Gaasch W H, Zile M R
Department of Medicine, Medical Center of Central Massachusetts, Worcester.
Eur Heart J. 1991 Jul;12 Suppl B:48-51. doi: 10.1093/eurheartj/12.suppl_b.48.
It is generally believed that mitral regurgitation (MR) creates a systolic 'unloading' effect by providing a low-resistance ejection into the left atrium; this is thought to increase the left ventricular ejection fraction (EF), and thus to mask a reduced contractile state. Similarly, mitral valve replacement (MVR), by removing the low-resistance regurgitant leak, has been thought to increase left ventricular afterload (systolic wall stress) and thereby cause the decrease in EF that is often seen postoperatively. These concepts have never been confirmed in patients with chronic MR. Accordingly, we evaluated systolic wall stress before and after MVR and assessed stress-shortening relations in two groups of patients with chronic MR (those with compensated and those with decompensated MR). Calculated values for circumferential and meridional wall stress were found to be normal or high in patients with chronic MR. This indicates that chronic MR is not associated with an unloading effect. In decompensated MR, systolic wall stress tends to increase after MVR; this can contribute to a postoperative decline in myocardial fibre shortening and a lower EF. By contrast, patients with compensated MR exhibit a decline in systolic wall stress after MVR; despite this postoperative decline in afterload, fibre shortening falls. This indicates that the fall in fibre shortening after MVR is not the result of increased systolic loading. In such patients, the valve replacement (with loss of integrity of papillary muscles and chordae, and a tethering of posterobasal wall motion by the prosthesis) is most likely responsible for the postoperative decline in fibre shortening and EF.
一般认为，二尖瓣反流（MR）通过向左心房提供低阻力射血产生收缩期“卸载”效应；据认为这会增加左心室射血分数（EF），从而掩盖收缩状态的降低。同样，二尖瓣置换术（MVR）通过消除低阻力反流漏，被认为会增加左心室后负荷（收缩期壁应力），从而导致术后常见的EF降低。这些概念从未在慢性MR患者中得到证实。因此，我们评估了MVR前后的收缩期壁应力，并评估了两组慢性MR患者（代偿性和失代偿性MR患者）的应力-缩短关系。发现慢性MR患者的圆周壁应力和子午线壁应力计算值正常或较高。这表明慢性MR与卸载效应无关。在失代偿性MR中，MVR后收缩期壁应力往往会增加；这可能导致术后心肌纤维缩短下降和EF降低。相比之下，代偿性MR患者在MVR后收缩期壁应力会下降；尽管术后后负荷下降，但纤维缩短仍会下降。这表明MVR后纤维缩短下降不是收缩期负荷增加的结果。在这类患者中，瓣膜置换（乳头肌和腱索完整性丧失，假体使后基底壁运动受限）很可能是术后纤维缩短和EF下降的原因。
