. Follow-up between 2 and 6 years postoperatively (mean, 32 +/- 17 months) was 98% complete. Four prostheses were inserted to permit a prospective evaluation of alternative valves: Björk-Shiley mechanical (n = 118), Ionescu-Shiley pericardial (n = 146), Carpentier-Edwards porcine (n = 38), and Hancock pericardial (n = 31). Hospital mortality was 6%, and actuarial survival at 5 years was 74% +/- 5%. Multivariate Cox regression analysis identified advancing age (less than 40 years, 88% +/- 7%; greater than 70 years, 50% +/- 14%) and poor left ventricular function (ejection fraction less than 0.20, 62% +/- 17%; ejection fraction greater than 0.60, 80% +/- 7%) as independent predictors of postoperative survival. Freedom from structural valve dysfunction, prosthetic valve endocarditis, reoperation, and valve-related mortality and morbidity were 86% +/- 4%, 91% +/- 4%, 81% +/- 4%, and 72% +/- 5%, respectively, at 5 years. The actuarial incidence of valve failure was inordinately high with the Hancock pericardial valve (p less than 0.05). Freedom from thromboembolic events (78% +/- 8% at 5 years) was significantly lower in patients with poor ventricular function (ejection fraction (less than 0.20, 54% +/- 20%; ejection fraction greater than 0.60, 73% +/- 11%; p less than 0.05). Survival after mitral valve replacement was determined by age and left ventricular function. Premature failure of the Hancock pericardial valve resulted in an unacceptable rate of valve-related complications.
Biochemical analyses and electron microscopy of mitral valve collagen were carried out in 29 patients with various mitral valve diseases. They were divided into 3 groups: (1) rheumatic heart disease (15 patients), (2) isolated rupture of chordae tendineae (8 patients), and (3) floppy mitral valve (6 patients). Normal mitral valves obtained at necropsy from 6 patients who died from extracardiac causes were used for control observations. Results of the electrophoretic analysis of the collagen of normal and diseased valves showed that all valves contained collagen types I, III, and AB collagen with similar electrophoretic patterns. Electron microscopic observations and comparisons of the segment-long-spacing crystallites of each type of collagen revealed similar band patterns, irrespective of the normal or diseased valves sources. It is concluded that the composition and primary molecular structure of mitral valve collagen are usually not altered in a wide variety of disease processes affecting the mitral valve.
Five patients with rheumatic mitral stenosis were observed to have mid-systolic clicks with murmurs of mitral regurgitation at various intervals after mitral commissurotomy. In two patients echocardiography showed an unusually rapid posterior deflection of the mitral valve coinciding exactly with a systolic nonejection click. It is speculated that the shortened, fused chordae tendineae, compromised by mitral commissurotomy, rigidly hold the valve leaflets fixed at the onset of systole. During systole, ventricular conformational changes, in the face of marginal coaptation of thickened and fibrotic mitral leaflets, allow the mitral valve to be forced abruptly towards the left atrium with great velocity. This is manifested by a loud systolic click and, in some patients, a near vertical posterior systolic deflection of the mitral valve on the echocardiogram. The systolic click may occur without echocardiographic or angiographic evidence of mitral valve prolapse. Unusually loud mid-systolic clicks can be heard in patients with rheumatic heart disease after mitral commissurotomy and may be accompanied by a distinctive echocardiographic appearance of the mitral valve.
OBJECTIVE: To assess by tissue Doppler echocardiography (TDE), the tissue velocities, both at rest and after exercise stress testing, in subjects with mitral valve prolapse (MVP) and those with thick mitral valve (TMV). METHODS: Twenty individuals with typical MVP, 30 with TMV, and 30 healthy controls were enrolled. TDE was performed at the basal-inferior wall and the parameters evaluated were the S, Em, and Am velocities, as well as the Em/Am ratio. RESULTS: The mean S-wave at rest was higher in subjects with MVP compared to that of the TMV (P < 0.01) and the control groups (P = 0.00005), whereas after exercise it was higher in the control group compared to either MVP (P = 0.013) or TMV group (P = 0.00002). The mean Em wave at rest was higher in the control individuals both at rest (P = 0.007 compared with MVP group and P = 0.013 compared with TMV group), and after exercise (P = 0.0002 and 0.0009, respectively). The Am wave in the MVP group was higher compared with TMV and control subjects at rest (P = 0.022 and 0.00001, respectively) but it was not after exercise (P = ns for both comparisons). The Em/Am ratio of the control group at rest was higher than that of the MVP (P = 0.0000) and TMV (P = 0.00028) groups. However, after exercise, it was higher only when compared with the MVP group (P = 0.016). CONCLUSIONS: Subjects with MVP and those with TMV exhibit a less effective contractile response to exercise compared to healthy individuals. Some degree of diastolic dysfunction, particularly after exercise, was also detected in the individuals with MVP.
An endoscope was used to study the anatomy and morphology of the native mitral valve inside an isolated pig heart working under physiological conditions. Annulus motion, valve leaflet function, and the anatomy of the chords and branching pattern are described. Anatomical and functional details relevant to mitral valve reconstruction and valve replacement are outlined. Because of the similarity with the human heart, we have assumed that the observations made in the pig heart also apply to humans.
Double-orifice mitral valve is an unusual condition of importance to surgeons, and usually associated with other cardiac anomalies. This article reports a case of isolated double-outlet mitral valve with torn chordae in which we successfully performed mitral valvuloplasty by placement of artificial chordae. The mitral valve was divided into anterolateral and posteromedial orifices by vertical bridging tissue. Two torn chordae at the posteromedial scallop surrounding the posteromedial mitral orifice were replaced with artificial chordae of two pairs of expanded polytetrafluoroethylene sutures. Because replacement of torn chordae with artificial chordae was not complicated and seemed to preserve very fine relationships among leaflet tissues, bridging tissue, chordae, and papillary muscles, we suggest this method may be used to reconstruct various kinds of mitral lesions causing mitral regurgitation.
Optimal mitral valve operation requires adequate exposure without impairment of atrial physiology, namely sinus node and atrioventricular node function. We used an extended vertical transseptal atrial approach in 34 consecutive patients. The extended vertical transseptal approach combines two semicircular atrial incisions circumscribing the tricuspid and mitral annuli anteriorly and superiorly, allowing exposure of the mitral valve by deflecting the ventricular side using stay sutures. The right atrium is opened anteriorly along the atrioventricular sulcus. The atrial septum is incised vertically through the fossa ovalis. The right atriotomy is extended superiorly in the right coronary fossa between the right atrial appendage and the atrioventricular sulcus to meet the septal incision. The two joint incisions are extended onto the left atrial roof transversely. At this point, the two semicircular incisions are performed and joined, and mitral valve operation is performed. There were 18 women and 16 men. Five patients had ischemic mitral valve regurgitation, 18 had mitral valve prolapse, and 11 had rheumatic heart disease. The mitral valve was replaced in 17 patients and repaired in 17. There were no perioperative complications associated with the atriotomies, ie, no bleeding, no atrioventricular nodal dysfunction, and no sinus node dysfunction. The extended vertical transatrial septal approach provides good mitral valve exposure without inherent complications.
To assess the reliability of M-mode echocardiographic patterns of mitral valve prolapse (MVP) (echo MVP) in detection of morphologic evidence of MVP (morphologic MVP), operatively excised mitral valves and corresponding M-mode echocardiograms from 65 patients with chronic, severe, isolated, pure mitral regurgitation (MR) were studied. Of the 65 patients, 45 (69%) had echo MVP (either holosystolic or mid-to-late systolic prolapse patterns on preoperative M-mode echograms) and 42 (93%) of them had morphologic MVP; of the 3 without morphologic MVP, 2 had ruptured chordae tendineae from infective endocarditis and 1 had papillary muscle dysfunction from atherosclerotic coronary heart disease. Of the 20 patients without echo MVP, 14 (70%) had no morphologic MVP (9 had papillary muscle dysfunction from coronary heart disease, 4 had infective endocarditis on previous normal valves and 1 had rheumatic heart disease). Of the 48 patients with morphologic MVP, 42 (88%) had echo MVP and most had considerably dilated mitral anulae; the other 6 had ruptured chordae tendineae with less degrees of anular dilatation. Of the 17 patients without morphologic MVP, 3 had echo MVP (coronary artery disease in 1 and infective endocarditis on a previous normal valve in 2); of the 14 with neither echo nor morphologic MVP, 9 had papillary muscle dysfunction from coronary artery disease, 4 had infective endocarditis on previously normal valves and 1 had rheumatic heart disease. The patients with very dilated mitral anuli and leaflet areas generally had holosystolic (hammocking) patterns on echo; the patients with small anuli and leaflet areas usually had mid-to-late systolic (buckling) prolapse patterns.
To avoid postoperative morbidity and mortality often associated with left ventricular dysfunction after mitral valve replacement (MVR) for chronic mitral insufficiency, reconstruction or preservation of the native mitral valve apparatus may be attempted during mitral prosthetic implantation (MPI). The effects of mitral surgery on heart function, studied with echocardiography and radionuclide angiography, were compared in seven patients with MPI (study group) and five with MVR (control group) who underwent complete preoperative, early postoperative and 3-6 months follow-up examinations. Preoperatively there was significant intergroup difference only in right ventricular ejection fraction measured at radionuclide angiography, which was lower in the MPI group (p < 0.05). At follow-up the MPI group had improved as regards this fraction (p < 0.005) and stroke volume index (p < 0.05). The number of patients with improved NYHA class at follow-up was significantly greater in the MPI group. Our preliminary experience with preservation of the native mitral valve apparatus thus suggests that the method offers haemodynamic advantages for postoperative right ventricular function.
We have investigated the application of an hydraulic orifice equation for the computation of diastolic mitral valve area in conditions of regurgitation. The new equation is given by Af = 21 Vf/T2, where Af is the total forward flow mitral valve area in cm2, Vf is the diastolic filling volume in ml, T is the diastolic filling period and 21 is a discharge coefficient derived from clinical haemodynamic data. Areas computed by the new formula correlate with valve areas as computed by the Gorlin formula at a level given by r = 0.93, n = 27. The results suggest that the new formula may be utilised in the context of mitral insufficiency and further, considerating the nature of the haemodynamic variables involved, an echographic quantification of this condition by M-mode or bidimensional echocardiography may be possible.
We studied 37 consecutive patients with mitral stenosis in sinus rhythm using transthoracic and transesophageal echocardiography to relate the presence of spontaneous echo contrast (SEC) in the left atrium with mitral valve area and left atrial dimensions. We also compared the value of left atrial area by planimetry with that of left atrial dimension by M mode in predicting presence of SEC and monitored the effect of anticoagulation on SEC. Transesophageal echocardiography demonstrated spontaneous echo contrast in 9/37 (24%) patients and thrombus in none. SEC continued to be present despite anticoagulation. Mitral valve orifice area by pressure half time method (P=0.001) and by planimetry (P=0.01), and left atrial area by planimetry (P<0.05) were predictors to presence of SEC. Left atrial dimension by M mode examination failed to predict SEC. Cut off values were mitral valve orifice </=1.4 cm(2) (agreement 86%) and left atrial area >/=25 cm(2) (agreement 81%). On multivariate analysis mitral valve area was the only independent predictor. SEC persisted despite anticoagulation. This supports the view that more than one mechanism is involved in the development of SEC.
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To evaluate the mitral reconstructive technique from the pathological and surgical points of view, 33 consecutive cases were analyzed. Eighteen patients (54.5%) were men, and the mean age was 40.9 +/- 19.8 (range 5 to 72 years). Ten patients (30.3%) had atrial fibrillation. The causes of mitral regurgitation were torn chordae tendinae in 17, elongated choradae tendinae in 14, annular dilatation in 8, papillary muscle dysfunction in 2, and congenital cleft in 4. The mitral regurgitation was due to prolapse of the anterior leaflet in 16, prolapse of the posterior leaflet in 10, and prolapse of both leaflets in 5. Resection and reconstruction of the leaflet was performed on anterior leaflet in 15, and on posterior leaflet in 15. The anterior mitral cleft was sutured in 3. The newly contrived wrapping and shortening chordoplasty was performed on anterior leaflet in 6, on posterior leaflet in 3, and on both leaflets in 2. Two patients had replacement of artificial chordae tendinae with EPTFE suture. Commissuroplasty was performed at anterolateral commissure in 5, at posteromedian commissure in 15, and at both commissures in 5. Thirty patients with dilated annulus underwent ring annuloplasty by Carpentier ring. There was no hospital death. Two patients required mitral valve replacement for redeveloping mitral regurgitation 2 weeks and one year after initial operation. All patients were in NYHA functional class I after surgery. The Doppler echo cardiographic study revealed no mitral regurgitation in 27, mild or trivial in 3, and moderate in 3. LVEDVI and LVESVI significantly decreased, and left ventricular volume overload was markedly reduced.
Mitral valve clicks with or without late systolic murmurs were detected in genetically unrelated marital partners of 5 families. The first family represented 2 successive nonconsanguineous marital unions with 3 generations of mitral valve clicks. The second family included 1 natural and 2 adopted children with clinical and echographic evidence of mitral valve prolapse. The third family was comprised of asymptomatic parents, both with nonejection clicks and mitral valve prolapse, whose daughter presented 3 years previously with syncope, palpitations, and combined mitral and tricuspid valve prolapse. The fourth family had 3 members with auscultatory and ultrasonic manifestations of billowing mitral valve, whereas the fourth member had "silent mitral valve prolapse." The fifth family represented a mother with auscultatory and echographic evidence of mitral valve prolapse; her 14-year-old daughter had both mitral and tricuspid valve prolapse, whereas the son had a bicuspid aortic valve. Both children were products of a prior marriage, and her husband has symptomatic mitral valve prolapse. We conclude that matrimonial mitral valve prolapse probably reflects the purported (6--10%) prevalence of this disorder in the general population. The consequences of such marital union on progeny is currently unclear and warrants future investigation.
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