Palta Sanjeev, Gill Kanwaljit S, Pai Ramdas G
Loma Linda University Loma Linda, CA 92354, USA.
J Heart Valve Dis. 2003 Sep;12(5):601-4.
Mitral regurgitation (MR) is frequent in patients with severe calcific aortic stenosis (AS). This complicates not only the clinical course of AS, but also its surgical management. The aim of the present study was to investigate the mechanism of genesis of MR in patients with severe AS.
The echocardiographic database was searched for subjects with severe AS defined as a calculated (continuity equation) aortic valve area < 0.7 cm2. Patients with previous valve surgery were excluded; thus, the study group comprised 123 patients.
Among 123 patients (mean age 75 +/- 10 years) with severe AS, 54 (44%) had no MR, 37 (30%) had mild MR, 20 (16%) had moderate MR, and 12 (10%) had severe MR. Hence, moderate or severe MR was present in approximately 25% of patients. Patients with moderate or severe MR had a larger left ventricular (LV) end-diastolic diameter (5.1 +/- 1.0 versus 4.8 +/- 0.8 cm; p = 0.08), larger LV end-systolic diameter (3.8 +/- 1.2 versus 3.1 +/- 0.8 cm; p = 0.001), lower LV ejection fraction (40 +/- 16 versus 58 +/- 18%; p = 0.0001), higher degree of aortic regurgitation (p = 0.002), larger left atrial diameter (4.7 +/- 0.9 versus 4.1 +/- 0.6 cm; p = 0.001), lower LV free wall thickness (1.1 +/- 0.2 versus 1.3 +/- 0.4 cm; p = 0.05), and lower combined wall thickness (2.4 +/- 0.3 versus 2.7 +/- 0.5 cm; p = 0.02) and relative wall thickness (0.5 +/- 0.1 versus 0.6 +/- 0.1 cm; p = 0.02). Both groups had similar degrees of AS and mitral annular calcification.
MR in severe AS is associated with a larger LV size and lesser wall thickness, and this may result from failure of adequate adaptive LV hypertrophy necessitated by the pressure overload imposed by AS. This might have important clinical implications in terms of timing of aortic valve replacement before the left ventricle begins to dilate, and also in the choice of pharmacologic therapy that may modulate the adaptive response of the left ventricle.
二尖瓣反流（MR）在重度钙化性主动脉瓣狭窄（AS）患者中很常见。这不仅使AS的临床病程复杂化，也使其外科治疗变得复杂。本研究的目的是探讨重度AS患者中MR的发生机制。
在超声心动图数据库中搜索重度AS患者，重度AS定义为通过连续方程计算的主动脉瓣面积<0.7cm²。排除既往有瓣膜手术史的患者；因此，研究组包括123例患者。
在123例重度AS患者（平均年龄75±10岁）中，54例（44%）无MR，37例（30%）有轻度MR，20例（16%）有中度MR，12例（10%）有重度MR。因此，约25%的患者存在中度或重度MR。中度或重度MR患者的左心室（LV）舒张末期直径较大（5.1±1.0对4.8±0.8cm；p = 0.08），LV收缩末期直径较大（3.8±1.2对3.1±0.8cm；p = 0.001），LV射血分数较低（40±16对58±18%；p = 0.0001），主动脉反流程度较高（p = 0.002），左心房直径较大（4.7±0.9对4.1±0.6cm；p = 0.001），LV游离壁厚度较低（1.1±0.2对1.3±0.4cm；p = 0.05），联合壁厚度较低（2.4±0.3对2.7±0.5cm；p = 0.02）和相对壁厚度较低（0.5±0.1对0.6±0.1cm；p = 0.02）。两组的AS程度和二尖瓣环钙化程度相似。
重度AS中的MR与较大的LV大小和较小的壁厚度相关，这可能是由于AS施加的压力过载所必需的适当适应性LV肥厚失败所致。这在左心室开始扩张之前进行主动脉瓣置换的时机方面以及在可能调节左心室适应性反应的药物治疗选择方面可能具有重要的临床意义。
