Quantification of mitral regurgitation using proximal isovelocity surface area method in dogs.
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The present study was performed to determine the accuracy and reproducibility of calculating the mitral regurgitant orifice area with the proximal isovelocity surface area (PISA) method in dogs with experimental mitral regurgitation and in canine patients with chronic mitral insufficiency and to evaluate the effect of general anesthesia on mitral regurgitation. Eight adult, Beagle dogs for experimental mitral regurgitation and 11 small breed dogs with spontaneous mitral regurgitation were used. In 8 Beagle dogs, mild mitral regurgitation was created by disrupting mitral chordae or leaflets. Effective regurgitant orifice (ERO) area was measured by the PISA method and compared with the measurements simultaneously obtained by quantitative Doppler echocardiography 4 weeks after creation of mitral regurgitation. The same procedure was performed in 11 patients with isolated mitral regurgitation and in 8 Beagle dogs under two different protocols of general anesthesia. ERO and regurgitant stroke volume (RSV) by the PISA method correlated well with values by the quantitative Doppler technique with a small error in experimental dogs (r = 0.914 and r = 0.839) and 11 patients (r = 0.990 and r = 0.996). The isoflurane anesthetic echocardiography demonstrated a significant decrease of RSV, and there was no significant change in fractional shortening (FS), ERO area, LV end-diastolic and LV end-systolic volume. ERO area showed increasing tendency after ketamine-xylazine administration, but not statistically significant. RSV, LV end-systolic and LV end-diastolic volume increased significantly (p < 0.01), whereas FS significantly decreased (p < 0.01). The PISA method is accurate and reproducible in experimental mitral regurgitation model and in a clinical setting. ERO area is considered and preferred as a hemodynamic-nondependent factor than other traditional measurements. (+info)
Lineage and morphogenetic analysis of the cardiac valves.
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We used a genetic lineage-labeling system to establish the material contributions of the progeny of 3 specific cell types to the cardiac valves. Thus, we labeled irreversibly the myocardial (alphaMHC-Cre+), endocardial (Tie2-Cre+), and neural crest (Wnt1-Cre+) cells during development and assessed their eventual contribution to the definitive valvar complexes. The leaflets and tendinous cords of the mitral and tricuspid valves, the atrioventricular fibrous continuity, and the leaflets of the outflow tract valves were all found to be generated from mesenchyme derived from the endocardium, with no substantial contribution from cells of the myocardial and neural crest lineages. Analysis of chicken-quail chimeras revealed absence of any substantial contribution from proepicardially derived cells. Molecular and morphogenetic analysis revealed several new aspects of atrioventricular valvar formation. Marked similarities are seen during the formation of the mural leaflets of the mitral and tricuspid valves. These leaflets form by protrusion and growth of a sheet of atrioventricular myocardium into the ventricular lumen, with subsequent formation of valvar mesenchyme on its surface rather than by delamination of lateral cushions from the ventricular myocardial wall. The myocardial layer is subsequently removed by the process of apoptosis. In contrast, the aortic leaflet of the mitral valve, the septal leaflet of the tricuspid valve, and the atrioventricular fibrous continuity between these valves develop from the mesenchyme of the inferior and superior atrioventricular cushions. The tricuspid septal leaflet then delaminates from the muscular ventricular septum late in development. (+info)
Cutting second-order chords does not prevent acute ischemic mitral regurgitation.
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BACKGROUND: Cutting anterior mitral leaflet second-order chordae has been proposed for repair in ischemic mitral regurgitation (IMR). We examined the efficacy of such chordal cutting in preventing acute IMR. METHODS AND RESULTS: Six sheep underwent radiopaque marker placement (left ventricle, mitral annulus, papillary muscles [PMs], and leaflets). The largest second-order chord from each PM was encircled with exteriorized wire snares. Three-dimensional marker coordinates were obtained with biplane videofluoroscopy before and during acute ischemia (80 seconds of mid-circumflex occlusion). Color Doppler transesophageal echocardiography was used to grade MR on a 0 to 4+ scale. Data were acquired immediately before and after dividing second-order chordae. Slope of the end-diastolic volume-stroke work relationship (PRSW) was calculated to assess systolic function. Chordal cutting increased anterior leaflet inflection angle (155+/-12 versus 162+/-9 degrees; P=0.03), resulting in a flatter leaflet, but did not increase effective leaflet length (1.97+/-0.24 versus 2.08+/-0.23 cm; P=0.15); PRSW decreased (63+/-15 versus 56+/-12 mm Hg; P=0.008). Both before and after chordal cutting, ischemia caused: Septal-lateral annular dilation (P=0.005), posterior PM displacement away from the mid-septal annulus (P=0.06), increased leaflet tenting area (P=0.001), and increased leaflet tenting volume (P=0.002). Before chordal cutting, MR increased significantly during ischemia (0.5+/-0.3 versus 1.7+/-0.4; P<0.001), and IMR increased similarly even after the second-order chords were cut (0.7+/-0.4 versus 1.9+/-0.9; P<0.001). CONCLUSIONS: Cutting second-order chordae resulted in LV systolic dysfunction and neither prevented nor decreased the severity of acute IMR, septal-lateral annular dilation, leaflet tenting area, or leaflet tenting volume. (+info)
Importance of mitral valve second-order chordae for left ventricular geometry, wall thickening mechanics, and global systolic function.
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BACKGROUND: Mitral valvular-ventricular continuity is important for left ventricular (LV) systolic function, but the specific contributions of the anterior leaflet second-order "strut" chordae are unknown. METHODS AND RESULTS: Eight sheep had radiopaque markers implanted to silhouette the LV, annulus, and papillary muscles (PMs); 3 transmural bead columns were inserted into the mid-lateral wall between the PMs. The strut chordae were encircled with exteriorized wire snares. Three-dimensional marker images and hemodynamic data were acquired before and after chordal cutting. Preload recruitable stroke work (PRSW) and end-systolic elastance (E(es)) were calculated to assess global LV systolic function (n=7). Transmural strains were measured from bead displacements (n=4). Chordal cutting caused global LV dysfunction: E(es) (1.48+/-1.12 versus 0.98+/-1.30 mm Hg/mL, P=0.04) and PRSW (69+/-16 versus 60+/-15 mm Hg, P=0.03) decreased. Although heart rate and time from ED to ES were unchanged, time of mid-ejection was delayed (125+/-18 versus 136+/-19 ms, P=0.01). Globally, the LV apex and posterior PM tip were displaced away from the fibrous annulus and LV base-apex length increased at end-diastole and end-systole (all +1 mm, P<0.05). Locally, subendocardial end-diastolic strains occurred: Longitudinal strain (E22) 0.030+/-0.013 and radial thickening (E33) 0.081+/-0.041 (both P<0.05 versus zero). Subendocardial systolic shear strains were also perturbed: Circumferential-longitudinal "micro-torsion" (E12) (0.099+/-0.035 versus 0.075+/-0.025) and circumferential radial shear (E13) (0.084+/-0.023 versus 0.039+/-0.008, both P<0.05). CONCLUSIONS: Cutting second-order chords altered LV geometry, remodeled the myocardium between the PMs, perturbed local systolic strain patterns affecting micro-torsion and wall-thickening, and caused global systolic dysfunction, demonstrating the importance of these chordae for LV structure and function. (+info)
Long-term results of cusp-level chordal shortening for anterior mitral leaflet prolapse.
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The technique and early results of cusp-level chordal shortening for isolated anterior mitral leaflet prolapse in rheumatic mitral regurgitation were presented by us earlier. Here we present our experience from January 1989 through December 2000. Two hundred twenty-six patients underwent this procedure. The mean age was 18 +/- 7.22 years. Preoperatively, 38 (16.8%) patients were in New York Heart Association functional class 11, 160 (70.8%) were in class IIl, and 28 (12.4%) were in class IV. All patients underwent chordal shortening at the cusp level. In addition, 8 patients (3.5%) underwent chordal transfer, and 4 patients (1.8%) received neochordae. Two hundred twenty-one (97.8%) patients underwent posterior annuloplasty using a C-shaped polytetrafluoroethylene collar. In 85 (37.6%) patients, cuspal thinning was also performed. Early mortality was 3.5% (8 patients). Follow-up ranged from 1 to 144 months (mean, 53.02 +/- 31.10 months) and was 94% complete. In 68% of survivors, there was no or trivial mitral regurgitation. Ten patients required reoperation. There were 8 late deaths. Actuarial survival, mitral regurgitation-free survival, and event-free survival were 93.3% +/- 1.7%, 41.8% +/- 8.4%, and 73.6% +/- 6.6%, respectively. Among the 210 survivors, 159 (75.7%) were in New York Heart Association class I, 26 (12.4%) were in class II, 22 (10.5%) were in class III, and 3 (1.4%) were in class IV. We conclude that cusp-level chordal shortening for isolated anterior mitral leaflet prolapse is an effective procedure for correction of anterior mitral leaflet prolapse. (+info)
Differentiating clinical and echocardiographic characteristics of chordal rupture detected in patients with rheumatic mitral valve disease and floppy mitral valve: impact of the infective endocarditis on chordal rupture.
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AIMS: We aimed to compare the clinical and echocardiographic correlates of chordal rupture in patients with rheumatic mitral valve disease and floppy mitral valve. METHODS AND RESULTS: The study group comprised of 224 patients who underwent transthoracic and transesophageal echocardiography because of the severe mitral regurgitation. Chordal rupture was detected in 58 (25.9%) out of the 224 patients, in 33 out of the 83 (39.7%) patients with floppy mitral valve, and in 25 out of the 141 (17.7%) patients with rheumatic mitral valve disease. Chordal rupture was more frequently associated with anterior leaflet (80%) in patients with rheumatic mitral valve disease, and posterior leaflet (72.7%) in patients with floppy mitral valve (p<0.05). Univariate correlates of chordal rupture were age, male sex, posterior mitral leaflet thickening and chordal elongation in patients with floppy mitral valve (p<0.05), and chordal shortening (p<0.0001) and infective endocarditis involving mitral anterior leaflet (p<0.05) in rheumatic group. Independent predictors of chordal rupture were age (>50 years), posterior mitral leaflet thickness (> or =0.45cm), and male sex (p<0.05) in patients with floppy mitral valve while infective endocarditis involving mitral anterior leaflet (p<0.05) in patients with rheumatic mitral valve disease. Patients with chordal rupture due to floppy mitral valve had an older age (p<0.0001), a male dominance, longer mitral leaflets and chordae, and a larger mitral annulus circumference (p<0.05) as compared to those with rheumatic chordal rupture. Despite the comparable severity of mitral regurgitation and left atrial diameters between the two groups of chordal rupture (p>0.05), functional class and pulmonary artery systolic pressure were higher, and atrial fibrillation, acute deterioration, infective endocarditis, mitral leaflet rupture and need for mitral valve surgery in the 3 months were more frequent in rheumatic chordal rupture subgroup (p<0.05). CONCLUSION: Chordal rupture seems to be more frequently associated with anterior mitral leaflet in rheumatic mitral valve disease, whereas it was the posterior leaflet in floppy mitral valve. Chordal rupture was related to male sex, older age, posterior leaflet thickening, and chordal elongation in patients with floppy mitral valve. However, infective endocarditis, acute deterioration, and need for early mitral surgery were more frequent in patients with rheumatic chordal rupture. (+info)
Total relief of severe left ventricular outflow obstruction after spontaneous rupture of chordae tendineae in a patient with hypertrophic cardiomyopathy.
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In hypertrophic cardiomyopathy (HCM), rupture of mitral chordae tendineae is infrequent and causes acute haemodynamic deterioration. A 38 year old male patient had chordae rupture leading to prolapse of both mitral leaflets and severe regurgitation, without change in symptomatic status. One year before, he had had mild mitral regurgitation and a resting left ventricle outflow tract of 105 mm Hg that disappeared in the present evaluation. In this unique case, worsening of mitral regurgitation was counterbalanced by total relief of the severe obstruction. This case report highlights the role of the mitral valve apparatus in the genesis of obstruction in HCM, further stimulating surgical techniques in which mitral repair can be the main procedure. (+info)
Normal distribution of melanocytes in the mouse heart.
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We report the consistent distribution of a population of pigmented trp-1-positive cells in several important septal and valvular structures of the normal mouse (C57BL/6) heart. The pigmented cell population was first apparent by E16.5 p.c. in the right atrial wall and extended into the atrium along the interatrial septum. By E17.5, these cells were found along the apical membranous interventricular septum near or below the surface of the endocardium. The most striking distribution of dark pigmented cells was found in the tricuspid and mitral valvular leaflets and chordae tendineae. The normal distribution of pigmented cells in the valvuloseptal apparatus of C57BL/6 adult heart suggests that a premelanocytic lineage may participate in the earlier morphogenesis of the valve leaflets and chordae tendineae. The origin of the premelanocyte lineage is currently unknown. The most likely candidate populations include the neural crest and the epicardially derived cells. The only cell type in the heart previously shown to form melanocytes is the neural crest. The presence of neural crest cells, but not melanocytes, in some of the regions we describe has been reported by others. However, previous reports have not shown a contribution of melanocytes or neural crest derivatives to the atrioventricular valve leaflets or chordae tendineae in mouse hearts. If these cells are of neural crest origin, it would suggest a possibly greater contribution and persistence of neural crest cells to the valvuloseptal apparatus than has been previously understood. (+info)