Department of Cardiovascular Medicine, Graduate School of Medicine, Kagoshima University, Kagoshima, Japan.
J Thorac Cardiovasc Surg. 2010 Sep;140(3):617-23. doi: 10.1016/j.jtcvs.2009.11.003. Epub 2010 Feb 1.
Diastolic subvalvular mitral leaflet tethering by left ventricular remodeling that restricts leaflet opening in the presence of annular size reduction by surgery for ischemic mitral regurgitation potentially causes functional mitral stenosis in the absence of organic leaflet lesions. Exercise, known to worsen systolic tethering and ischemic mitral regurgitation, might also dynamically exacerbate such mitral stenosis by increasing tethering. This study evaluates the mechanism and response of such mitral stenosis to exercise.
We measured the diastolic mitral valve area, annular area, and peak and mean transmitral pressure gradient by echocardiography in 20 healthy individuals and 31 patients who underwent surgical annuloplasty for ischemic mitral regurgitation.
Although the mitral valve area and annular area did not significantly differ in healthy individuals (4.7 +/- 0.6 cm(2) vs 5.2 +/- 0.6 cm(2), not significant), mitral valve area was significantly smaller than the annular area in patients after annuloplasty (1.6 +/- 0.2 cm(2) vs 3.3 +/- 0.5 cm(2), P < .01). The mitral valve area was less than 1.5 cm(2) only after the surgery (P < .01) and was significantly correlated with restricted leaflet opening (r(2) = 0.74, P < .001), left ventricular dilatation (r(2) = 0.17, P < .05), and New York Heart Association functional class (P < .05). Exercise stress echocardiography of 12 patients demonstrated dynamic worsening in functional mitral stenosis (mitral valve area: 2.0 +/- 0.5 cm(2) to 1.4 +/- 0.2 cm(2), P < .01; mean pressure gradient: 1.5 +/- 0.9 mm Hg to 6.0 +/- 2.2 mm Hg, P < .01).
Persistent subvalvular leaflet tethering in the presence of annular size reduction by surgery in ischemic mitral regurgitation frequently causes functional mitral stenosis at the leaflet tip level, which is related to heart failure symptoms and can be dynamic with significant exercise-induced worsening.
左心室重构导致二尖瓣下叶瓣叶游离壁在瓣环缩小时发生牵张,限制瓣叶开放,从而导致缺血性二尖瓣反流患者手术治疗后出现功能性二尖瓣狭窄,而瓣叶本身并无器质性病变。运动已知会加重收缩期牵张和缺血性二尖瓣反流,也可能通过增加牵张作用而使二尖瓣狭窄加重。本研究旨在评估这种二尖瓣狭窄的机制和对运动的反应。
我们对 20 名健康个体和 31 名因缺血性二尖瓣反流而行手术瓣环成形术的患者进行了超声心动图检查,测量了舒张期二尖瓣瓣口面积、瓣环面积、二尖瓣口峰值和平均跨瓣压力梯度。
虽然健康个体的二尖瓣瓣口面积和瓣环面积无显著差异(4.7 ± 0.6 cm² vs. 5.2 ± 0.6 cm²,无统计学意义),但瓣环成形术后患者的二尖瓣瓣口面积明显小于瓣环面积(1.6 ± 0.2 cm² vs. 3.3 ± 0.5 cm²,P <.01)。仅在手术后,二尖瓣瓣口面积才小于 1.5 cm²(P <.01),并且与瓣叶开放受限显著相关(r² = 0.74,P <.001)、左心室扩张(r² = 0.17,P <.05)和纽约心脏协会心功能分级(P <.05)。12 例患者的运动负荷超声心动图显示功能性二尖瓣狭窄明显恶化(二尖瓣瓣口面积:2.0 ± 0.5 cm²至 1.4 ± 0.2 cm²,P <.01;平均压力梯度:1.5 ± 0.9 mm Hg 至 6.0 ± 2.2 mm Hg,P <.01)。
缺血性二尖瓣反流患者手术治疗后瓣环缩小时持续存在瓣下叶瓣叶游离壁牵张,常导致瓣尖水平出现功能性二尖瓣狭窄,与心力衰竭症状有关,并可能因剧烈运动而明显恶化。