Cerfolio R J, Orszulak T A, Daly R C, Schaff H V
Section of Cardiovascular Surgery, Mayo Clinic, Rochester, MN 55905, USA.
Eur J Cardiothorac Surg. 1997 Mar;11(3):479-84. doi: 10.1016/s1010-7940(96)01091-3.
To identify the possible cause(s) of hemolysis after mitral valve repair for mitral regurgitation (MR) and to evaluate the late outcome of surgical treatment.
We reviewed all patients who had reoperation after valve repair for mitral regurgitation. Ten patients had reoperation because of hemolytic anaemia. The diagnosis of hemolysis was made by decreased serum haptoglobin, elevation of serum lactate dehydrogenase (LDH), and schistocytosis. No other causes of anaemia or hemolysis were identified in these six men and four women (ages 35-84 years; median 59 years). Interval between initial mitral valve repair and reoperation ranged from 40 to 165 days (median 87 days), and prior to reoperation, red cell transfusions (range 2-12 units; median 5 units) were required in all patients. Seven patients were symptomatic: two complained of easy fatigability and five were severely limited. Transesophageal echocardiogram during hemolytic evaluation showed only mild MR in two patients, moderate in five, moderately severe in two and severe in one.
Etiology of hemolysis was suggested from echocardiography and confirmed at reoperation. In one patient, an eccentric MR jet struck a pledget of a commissural annuloplasty. In the remaining nine patients, the regurgitant jet struck a non-endothelialized portion of the annuloplasty ring (Carpentier-Edwards n = 5; Duran n = 2; Cosgrove-Edwards n = 2). Seven patients had prosthetic replacement and three patients had re-repair. There were no operative deaths and all patients had resolution of hemolytic anaemia.
Relatively minor degrees of regurgitation after mitral valve repair can produce hemolytic anaemia which is manifested within the first few postoperative months. Most patients are highly symptomatic because of anaemia. The mechanism of red cell destruction is a high velocity eccentric stream of blood impacting on a small area of a prosthetic ring or pledget. This process retards endothelialization of the ring. Reoperation with re-repair or mitral valve replacement is safe and effectively relieves the hemolysis.
确定二尖瓣反流（MR）二尖瓣修复术后溶血的可能原因，并评估手术治疗的远期效果。
我们回顾了所有二尖瓣反流瓣膜修复术后再次手术的患者。10例患者因溶血性贫血再次手术。溶血的诊断依据血清触珠蛋白降低、血清乳酸脱氢酶（LDH）升高和破碎红细胞增多。这6名男性和4名女性（年龄35 - 84岁；中位数59岁）未发现其他贫血或溶血原因。初次二尖瓣修复与再次手术的间隔时间为40至165天（中位数87天），所有患者在再次手术前均需要输注红细胞（范围2 - 12单位；中位数5单位）。7例患者有症状：2例主诉易疲劳，5例严重受限。溶血评估期间的经食管超声心动图显示，2例患者仅有轻度MR，5例为中度，2例为中重度，1例为重度。
超声心动图提示溶血病因并在再次手术时得到证实。1例患者，偏心的MR血流束冲击连合瓣环成形术的垫片。其余9例患者，反流束冲击瓣环成形环的非内皮化部分（Carpentier - Edwards型n = 5；Duran型n = 2；Cosgrove - Edwards型n = 2）。7例患者进行了人工瓣膜置换，3例患者进行了再次修复。无手术死亡，所有患者的溶血性贫血均得到缓解。
二尖瓣修复术后相对较小程度的反流可导致溶血性贫血，在术后最初几个月内出现。大多数患者因贫血症状严重。红细胞破坏的机制是高速偏心血流冲击人工瓣环或垫片的小面积区域。这个过程会阻碍瓣环的内皮化。再次手术进行再次修复或二尖瓣置换是安全的，可有效缓解溶血。
