Filiberto Rodriguez

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 (≥ 2+, n=10 versus ≤ 1+, n=6). End-systolic mitral annulus dimensions, components of papillary muscle and leaflet displacement, were calculated. After inferior myocardial infarction, total displacement of the posterior papillary muscle from the midseptal annulus (“saddle horn”) was greater in CIMR(+) animals: 6.5±3.2 versus 3.1±2.7 (P =0.02), with the posterior papillary muscle moving more laterally (6.8±3.4 versus 2.5±3.5 mm, P =0.01). Increase in mitral annular septal-lateral diameter was greater in animals with CIMR (4.9±2.7 versus 2.3±2.0, P =0.02), and apical displacement of the posterior leaflet (PL) margin was also greater in the CIMR(+) group (1.7±1.0 versus 0.3±0.5, P =0.01). Conclusions—The CIMR(+) group had greater septal-lateral annular dilatation, lateral posterior papillary muscle displacement, and apical PL restriction, indicating that these associated geometric alterations may be important in the pathogenesis of CIMR. Treatment of CIMR should address both annular septal-lateral dilatation and lateral displacement of the posterior papillary muscle.

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 (Ees) 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: Ees (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). Conclusion—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 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 (&phgr;max, rotation of the LV apex with respect to the base), and torsional recoil in early diastole (&phgr;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° to 3.9±1.9°* versus 4.4±2.5° to 2.8±2.0°; mean±SD, baseline to chronic, *P<0.05) and anterior torsional recoil (−1.4±1.1° to −0.2±1.0° versus −1.2±1.0° to −1.3±1.6°). Conclusion—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.

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.

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

BackgroundAlfieri 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. MethodsSeventeen 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). ResultsSeverity 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. ConclusionsAlfieri repair did not prevent acute IMR nor alter ischemic valvular or subvalvular geometric perturbations. Adjunct surgical procedures, such as ring annuloplasty, are also necessary.

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.

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.

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, SLACCENT, had a significantly greater effect on reducing the magnitude of IMR than SLACPCOM or SLACACOM (mean grade of IMR reduction=1.0±0.5, 1.8±0.5, and 0.9±0.2 for SLACACOM, SLACCENT, and SLACPCOM, respectively; P=0.044). Although ACOM and PCOM cinching reduced SLCENT somewhat, only SLACCENT simultaneously reduced both SLACOM and SLPCOM 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.

Transmural Strains in the Ovine Left Ventricular Lateral Wall During Diastolic Filling

Rapid early diastolic left ventricular (LV) filling requires a highly compliant chamber immediately after systole, allowing inflow at low driving pressures. The transmural LV deformations associated with such filling are not completely understood. We sought to characterize regional transmural LV strains during diastole, with focus on early filling, in ovine hearts at 1 week and 8 weeks after myocardial marker implantation. In seven normal sheep hearts, 13 radiopaque markers were inserted to silhouette the LV chamber and a transmural beadset was implanted into the lateral equatorial LV wall to measure transmural strains. Four-dimensional marker dynamics were obtained 1 week and 8 weeks thereafter with biplane videofluoroscopy in closed-chest, anesthetized animals. LV transmural strains in both cardiac and fiber-sheet coordinates were studied from filling onset to the end of early filling (EOEF, 100 ms after filling onset) and at end diastole. At the 8 week study, subepicardial circumferential strain (ECC) had reached its final value already at EOEF, while longitudinal and radial strains were nearly zero at this time. Subepicardial ECC and fiber relengthening (Eff) at EOEF were reduced to 1 compared with 8 weeks after surgery (ECC:0.02+/-0.01 to 0.08+/-0.02 and Eff:0.00+/-0.01 to 0.03+/-0.01, respectively, both P<0.05). Subepicardial ECC during early LV filling was associated primarily with fiber-normal and sheet-normal shears at the 1 week study, but to all three fiber-sheet shears and fiber relengthening at the 8 week study. These changes in LV subepicardial mechanics provide a possible mechanistic basis for regional myocardial lusitropic function, and may add to our understanding of LV myocardial diastolic dysfunction.

Transmural LV Systolic Wall Thickening Gradients and Models of Heart Wall Mechanics

We implanted arrays of radiopaque markers to measure lateral equatorial wall transmural strains and global and regional LV geometry in 7 sheep. Without intervening procedures, one and eight weeks after surgery, 4-D datasets from stereo radiographic studies were processed to yield transmural strains from each heart. In accordance with previous theoretical predictions and experimental results, we hypothesized that systolic radial strain (i.e., wall thickening) would exhibit a transmural gradient, increasing from subepicardium to subendocardium, and, as previous work suggested that this was a fundamental mechanism, this gradient would be observed at both the one- and eight-week studies. The one-week studies yielded the expected gradient. This gradient, however, was not present in the eight-week studies, although LV shape and hemodynamics were virtually identical to their one-week values. We discuss the implications of these findings to mechanistic theories of heart wall mechanics.Copyright