Rodriguez Filiberto, Langer Frank, Harrington Katherine B, Tibayan Frederick A, Zasio Mary K, Cheng Allen, Liang David, Daughters George T, Covell James W, Criscione John C, Ingels Neil B, Miller D Craig
Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, Calif 94305-5247, USA.
Circulation. 2004 Sep 14;110(11 Suppl 1):II115-22. doi: 10.1161/01.CIR.0000138580.57971.b4.
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.
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).
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.
二尖瓣 - 心室连续性对左心室(LV)收缩功能很重要,但前叶二级“支柱”腱索的具体作用尚不清楚。
八只绵羊植入不透射线的标记物以勾勒左心室、瓣环和乳头肌(PMs);在乳头肌之间的左心室中外侧壁插入3个跨壁珠柱。用外置钢丝圈套环绕支柱腱索。在腱索切断前后采集三维标记物图像和血流动力学数据。计算预负荷可募集搏功(PRSW)和收缩末期弹性(E(es))以评估整体左心室收缩功能(n = 7)。从珠柱位移测量跨壁应变(n = 4)。腱索切断导致整体左心室功能障碍:E(es)(1.48±1.12对0.98±1.30 mmHg/mL,P = 0.04)和PRSW(69±16对60±15 mmHg,P = 0.03)降低。虽然心率和从舒张末期到收缩末期的时间不变,但射血中期时间延迟(125±18对136±19 ms,P = 0.01)。整体上,左心室心尖和后乳头肌尖端在舒张末期和收缩末期远离纤维环移位,左心室心底 - 心尖长度增加(均增加1 mm,P < 0.05)。局部上,出现心内膜下舒张末期应变:纵向应变(E22)0.030±0.013和径向增厚(E33)0.081±0.041(两者与零相比P < 0.05)。心内膜下收缩期剪切应变也受到干扰:周向 - 纵向“微扭转”(E12)(0.099±0.035对0.075±0.025)和周向 - 径向剪切(E13)(0.084±0.023对0.039±0.008,两者P < 0.05)。
切断二级腱索改变了左心室几何形状,重塑了乳头肌之间的心肌,干扰了影响微扭转和壁增厚的局部收缩期应变模式,并导致整体收缩功能障碍,证明了这些腱索对左心室结构和功能的重要性。