Ishihara K, Zile M R, Kanazawa S, Tsutsui H, Urabe Y, DeFreyte G, Carabello B A
Department of Medicine, Medical University of South Carolina, Charleston 29425-2221.
Circulation. 1992 Nov;86(5 Suppl):II16-25.
Contractile function improves after correction of experimental mitral regurgitation, but ejection performance becomes depressed when mitral valve replacement involves chordal transection. A role for chordal transection in producing the depressed ejection performance was suspected but uncertain. Therefore, in this study, we tested two specific hypotheses: 1) that contractile function would improve and, in conjunction with chordal preservation, would allow for preserved ejection performance and 2) that improved left ventricular contractile function after surgery would be reflected in the function of myocytes isolated from the affected left ventricles.
We examined ventricular contractile function and ejection performance and isolated myocyte function after correction of experimental mitral regurgitation (chordal rupture) with mitral valve replacement that involved chordal preservation. After 3 months of chronic mitral regurgitation, the average regurgitant fraction of seven dogs was 0.77 +/- 0.04. End-diastolic volume had increased from 79 +/- 5 to 132 +/- 10 cm3 (p < 0.05). At that time, all indexes of left ventricular contractile function were depressed. Three months after mitral valve replacement with chordal preservation, end-diastolic volume fell to 100 +/- 4 cm3 (p < 0.05). At this time, all indexes of contractile function had returned to normal. End-systolic stress and ejection fraction after mitral valve replacement were similar to their baseline levels. Viscosity-velocity curves (analogous to force-velocity curves) of myocytes isolated from the affected left ventricles were similar to those of myocytes isolated from normal left ventricles.
We conclude that mitral valve replacement with chordal preservation allows ventricular contractile function to return to normal. Normal global ventricular function, in turn, is associated with normal function of the individual myocytes that compose the left ventricular chamber. Further, chordal preservation allowed for loading and ejection performance to return to premorbid levels.
实验性二尖瓣反流纠正后收缩功能有所改善，但当二尖瓣置换术涉及腱索横断时，射血功能会受到抑制。腱索横断在导致射血功能受抑制方面的作用虽被怀疑，但尚不明确。因此，在本研究中，我们检验了两个特定假设：1）收缩功能会改善，并且与腱索保留相结合，将允许保留射血功能；2）手术后左心室收缩功能的改善将反映在从受影响的左心室分离出的心肌细胞的功能上。
我们在二尖瓣置换术（腱索断裂）纠正实验性二尖瓣反流并保留腱索后，检查了心室收缩功能、射血功能以及分离出的心肌细胞功能。在慢性二尖瓣反流3个月后，7只犬的平均反流分数为0.77±0.04。舒张末期容积从79±5增加到132±10 cm³（p<0.05）。此时，左心室收缩功能的所有指标均受到抑制。保留腱索的二尖瓣置换术后3个月，舒张末期容积降至100±4 cm³（p<0.05）。此时，收缩功能的所有指标均恢复正常。二尖瓣置换术后的收缩末期应力和射血分数与基线水平相似。从受影响的左心室分离出的心肌细胞的黏度-速度曲线（类似于力-速度曲线）与从正常左心室分离出的心肌细胞的曲线相似。
我们得出结论，保留腱索的二尖瓣置换术可使心室收缩功能恢复正常。正常的整体心室功能反过来与构成左心室腔的单个心肌细胞的正常功能相关。此外，腱索保留使负荷和射血功能恢复到病前水平。
