Biomedical subjects

David Liang

Publications and source records attributed to David Liang.

At least 19 recordsLinked to original sources

PubMed2007

Septal-lateral annnular cinching perturbs basal left ventricular transmural strains.

OBJECTIVE: Septal-lateral annular cinching ('SLAC') corrects both acute and chronic ischemic mitral regurgitation in animal experiments, which has led to the development of therapeutic surgical and interventional strategies incorporating this concept (e.g., Edwards GeoForm ring, Myocor Coapsys, Ample Medical PS3). Changes in left ventricular (LV) transmural cardiac and fiber-sheet strains after SLAC, however, remain unknown. METHODS: Eight normal sheep hearts had two triads of transmural radiopaque bead columns inserted adjacent to (anterobasal) and remote from (midlateral equatorial) the mitral annulus. Under acute, open chest conditions, 4D bead coordinates were obtained using videofluoroscopy before and after SLAC. Transmural systolic strains were calculated from bead displacements relative to local circumferential, longitudinal, and radial cardiac axes. Transmural cardiac strains were transformed into fiber-sheet coordinates (X(f), X(s), X(n)) oriented along the fiber (f), sheet (s), and sheet-normal (n) axes using fiber (alpha) and sheet (beta) angle measurements. RESULTS: SLAC markedly reduced (approximately 60%) septal-lateral annular diameter at both end-diastole (ED) (2.5+/-0.3 to 1.0+/-0.3 cm, p=0.001) and end-systole (ES) (2.4+/-0.4 to 1.0+/-0.3 cm, p=0.001). In the LV wall remote from the mitral annulus, transmural systolic strains did not change. In the anterobasal region adjacent to the mitral annulus, ED wall thickness increased (p=0.01) and systolic wall thickening was less in the epicardial (0.28+/-0.12 vs 0.20+/-0.06, p=0.05) and midwall (0.36+/-0.24 vs 0.19+/-0.11, p=0.04) LV layers. This impaired wall thickening was due to decreased systolic sheet thickening (0.20+/-0.8 to 0.12+/-0.07, p=0.01) and sheet shear (-0.15+/-0.07 to -0.11+/-0.04, p=0.02) in the epicardium and sheet extension (0.21+/-0.11 to 0.10+/-0.04, p=0.03) in the midwall. Transmural systolic and remodeling strains in the lateral midwall (remote from the annulus) were unaffected. CONCLUSIONS: Although SLAC is an alluring concept to correct ischemic mitral regurgitation, these data suggest that extreme SLAC adversely effects systolic wall thickening adjacent to the mitral annulus by inhibiting systolic sheet thickening, sheet shear, and sheet extension. Such alterations in LV strains could result in unanticipated deleterious remodeling and warrant further investigation.

Animals↗

PubMed2007

Altered myocardial shear strains are associated with chronic ischemic mitral regurgitation.

BACKGROUND: Ischemic mitral regurgitation (IMR) limits life expectancy and can lead to postinfarction global left ventricular (LV) dilatation and remodeling, the pathogenesis of which is not completely known. We tested the hypothesis that IMR perturbs adjacent myocardial LV systolic strains. METHODS: Thirteen sheep had three columns of miniature beads inserted across the lateral LV wall, with additional epicardial markers silhouetting the ventricle. One week later posterolateral infarction was created. Seven weeks thereafter, the animals were divided into two groups according to severity of IMR (< or = 1+, n = 7, IMR[-] vs > or = 2+, n = 6, IMR[+]). Four dimensional marker coordinates and quantitative histology were used to calculate ventricular volumes, transmural myocardial systolic strains, and systolic fiber shortening. RESULTS: Seven weeks after infarction, end-diastolic (ED) volume increased similarly in both groups, end-systolic (ES) E13 (circumferential-radial) shear increased in both groups, but more so in IMR(+) than IMR(-) (+0.12 vs 0.04, p < 0.005), and E12 (circumferential-longitudinal) shear increased in IMR(-) but not IMR(+) (+0.04 vs -0.01, p < 0.005). There were no significant differences in ED or ES remodeling strains or systolic fiber shortening between IMR(-) and IMR(+). CONCLUSIONS: An equivalent increase in LV end-diastolic (ED) volume in both groups, coupled with unchanged ED and end-systolic remodeling strains as well as systolic circumferential, longitudinal, and radial strains, argue against a global LV or regional myocardial geometric basis for the cardiomyopathy associated with IMR. Further, similar systolic fiber shortening in both groups militates against an intracellular (cardiomyocyte) mechanism. The differences in subepicardial E12 and E13 shears, however, suggest a causal role of altered interfiber (cytoskeleton and extracellular-matrix) interactions.

Animals↗

PubMed2006

Mitral leaflet remodeling in dilated cardiomyopathy.

BACKGROUND: Normal mammalian mitral leaflets have regional heterogeneity of biochemical composition, collagen fiber orientation, and geometric deformation. How leaflet shape and regional geometry are affected in dilated cardiomyopathy is unknown. METHODS AND RESULTS: Nine sheep had 8 radio-opaque markers affixed to the mitral annulus (MA), 4 markers sewn on the central meridian of the anterior mitral leaflet (AML) forming 4 distinct segments S1 to S4 and 2 on the posterior leaflet (PML) forming 2 distinct segments S5 and S6. Biplane videofluoroscopy and echocardiography were performed before and after rapid pacing (180 to 230 bpm for 15+/-6 days) sufficient to develop tachycardia-induced cardiomyopathy (TIC) and functional mitral regurgitation (FMR). Leaflet tethering was defined as change of displacement of AML and PML edge markers from the MA plane from baseline values while leaflet length was obtained by summing the segments between respective leaflet markers. With TIC, total AML and PML length increased significantly (2.11+/-0.16 versus 2.43+/-0.23 cm and 1.14+/-0.27 versus 1.33+/-0.25 cm before and after pacing for AML and PML, respectively; P<0.05 for both), but only segments near the edge of each leaflet (S4 lengthened by 23+/-17% and S5 by 24+/-18%; P<0.05 for both) had significant regional remodeling. AML shape did not change and no leaflet tethering was observed. CONCLUSIONS: TIC was not associated with leaflet tethering or shape change, but both anterior and posterior leaflets lengthened because of significant remodeling localized near the leaflet edge. Leaflet remodeling accompanies mitral regurgitation in cardiomyopathy and casts doubt on FMR being purely "functional" in etiology.

Animals↗

PubMed2006

Effects of undersized mitral annuloplasty on regional transmural left ventricular wall strains and wall thickening mechanisms.

BACKGROUND: Undersized mitral annuloplasty, widely used for ischemic and functional mitral regurgitation (MR), has been proposed as an "annular solution to a ventricular problem." Beyond relief of MR, it is thought to improve global left ventricular (LV) shape, hence potentially reducing myocardial stress and promoting beneficial reverse LV remodeling. We previously observed that undersized annuloplasty inhibited systolic wall thickening at the LV base near the mitral annulus. In this study, we measured the effects of undersized annuloplasty on regional transmural LV wall fiber and sheet strains and wall thickening mechanisms. METHODS AND RESULTS: Nine sheep had transmural radiopaque beadsets surgically inserted into anterobasal and lateral equatorial LV regions, with additional markers silhouetting the LV and mitral annulus. 4-Dimensional marker dynamics were studied with biplane videofluoroscopy before and after tightening an adjustable Paneth-type mitral annuloplasty suture. Transmural circumferential, longitudinal, and radial systolic and remodeling strains in the subepicardium (20% depth), midwall (50%), and subendocardium (80%) in both regions were computed. Fiber and sheet angles from quantitative regional histology allowed transformation of these strains into local fiber (f), sheet (s), and sheet-normal (n) coordinates. Further analysis calculated the transmural contributions of sheet extension (E(ssc)), sheet thickening (E(nnc)), and sheet shear (E(snc)) to systolic wall thickening (E(33)). In the anterobasal region, undersized annuloplasty reduced systolic wall thickening (E33) by &50% at all transmural depths by inhibiting: (1) subendocardial systolic fiber shortening (-0.10+/-0.05 versus -0.04+/-0.05; P<0.05); (2) subepicardial (0.16+/-0.15 versus 0.09+/-0.08; P<0.05) and subendocardial (0.45+/-0.40 versus 0.19+/-0.18; P<0.05) systolic sheet thickening; (3) midwall sheet extension (0.22+/-0.12 versus 0.11+/-0.06; P<0.05); and (4) transmural sheet shear (subepicardium, -0.14+/-0.07 versus -0.08+/-0.07; midwall, 0.21+/-0.12 versus 0.10+/-0.11; subendocardium, -0.19+/-0.23 versus -0.11+/-0.16; P<0.05). In the remote lateral equatorial region, fiber-sheet strains and E33 were unchanged. CONCLUSIONS: In this acute animal study, undersized annuloplasty inhibited systolic wall thickening in the anterobasal region by reducing subendocardial systolic fiber shortening and laminar sheet wall thickening, but had no effects in a more distant LV region. This suggests that undersized mitral annuloplasty may have potentially deleterious effects on local myocardial mechanics.

Animals↗

PubMed2006

Passive ventricular constraint prevents transmural shear strain progression in left ventricle remodeling.

BACKGROUND: Passive ventricular constraint provides external cardiac support to reduce left ventricular (LV) wall stress and myocardial stretch, which are primary determinants of LV remodeling. Altered wall strain results in cytokine and reactive oxygen species production, which, in turn, stimulates apoptosis and extracellular matrix disruption and could be an important trigger for adverse global LV dilatation and remodeling. The effects of the Acorn cardiac support device (CSD) on regional transmural LV wall strains, however, remain unknown. METHODS AND RESULTS: Thirty-three sheep had transmural radiopaque beadsets surgically inserted into the anterior basal and lateral equatorial LV walls, with additional markers silhouetting the left ventricle. Eight animals had CSD implanted (myocardial infarction [MI]+CSD). One week thereafter, the MI+CSD group and 10 animals without CSD (MI) underwent posterior LV infarction by snaring obtuse marginal coronary arteries. Fifteen animals (Sham) had no infarction or CSD. 4D marker dynamics were measured with biplane videofluoroscopy 1 and 8 weeks postoperatively. LV volumes, sphericity index, and transmural circumferential, longitudinal, and radial systolic strains were analyzed. Compared with Sham, infarction (MI) dilated the heart, reduced sphericity index (LV length/width), and increased longitudinal-radial shear strains in the inner half of both the anterior and lateral LV walls. CSD prevented this shear strain perturbation, minimized LV end diastolic volume increase, and augmented the LV sphericity index. CONCLUSIONS: Prophylactic CSD prevented infarct-induced shear strain progression not only in myocardium adjacent to, but also remote from, the infarct. CSD also prevented LV dilatation and sphericalization. By attenuating shear strain abnormalities, CSD could prevent the heart from entering into a positive feedback loop of further LV dilatation and exaggeration of LV wall stress and may reduce biochemical triggers portending adverse LV remodeling.

Animals↗

PubMed2006

Posterior mitral leaflet extension: an adjunctive repair option for ischemic mitral regurgitation?

BACKGROUND: Residual or recurrent mitral regurgitation frequently occurs after mitral valve repair for ischemic mitral regurgitation with an annuloplasty ring. Because annuloplasty primarily addresses annular dilatation, we studied an adjunctive technique that might correct restricted leaflet (Carpentier type IIIb) systolic closing motion, which often accompanies annular dilatation in patients with ischemic mitral regurgitation. METHODS: Six sheep had radiopaque markers placed on the left ventricle, mitral leaflets and annulus, and mitral subvalvular apparatus. A pericardial patch was sutured into the middle scallop of the posterior mitral valve leaflet and furled in with a reefing stitch placed in the radial axis. Posterolateral left ventricular myocardial ischemia was created by using proximal circumflex occlusion to induce acute ischemic mitral regurgitation. Under open-chest conditions, 3-dimensional marker coordinates were measured by using biplane videofluoroscopy at baseline and during acute ischemia both before and after release of the reefing stitch (leaflet extension); transesophageal echocardiography was used to grade ischemic mitral regurgitation. RESULTS: Leaflet apical systolic tethering was not improved by leaflet extension, but ischemic mitral regurgitation decreased (control, 0.9 +/- 0.3*; ischemia, 2.4 +/- 0.3; leaflet extension, 1.5 +/- 0.3; *P < 0.002). Posterior mitral valve leaflet midline length (control, 1.45 +/- 0.09*; ischemia, 1.53 +/- 0.10; leaflet extension, 1.83 +/- 0.13*; *P < 0.001) and posterior mitral valve leaflet middle scallop area (control, 1.66 +/- 0.20 cm2*; ischemia, 1.91 +/- 0.22 cm2; leaflet extension, 2.36 +/- 0.22 cm2*; *P < 0.006) increased with leaflet extension because of patch unfurling (mean +/- 1 standard error of the mean; repeated-measures analysis of variance, Dunnet post-hoc test vs ischemia). CONCLUSIONS: Posterior mitral valve leaflet extension ameliorated acute ischemic mitral regurgitation but did not correct the abnormal apically restricted systolic posterior mitral valve leaflet closing motion. This technique might be a useful adjunct repair in combination with ring annuloplasty for ischemic mitral regurgitation, but the clinical role of this adjunct remains to be defined in patients.

Animals↗

PubMed2005

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.

Acute Disease↗

PubMed2005

Annular height-to-commissural width ratio of annulolasty rings in vivo.

BACKGROUND: A "saddle-shaped" mitral annulus with an optimal ratio between annular height and commissural diameter may reduce leaflet and chordal stress and is purported to be conserved across mammalian species. Whether annuloplasty rings maintain this relationship is unknown. METHODS AND RESULTS: Twenty-three adult sheep underwent implantation of radiopaque markers on the left ventricle and mitral annulus. Eight animals underwent implantation of a Carpentier-Edwards Physio ring, 7 underwent a Medtronic Duran flexible ring, and 8 served as controls. Animals were studied with biplane videofluoroscopy 7 to 10 days postoperatively. Annular height and commissural width (CW) were determined from 3D marker coordinates, and annular height:CW ratio (AHWCR) was calculated. Annular height was similar in Control and Duran animals but significantly lower in the Physio group at end diastole (8.4+/-3.8, 6.7+/-2.3, and 3.4+/-0.6 mm, respectively, for Control, Duran, and Physio; ANOVA=0.005) and at end systole (14.5+/-6.2, 10.5+/-5.5, and 5.8+/-2.5 mm, respectively, for Control, Duran, and Physio; ANOVA=0.004). Both ring groups reduced CW significantly relative to Control. AHCWR did not differ between Control and Duran but was lower in Physio (23+/-11%, 24+/-7%, and 12+/-2% at end diastole and 42+/-17%, 37+/-17%, and 21+/-10% at end systole, respectively, for Control, Duran, and Physio, respectively; ANOVA <0.05 for both). CONCLUSIONS: Mitral annular height and AHWCR of the native valve were unchanged by a Duran ring, whereas the Physio ring led to a lower AHWCR. Theoretically, such a flexible annuloplasty ring may provide better leaflet stress distribution by maintaining normal AHWCR.

Animals↗

PubMed2005

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.

Animals↗

PubMed2005

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.

Animals↗

PubMed2005

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.

Animals↗

PubMed2004

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.

Animals↗

PubMed2004

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.

Acute Disease↗

PubMed2004

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.

Acute Disease↗

PubMed2004

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.

Animals↗

PubMed2004

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.

Acute Disease↗

PubMed2004

Fixed-apex mitral annular descent correlates better with left ventricular systolic function than does free-apex left ventricular long-axis shortening.

Echocardiographic measures of mitral annular descent (MAD) assume a fixed left ventricular (LV) apex throughout the cardiac cycle, ignoring the apical component of LV long-axis shortening (LAS). We tested whether apical motion contributes significantly to LAS, making LAS a better surrogate of LV systolic function than MAD. Three-dimensional LV systolic MAD, LAS, and apical motion were measured in sheep using implanted radiopaque markers and biplane videofluoroscopy. End-diastolic volume-stroke work relationship (preload recruitable stroke work) was computed as a load-independent index of LV systolic function. Apical motion was 1.4 +/- 0.8 mm, representing 22% of LAS (P <.05). Linear regression demonstrated that MAD correlated slightly better with preload recruitable stroke work (r = 0.808) than LAS (r = 0.792, both P <.001). Receiver operating characteristic curves demonstrated MAD was more accurate in predicting depressed LV function than LAS (93% vs 84%, respectively). Although LV apical motion contributed significantly to LAS, MAD measured with a fixed-apex assumption, as currently done echocardiographically, correlated more closely with LV preload recruitable stroke work.

Animals↗

PubMed2004

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.

Animals↗