Tenting volume: three-dimensional assessment of geometric perturbations in functional mitral regurgitation and implications for surgical repair.

BACKGROUND AND AIM OF THE STUDY: Functional mitral regurgitation (FMR) often complicates dilated cardiomyopathy (DCM), and portends a poor prognosis. Debate over the optimal treatment continues, underscoring the present incomplete understanding of the patho-anatomic mechanisms of this disease. Studies of mitral tenting volume and tenting area, and echocardiographic measures of abnormal apical systolic leaflet geometry have linked mitral leaflet deformation with subvalvular left ventricular (LV) remodeling in chronic ischemic MR. The relative contributions of annular versus subvalvular remodeling in FMR due to DCM are less clear. Here, the validity of 3-D measurement of mitral deformation, tenting volume, as a correlate of MR in DCM, was tested. The ability of annular and subvalvular remodeling to predict mitral deformation was then determined. METHODS: Eight sheep underwent placement of radiopaque markers on the mitral annulus and leaflets. Global LV, annular and subvalvular geometry, as well as mitral tenting height, area and volume were calculated before (Control) and after the development of pacing-induced cardiomyopathy and MR (DCM). Multivariable regression determined which measure of mitral deformation was the best predictor of MR. Regression analysis was also used to find geometric predictors of mitral tenting volume. RESULTS: In a multivariable analysis, mitral tenting volume was the only independent predictor of severity of MR (r(2) = 0.79, standard error of estimate (SEE) = 0.58). Increased tenting volume correlated best with increased mitral annular septal-lateral diameter (r(2) = 0.67, SEE = 0.72). CONCLUSION: The 3-D tenting volume correlates best with severity of FMR. Mitral deformation (increased tenting volume) observed in DCM is predicted by annular dilation, but not by subvalvular LV remodeling. These data support the use of an undersized annuloplasty in DCM complicated by FMR, and may guide the rational design of new therapies for this vexing disease.

Subvalvular repair: the key to repairing ischemic mitral regurgitation?

BACKGROUND: Residual or recurrent mitral regurgitation frequently occurs after mitral ring annuloplasty repair for ischemic mitral regurgitation (IMR), because annuloplasty primarily addresses annular dilatation. We describe a subvalvular repair technique addressing posterior papillary muscle (PPM) displacement. METHODS AND RESULTS: Ten sheep had radiopaque markers placed on the left ventricle (LV) and mitral apparatus. A suture was anchored at the right fibrous trigone, passed through the PPM tip and LV wall, and exteriorized through a tourniquet (STRING-1). A second suture was anchored transmurally in the high septum (anterobasal LV wall) and passed through the PPM and LV wall (STRING-2). Reversible posterolateral ischemia was induced by temporarily occluding the proximal circumflex artery. Under open chest conditions, 3D marker coordinates were obtained with biplane videofluoroscopy at baseline and during acute ischemia before and after tightening of each STRING using transesophageal echocardiography to grade IMR. IMR decreased (mean+/-SEM, 2.0+/-0.1 to 1.2+/-0.1; P<0.05) when STRING-1 was tightened, did not change after tightening STRING-2 (2.3+/-0.1 to 2.3+/-0.1), and decreased after tightening both sutures (STRING-1+2, 2.3+/-0.2 to 1.3+/-0.2; P<0.05). STRING-1 and STRING-1+2 (STRING-1, 1.7+/-0.4 mm; STRING-2, 0.7+/-0.5 mm; STRING-1+2, 1.5+/-0.3 mm; P<0.05) resulted in significant PPM basal repositioning. Tightening of any STRING sutures did not affect anterior mitral leaflet excursion. CONCLUSIONS: Basal repositioning of the PPM with STRING-1 reduced acute IMR without concomitant annular reduction. This technique may be a useful adjunct if residual IMR is likely after undersized ring annuloplasty.

Left ventricular volume shifts and aortic root expansion during isovolumic contraction.

BACKGROUND AND AIM OF THE STUDY: Aortic valve opening involves conformational changes of the aortic root, including the ventricular-aortic junction (VAJ), sinotubular junction (STJ), and cusps. Moreover, the aortic root is contiguous with the left ventricular outflow tract (LVOT), which changes diameter throughout the cardiac cycle. Aortic root expansion prior to valve opening facilitates outward displacement of aortic cusp attachments, which helps flatten the cusps, thereby reducing cusp stress and fatigue, ultimately enhancing functional valve durability. The mechanisms underlying aortic root expansion prior to valve opening, however, remain incompletely characterized. The study aim was to establish a link between such aortic root expansion and intraventricular volume shifts into the LVOT during isovolumic contraction (IVC). METHODS: Miniature radiopaque markers were implanted on the left ventricle, VAJ, STJ, and aortic cusps of six sheep. After one week, 3-D marker coordinates were obtained using biplane videofluoroscopy (60 Hz). Triangular areas at the VAJ and STJ were calculated; LV main chamber (non-LVOT) and LVOT volumes were calculated using multiple tetrahedra. End-diastole was defined as the peak of the electrocardiogram R-wave, and end-IVC when aortic cusp separation began. RESULTS: During IVC, blood within the left ventricle was redistributed to the LVOT: mean LVOT volume was increased (+0.2 +/- 0.1 ml, p = 0.009) as non-LVOT volume fell (-0.8 +/- 0.4 ml, p = 0.006). Concomitantly, the aortic root expanded as both VAJ and STJ areas increased (+0.23 +/- 0.12 cm2 (p = 0.005) and +0.25 +/- 0.14 cm2 (p = 0.007), respectively) prior to aortic cusp separation. CONCLUSION: Aortic root expansion prior to valve opening is closely related to intraventricular volume shifts into the LVOT during IVC. Such volume shifts may 'prime' the aortic valve for ejection. These findings expand our understanding of cardiac dynamics by showing that blood acts as a coupling link between various cardiac units. Preservation of these normal aortic root dynamics may enhance the efficacy and durability of aortic surgical interventions.

Paneth suture annuloplasty abolishes acute ischemic mitral regurgitation but preserves annular and leaflet dynamics.

BACKGROUND: Ring annuloplasty, the standard treatment for ischemic mitral regurgitation (IMR), abolishes normal annular dynamics and freezes the posterior leaflet. We examined the impact of Paneth suture annuloplasty during acute IMR on motion of the mitral annulus and leaflets in an ovine model. METHODS AND RESULTS: Eight sheep had radiopaque markers placed on the left ventricle, anterior mitral leaflet, posterior mitral leaflet, and mitral annulus. A Paneth suture annuloplasty that could be reversibly tightened was anchored to each fibrous trigone and externalized through the mid-lateral mitral annulus. Acute IMR was induced by proximal circumflex artery occlusion. Transesophageal echocardiography assessed the degree of IMR, and biplane cinefluoroscopy measured 3-dimensional marker coordinates before and during circumflex ischemia, and tightening of the Paneth suture. Paneth suture annuloplasty eliminated acute IMR, and reduced septal-lateral and commissure-commissure mitral annular dimensions. Tightening of the annuloplasty sutures, even beyond the degree necessary to eliminate mitral regurgitation (MR), did not reduce septal-lateral or commissure-commissure annular shortening, shortening of the muscular annular perimeter, annular flexion, or angular excursion of the anterior or posterior leaflets relative to ischemic conditions. CONCLUSIONS: In contrast to ring annuloplasty, annular reduction sufficient to restore mitral competence during acute IMR can be achieved with a Paneth suture annuloplasty while simultaneously maintaining normal annular and leaflet dynamic motion. These findings should prompt additional investigation and design of repair methods that preserve the mobility of the mitral apparatus.

Effects of paracommissural septal-lateral annular cinching on acute ischemic mitral regurgitation.

BACKGROUND: Previous experimental studies demonstrated that central septal-lateral (SL) annular cinching (SLAC) abolishes acute ischemic mitral regurgitation (IMR), but whether localized cinching near the anterior (ACOM) or posterior (PCOM) commissure is equally effective is unknown. METHODS: Six adult sheep underwent implantation of 9 radiopaque markers on the left ventricle, 8 around the mitral annulus (MA) and 1 on each papillary muscle (PM) tip. Transannular SL sutures were placed at the valve center (CENT) and near ACOM and PCOM and externalized. Acute IMR was induced by proximal circumflex coronary snare occlusion. Biplane videofluoroscopy and transesophageal echocardiography were performed before and continuously during 3 episodes of myocardial ischemia including 20 seconds of SLAC at each different location. End-systolic MA SL dimension at each suture location and distances between the anterior and posterior PM tips and mid-septal annulus ("saddle horn") were calculated from the 3-dimensional (3D) marker coordinates. RESULTS: SLAC interventions in all 3 locations reduced the degree of IMR, but cinching at the center, SLAC(CENT), had a significantly greater effect on reducing the magnitude of IMR than SLAC(PCOM) or SLAC(ACOM) (mean grade of IMR reduction=1.0+/-0.5, 1.8+/-0.5, and 0.9+/-0.2 for SLAC(ACOM), SLAC(CENT), and SLAC(PCOM), respectively; P=0.044). Although ACOM and PCOM cinching reduced SL(CENT) somewhat, only SLAC(CENT) simultaneously reduced both SL(ACOM) and SL(PCOM) and also repositioned both PM tips closer to the annular saddle horn. CONCLUSIONS: SLAC in all 3 positions reduced acute IMR, but central SLAC cinching was most effective, reduced all mitral annular SL dimensions, and relocated both PM tips closer to the mid-septal annulus. Central SLAC is most capable of correcting the annular and subvalvular perturbations accompanying acute left ventricular ischemia that lead to IMR.

Cutting second-order chords does not prevent acute ischemic mitral regurgitation.

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.

Undersized mitral annuloplasty alters left ventricular shape during acute ischemic mitral regurgitation.

BACKGROUND: Underlying left ventricular (LV) dysfunction contributes to poor survival after operation to correct ischemic mitral regurgitation (IMR). Many surgeons do not appreciate that a key component of the Bolling undersized mitral ring annuloplasty concept is to decrease LV wall stress by altering LV shape, but precise 3-dimensional (3-D) geometric data do not exist substantiating this effect. We tested the hypothesis that annular reduction decreases regional circumferential LV radius of curvature (ROC) in a model of acute IMR. METHODS: Eight adult sheep underwent insertion of an adjustable Paneth-type annuloplasty suture and radiopaque markers on the LV and mitral annulus. The animals were studied with biplane videofluoroscopy during baseline conditions, then before and after tightening the annuloplasty suture during proximal left circumflex occlusion. End-systolic circumferential regional LV ROC and mitral annular area were computed. RESULTS: Acute IMR was eliminated (MR grade 2.1+/-0.4 to 0.4+/-0.4, mean+/-SD, P<0.05) by tightening the Paneth annuloplasty suture. Paneth suture tightening during circumflex occlusion also decreased end-systolic regional circumferential radii of curvature at the basal (anterior, 3.40+/-0.16 to 3.34+/-0.14 cm; posterior, 3.31+/-0.23 to 3.24+/-0.26 cm; P<0.05) and equatorial levels (anterior, 2.99+/-0.21 to 2.89+/-0.29 cm; posterior, 2.86+/-0.38 to 2.81+/-0.41 cm; P<0.05). CONCLUSIONS: Acute proximal circumflex occlusion caused IMR and increased end-systolic LV radii of curvature in this experimental preparation. Annular reduction sufficient to abolish IMR also decreased end-systolic anterior and posterior LV ROC, which would be expected to reduce LV wall stress and oxygen consumption in these regions, both potentially beneficial effects. The long-term effects of undersized annuloplasty on LV remodeling and function, however, will require further study in chronic animal preparations or patients with chronic IMR.

Alterations in left ventricular torsion and diastolic recoil after myocardial infarction with and without chronic ischemic mitral regurgitation.

BACKGROUND: Chronic ischemic mitral regurgitation (CIMR) is associated with heart failure that continues unabated whether the valve is repaired, replaced, or ignored. Altered left ventricular (LV) torsion dynamics, with deleterious effects on transmural gradients of oxygen consumption and diastolic filling, may play a role in the cycle of the failing myocardium. We hypothesized that LV dilatation and perturbations in torsion would be greater in animals in which CIMR developed after inferior myocardial infarction (MI) than in those that it did not. METHODS: 8+/-2 days after marker placement in sheep, 3-dimensional fluoroscopic marker data (baseline) were obtained before creating inferior MI by snare occlusion. After 7+/-1 weeks, the animals were restudied (chronic). Inferior MI resulted in CIMR in 11 animals but not in 9 (non-CIMR). End-diastolic septal-lateral and anterior-posterior LV diameters, maximal torsional deformation (phi(max), rotation of the LV apex with respect to the base), and torsional recoil in early diastole (phi(5%), first 5% of filling) for each LV free wall region (anterior, lateral, posterior) were measured. RESULTS: Both CIMR and non-CIMR animals demonstrated derangement of LV torsion after inferior MI. In contrast to non-CIMR, CIMR animals exhibited greater LV dilation and significant reductions in posterior maximal torsion (6.1+/-4.3 degrees to 3.9+/-1.9 degrees * versus 4.4+/-2.5 degrees to 2.8+/-2.0 degrees; mean+/-SD, baseline to chronic, *P<0.05) and anterior torsional recoil (-1.4+/-1.1 degrees to -0.2+/-1.0 degrees versus -1.2+/-1.0 degrees to -1.3+/-1.6 degrees ). CONCLUSIONS: MI associated with CIMR resulted in greater perturbations in torsion and recoil than inferior MI without CIMR. These perturbations may be linked to more LV dilation in CIMR, which possibly reduced the effectiveness of fiber shortening on torsion generation. Altered torsion and recoil may contribute to the "ventricular disease" component of CIMR, with increased gradients of myocardial oxygen consumption and impaired diastolic filling. These abnormalities in regional torsion and recoil may, in part, underlie the "ventricular disease" of CIMR, which may persist despite restoration of mitral competence.

Geometric distortions of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation.

BACKGROUND: Better understanding of the precise 3-dimensional geometric changes of the mitral valvular-ventricular complex in chronic ischemic mitral regurgitation (CIMR) is needed in order to devise better surgical repair techniques. We hypothesized that changes after inferior myocardial infarction would be different in hearts that developed CIMR compared with those that did not. METHODS AND RESULTS: Twenty-four sheep underwent coronary snare and marker placement (annulus, papillary muscles, and anterior and posterior leaflets). After 8 days, cinefluoroscopy provided 3-dimensional marker data, and snare occlusion of obtuse marginal branches created inferior myocardial infarction, including the posterior papillary muscle. After 7 weeks, the 16 surviving animals were studied again and grouped by mitral regurgitation grade (>or= 2+, n=10 versus

Edge-to-edge mitral valve repair without ring annuloplasty for acute ischemic mitral regurgitation.

BACKGROUND: Alfieri edge-to-edge mitral repair has been used clinically with ring annuloplasty to correct ischemic mitral regurgitation (IMR), but its efficacy without concomitant ring annuloplasty has not been described in this setting. METHODS: Seventeen sheep underwent implantation of 9 radiopaque markers on the left ventricle, 8 on the mitral annulus (MA), 1 on each papillary muscle (PM) tip, and 1 on the anterior and posterior leaflet edges near the anterior and posterior commissures. Alfieri repair was performed in 7 animals, and 10 were controls. Biplane videofluoroscopy and transesophageal echocardiography (TEE) were performed (open chest) before and continuously during left circumflex coronary artery occlusion to induce acute IMR. MA area (MAA), anterior (APM), and posterior (PPM) papillary muscle tip distances to midseptal MA ("saddle horn"), and distance of each leaflet marker to the mitral annular plane were calculated from 3-dimensional marker coordinates at end-systole (ES). RESULTS: Severity of IMR was not different between groups (+1.9+/-0.7 versus +1.4+/-0.5 for Control and Alfieri, respectively; P=not significant [NS]). Mitral annular area (MAA; 21+/-15 versus 19+/-9%; P =NS) and septal-lateral (SL) annular diameter (12+/-6 versus 12+/-11%; P =NS) increased similarly during ischemia. While PPM-saddle horn distance increased in both groups (1.5+/-1.3 and 1.6+/-1.4 mm for Control and Alfieri, respectively; P<0.05 versus preischemia), APM-saddle horn distance increased in Control (1.0+/-1.2 mm; P=0.03) but not in the Alfieri animals (0.8+/-08 mm; P=0.07). Leaflet edge displacements from the annular plane during ischemia were similar in both groups. CONCLUSIONS: Alfieri repair did not prevent acute IMR nor alter ischemic valvular or subvalvular geometric perturbations. Adjunct surgical procedures, such as ring annuloplasty, are also necessary.

Annular versus subvalvular approaches to acute ischemic mitral regurgitation.

BACKGROUND: Ischemic mitral regurgitation (IMR) has been attributed to annular dilatation, papillary muscle (PM) displacement ("apical leaflet tenting"), or both. We compared the efficacy of reducing annular or subvalvular dimensions to gain more mechanistic insight into acute IMR. METHODS: Eight adult sheep underwent implantation of radiopaque markers on the LV, mitral annulus (MA), each leaflet edge, and each PM tip. Trans-annular septal-lateral (SL) and inter-PM tip sutures were placed and externalized. Biplane videofluoroscopy and transesophageal echocardiography were performed before and continuously during LCx occlusion-induced IMR with SL annular (SLAC) or inter-PM (PAPS) suture tightening (4 to 5 mm of cinching for 5 seconds during ischemia). MA SL dimension, inter-papillary distance (APM-PPM), and the distances between the anterior (APM) and posterior (PPM) PM tips and the mid-septal annulus ("saddle horn") were calculated from 3-D marker coordinates at end-systole. RESULTS: SLAC reduced IMR (grade=2.1+/-0.6 versus 0.7+/-0.5, P.001), SL annular diameter (4.9+/-2.5 mm smaller versus pre-cinching; P.001), and PM-"saddle horn" distances (0.9+/-0.7 and 1.0+/-0.8 mm reduction for APM and PPM, respectively; P.005). PAPS reduced APM-PPM distance (3.7+/-1.8 mm reduction versus precinching; P.001), only slightly decreased the PPM-"saddle horn" distance (0.3+/-0.3 mm reduction; P.03), and had no effect on IMR. CONCLUSIONS: Acute IMR was abolished by annular SL reduction, which also repositioned both PM tips closer to the mid-septal annulus and paradoxically increased leaflet "apical tenting"; reducing inter-papillary dimension was not effective, even though it displaced the leaflets toward the annular plane (less "apical tenting").

Importance of mitral valve second-order chordae for left ventricular geometry, wall thickening mechanics, and global systolic function.

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.

Alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion.

OBJECTIVE: Helically oriented left ventricular fibers assemble into transmural sheets, which are important for wall-thickening mechanics: 15% fiber shortening results in 40% cross-fiber left ventricular wall thickening and a 60% ejection fraction through sheet extension, thickening, and shear. Normal cardiac microstructure and strains are optimized; deviations could result in apoptosis and deleterious matrix remodeling, which degenerates into global cardiomyopathy. We studied alterations in transmural strains adjacent to ischemic myocardium during acute midcircumflex occlusion. METHODS: Nine sheep had radiopaque markers implanted to measure left ventricular systolic fractional area shortening; 3 transmural bead columns were inserted into the midlateral wall for strain analysis. Three-dimensional marker coordinates were obtained with biplane videofluoroscopy before and during 70 seconds of ischemia. Systolic strains were quantified along circumferential, longitudinal, and radial axes (n = 9) and were transformed into fiber-sheet coordinates by using quantitative microstructural measurements (n = 5). RESULTS: A functional border was defined in the midlateral left ventricle; ischemia decreased posterolateral fractional area shortening, and anterolateral fractional area shortening increased. In this demarcation junction, subepicardial end-systolic radial wall thickening decreased (0.16 +/- 0.08 vs 0.11 +/- 0.06) and sheet-normal shear was abolished (0.08 +/- 0.04 vs -0.01 +/- 0.03). Longitudinal shortening decreased in the subepicardium and midwall (-0.05 +/- 0.04 vs +/- -0.01 +/- 0.06), but circumferential-radial shear increased at these depths (0.04 +/- 0.04 vs 0.11 +/- 0.05). Subendocardial fiber stretch occurred during early systole (-0.01 +/- 0.03 vs 0.02 +/- 0.03), and end-systolic fiber-sheet shear increased (0.07 +/- 0.01 vs 0.11 +/- 0.04, all P < .05). CONCLUSIONS: Increased circumferential-radial shear and altered fiber-sheet strains reflect mechanical interactions between ischemic and nonischemic myocardium, which might be important in triggering remodeling processes that evolve into global ischemic cardiomyopathy.

Annular or subvalvular approach to chronic ischemic mitral regurgitation?

OBJECTIVE: We sought to investigate whether annular or subvalvular interventions corrected chronic ischemic mitral regurgitation differently. METHODS: Sheep underwent placement of markers on the left ventricle, mitral annulus, papillary muscles (anterior and posterior), and both leaflet edges. A transannular suture (septal-lateral annular cinching) was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. Another suture (papillary muscle repositioning) from the posterior papillary muscle was passed through the mitral annulus near the posterior commissure and externalized. After 7 days, 3-dimensional marker data were obtained before inducing posterolateral myocardial infarction. After 7 weeks, animals in whom chronic ischemic mitral regurgitation developed (n = 10) were restudied before and after pulling septal-lateral annular cinching or papillary muscle repositioning sutures. End-systolic septal-lateral annular diameter and 3-dimensional displacement of the papillary muscles and leaflet edges were computed. RESULTS: Infarction increased mitral regurgitation (0.6 +/- 0.5 to 2.3 +/- 1.1); mitral annular septal-lateral dilation (4 +/- 1 mm); posterior papillary muscle displacement laterally (4 +/- 2 mm), posteriorly (9 +/- 3 mm), and toward the annulus (2 +/- 1 mm); posterior mitral leaflet apical tethering (3 +/- 1 mm); and interleaflet separation (+3 +/- 1 mm, P < .05 baseline vs chronic ischemic mitral regurgitation). Septal-lateral annular cinching reduced septal-lateral dimension (-9 +/- 3 mm), corrected lateral posterior papillary muscle displacement (4 +/- 1 mm) and septal-lateral interleaflet separation (-4 +/- 2 mm), and decreased mitral regurgitation (0.6 +/- 0.6, P < .05 septal-lateral annular cinching vs chronic ischemic mitral regurgitation) without affecting posterior leaflet restriction. Papillary muscle repositioning reduced septal-lateral diameter (-4 +/- 1 mm), moved the anterior papillary muscle closer to the annulus (2 +/- 1 mm), and relieved posterior leaflet apical restriction (2 +/- 1 mm, P < .05 papillary muscle repositioning vs chronic ischemic mitral regurgitation) but did not change lateral posterior papillary muscle displacement or decrease mitral regurgitation (1.9 +/- 1.2). CONCLUSIONS: Septal-lateral annular cinching moved the lateral annulus and the posterior papillary muscle closer to the septum and reduced mitral regurgitation unlike posterior papillary muscle repositioning, and thus the key mitral subvalvular repair component must correct posterior papillary muscle lateral displacement.

Effect of cutting second-order chordae on in-vivo anterior mitral leaflet compound curvature.

BACKGROUND AND AIM OF THE STUDY: Leaflet curvature determines leaflet stress. In order to assess the influence of second-order chordae (2 degrees CT) on anterior mitral valve leaflet (AMVL) geometry, AMVL curvature was measured before (Baseline) and after (CUT) cutting the 2 degrees CT. METHODS: Miniature radiopaque markers were sutured onto the AMVL in eight sheep: four along the central-meridian from mid-septal annulus to the free-margin; and one each at the 2 degrees CT insertion. Biplane videofluoroscopic data were acquired (open-chest) before and after CUT. Marker-triplet 3-D coordinates were used to calculate radii-of-curvature at LVPmax along the central-meridian (ROCm) and across the AMVL belly (commissure-commissure axis, ROCc-c). RESULTS: CUT did not change LVPmax (111 +/- 12 versus 106 +/- 11 mmHg; p = 0.19). At baseline, the AMVL central-meridian had compound curvature: Convex to the left ventricle near the annulus (-ROCm) and concave near the free-margin (+ROCm). After CUT, the AMVL flattened: ROCm increased near the annulus (from -1.37 +/- 0.52 to -12.58 +/- 29.04 cm; p = 0.02), but did not change near the edge. In the commissure-commissure axis, ROCc-c was concave to the left ventricle at baseline and increased after CUT in all eight animals. In five sheep, ROCc-c was increased (from 1.93 +/- 1.01 to 2.80 +/- 1.36 cm; p = 0.03), but in three sheep ROCc-c was increased and inverted (from 3.65 +/- 2.17 to -1.72 +/- 0.53 cm; p = 0.03), becoming convex to the left ventricle. CONCLUSION: Compound curvature along the AMVL central-meridian appears to be an intrinsic leaflet property that persists even without support from second-order chordae, whereas concave curvature in the commissure-commissure axis is more dependent on intact second-order chordae. Leaflet compound curvature must be incorporated into future finite element models to characterize leaflet stresses accurately. The importance of second-order chordae in maintaining leaflet shape must be considered during mitral repair. A larger ROC increases leaflet stresses, while reversal of ROC changes tensile stress to compressive stress; this might trigger deleterious leaflet remodeling after chordal cutting.

Altered mitral valve kinematics with atrioventricular and ventricular pacing.

BACKGROUND AND AIM OF THE STUDY: Pacing-induced mitral regurgitation contributes to the 'pacemaker syndrome', which usually is observed with ventricular (V) pacing, but has also been reported with atrioventricular (AV) sequential pacing. Effects of different pacing modes on 3-D kinematics of the mitral apparatus are incompletely understood. METHODS: Radio-opaque markers were placed on the left ventricular (LV) and mitral apparatus including the annulus, leaflets and papillary muscles of eight sheep. Hemodynamic and 3-D dynamic marker geometry were obtained one week later with biplane videofluoroscopy (60 Hz) during atrial (pacing site = left atrium), AV-sequential (140 ms interval) and (anterolateral LV epicardial) ventricular pacing. RESULTS: Compared with A-pacing (*p <0.05): 1) The regurgitant fraction increased with both AV- and V-pacing (A: 6 +/- 3%, AV: 13 +/- 3%*, V: 15 +/- 2%*); 2) AV and V-pacing delayed closure at the leaflet center (A: 21 +/- 10 ms, AV: 52 + 5 ms*, V: 92 +/- 6 ms*) and posterior commissure (A: 17 +/- 10 ms, AV: 46 +/- 8 ms*, V: 94 +/- 6 ms*). V-pacing delayed valve closure at the anterior commissure (A: 27 +/- 9 ms, V: 94 +/- 6 ms*); 3) The end-diastolic leaflet opening angle was greater with AV- and V-pacing (anterior mitral leaflet (AML): A: 32 +/- 2 degrees, AV: 41 +/- 4 degrees*, V: 46 +/- 4 degrees*; posterior mitral leaflet (PML): A: 56 +/- 4 degrees, AV: 62 +/- 3 degrees*, V: 68 +/- 3 degrees*); 4) 'Effective' end-diastolic PML midline length was reduced with AV- and V-pacing (A: 11.2 +/- 0.7 mm, AV: 10.0 +/- 0.4 mm*, V: 10.2 +/- 0.3 mm*), as was the distance from each papillary muscle (PM) tip to the AML edge ('effective' chordal length) close to the commissures (anterior PM-AML: A: 31.5 +/-1.8 mm, AV: 30.5 +/- 1.9 mm*, V: 29.7 +/- 1.8 mm*; posterior PM-AML: A: 33.7 +/- 1.8 mm, AV: 33.1 +/- 1.9 mm*, V: 32.8 +/- 1.9 mm*). CONCLUSION: Both ventricular and AV-sequential-pacing resulted in a more widely opened valve at end-diastole and leaflet dyssynchrony with delayed mitral valve closure and early systolic mitral regurgitation. These alterations which result in pacing-induced mitral regurgitation may be clinically important in patients with impaired LV function.

Does septal-lateral annular cinching work for chronic ischemic mitral regurgitation?

OBJECTIVES: Ring annuloplasty, the current treatment of choice for chronic ischemic mitral regurgitation, abolishes dynamic annular motion and immobilizes the posterior leaflet. In a model of chronic ischemic mitral regurgitation, we tested septal-lateral annular cinching aimed at maintaining normal annular and leaflet dynamics. METHODS: Twenty-five sheep had radiopaque markers placed on the mitral annulus and anterior and posterior mitral leaflets. A transannular suture was anchored to the midseptal mitral annulus and externalized through the midlateral mitral annulus. After 7 days, biplane cinefluoroscopy provided 3-dimensional marker data (baseline) prior to creating inferior myocardial infarction by snare occlusion of obtuse marginal branches. After 7 weeks, the 9 animals that developed chronic ischemic mitral regurgitation were restudied before and after septal-lateral annular cinching. Anterior and posterior mitral leaflet angular excursion and annular septal-lateral and commissure-commissure dimensions and percent shortening were computed. RESULTS: Septal-lateral annular cinching reduced septal-lateral dimension (baseline: 3.0 +/- 0.2; chronic ischemic mitral regurgitation: 3.5 +/- 0.4 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 2.4 +/- 0.3 cm; maximum dimension) and eliminated chronic ischemic mitral regurgitation (baseline: 0.6 +/- 0.5; chronic ischemic mitral regurgitation: 2.3 +/- 1.0 [P <.05 vs baseline by repeated measures analysis of variance and Dunnett's test]; septal-lateral annular cinching: 0.6 +/- 0.6; mitral regurgitation grade [0 to 4+]) but did not alter dynamic annular shortening (baseline: 7 +/- 3; chronic ischemic mitral regurgitation: 10 +/- 5; septal-lateral annular cinching: 6 +/- 2, percent septal-lateral shortening) or posterior mitral leaflet excursion (baseline: 46 degrees +/- 8 degrees; chronic ischemic mitral regurgitation: 41 degrees +/- 13 degrees; septal-lateral annular cinching: 46 degrees +/- 8 degrees ). CONCLUSIONS: In this model, septal-lateral annular cinching decreased chronic ischemic mitral regurgitation, reduced annular septal-lateral diameter (but not commissure-commissure diameter), and maintained normal annular and leaflet dynamics. These findings provide additional insight into the treatment of chronic ischemic mitral regurgitation.

Is medical therapy still the optimal treatment strategy for patients with acute type B aortic dissections?

OBJECTIVE: The optimal treatment of patients with acute type B dissections continues to be debated. METHODS: A 36-year clinical experience of medical and surgical treatments in 189 patients was retrospectively analyzed (multivariable Cox proportional hazards model) with respect to three outcome end points: all deaths, freedom from reoperation, and freedom from late aortic complications or death. Propensity score analysis identified 2 quintiles (quintiles I and II, consisting of 142 comparable patients) for further comparison of the effects of surgical versus medical treatment. RESULTS: Shock (hazard ratio 14.5, 95% confidence interval 4.7-44.5, P <.001) and visceral ischemia (hazard ratio 10.9, 95% confidence interval 3.9-30.3, P <.001) largely predominated as determinants of death, along with 6 other risk factors (arch involvement, rupture, stroke, previous sternotomy, and coronary or lung disease), which roughly doubled the hazard of death. Female sex was a significant but weaker predictor of death. Renal dysfunction, year of presentation, age, and mode of therapy (medical vs surgical) had no important bearing on overall survival. The actuarial survival estimates for all patients were 71%, 60%, 35%, and 17% at 1, 5, 10, and 15 years, respectively, and were similar for the medical and surgical patients. Reoperation and late aortic complications were predicted by the presence of Marfan syndrome. For the propensity-matched patients in quintiles I and II, survival, freedom from reoperation, and freedom from aortic complications were almost identical in the medically treated and surgical subsets. CONCLUSIONS: The prognosis for patients with acute type B aortic dissection is bleak and determined primarily by dissection-related and patient-specific risk factors, which do not appear to be readily modifiable.

Annular remodeling in chronic ischemic mitral regurgitation: ring selection implications.

BACKGROUND: More precise understanding of annular remodeling in the evolution of chronic ischemic mitral regurgitation is needed to provide a more rational basis for optimal annuloplasty ring sizing and selection as well as the design of new reparative techniques. Three-dimensional in vivo data describing these geometric perturbations however are lacking. Using an ovine model of chronic myocardial infarction we determined the three-dimensional distortions of the mitral annulus associated with the development of chronic ischemic mitral regurgitation. METHODS: Ten sheep underwent placement of radiopaque markers on the left ventricle and mitral annulus as well as placement of snares around the second and third obtuse marginal coronary arteries. After 8 days biplane cinefluoroscopy provided three-dimensional marker data and snare occlusion created an inferior infarction. After 7 more weeks the animals were studied again. RESULTS: Severity of mitral regurgitation increased (0.6 +/- 0.5 to 2.5 +/- 0.7). Septal-lateral (2.99 +/- 0.20 cm to 3.64 +/- 0.35 cm, maximum dimension) and commissure-commissure (3.71 +/- 0.32 cm to 4.40 +/- 0.30 cm) mitral annular diameters and the lengths of the muscular (7.77 +/- 0.39 cm to 9.51 +/- 0.72 cm) and fibrous annular perimeters (3.36 +/- 0.37 cm to 3.85 +/- 0.39 cm, p < 0.0001 for all) increased while the height of the annular "saddle horn" above a best-fit plane fell (0.73 +/- 0.52 cm to 0.57 +/- 0.42 cm, minimum dimension, p = 0.01). CONCLUSIONS: These three-dimensional in vivo data reflect annular remodeling in chronic ischemic mitral regurgitation and suggest that mitral repair in this context should be aimed at preventing further lengthening of the intertrigonal distance, reducing the septal-lateral annular diameter to reestablish adequate leaflet coaptation, and restoring the saddle shape of the annulus.

Aorto-mitral annular dynamics.

BACKGROUND: The aortic and mitral valves are coupled through fibrous aorto-mitral continuity, but their synchronous dynamic physiology has not been completely characterized. METHODS: Seven sheep underwent implantation of five radiopaque markers on the left ventricle, 10 on the mitral annulus, and 3 on the aortic annulus. One of the mitral annulus markers was placed at the center of aorto-mitral continuity (mitral annulus "saddle horn"). Animals were studied with bi-plane videofluoroscopy 7 to 10 days postoperatively. Total circumference and lengths of mitral fibrous annulus, mitral muscular annulus, aortic fibrous annulus, and aortic muscular annulus were calculated throughout the cardiac cycle from three dimensional marker coordinates as was mitral annular area and aortic annular area. Aorto-mitral angle was determined as the angle between the centroid of the aortic annulus markers, the saddle horn, and the centroid of the mitral annulus markers. Aortic annulus and mitral annulus flexion was expressed as the difference between maximum and minimum values of the aortic and mitral annulus angles during the cardiac cycle. RESULTS: Mitral and aortic annular areas changed in roughly a reciprocal fashion during late diastole and early systole with an overall 32 +/- 8% change in aortic annular area and a 13 +/- 13% change in mitral annular area. Aortic fibrous annulus changed much less than aortic muscular annulus (6 +/- 2% vs 18 +/- 4%; p = 0.0003) as did mitral fibrous annulus relative to mitral muscular annulus (4 +/- 1% vs 8 +/- 2%; p = 0.004). Aortic annulus and mitral annulus flexion was 8 +/- 2 degrees and increased to 11 +/- 2 degrees (p = 0.009) with inotropic stimulation. CONCLUSIONS: Dynamic aortic and mitral annular area changes were not mediated through the anatomic fibrous continuity. Aorto-mitral flexion, which increased with enhanced contractility, may facilitate left ventricle ejection. The effect of valvular surgical interventions on aorto-mitral flexion needs further investigation.