Department of Medicine and Geriatrics, Kochi Medical School, Kochi, Japan.
J Cardiol. 2010 Jan;55(1):125-9. doi: 10.1016/j.jjcc.2009.03.013. Epub 2009 May 9.
A 66-year-old woman was referred for further evaluation and treatment of normocytic and normochromic anemia with hemoglobin level of 8.6 g/dL. A peripheral blood smear showed fragmented erythrocytes. The patient was then referred to the department of cardiology because of systolic murmur, ECG abnormality, and red cell fragmentation. Transthoracic echocardiography revealed hypertrophic cardiomyopathy with particularly increased interventricular septal thickness of 24 mm and a hyperkinetic wall motion, resulting in marked obstruction to left ventricular outflow tract (pressure gradient of 200 mmHg). Mitral regurgitation due to systolic anterior motion of the mitral valve leaflets was also seen. The cause of anemia was thought to be mechanical intravascular hemolysis due to left ventricular outflow tract obstruction and mitral regurgitation. She was treated with atenolol and the class Ia antiarrhythmic drug cibenzoline to relieve the outflow tract obstruction, and the pressure gradient was reduced to 70 mmHg. After 3 months of treatment, her hemoglobin level had increased to 11.4 g/dL without additional treatment for anemia.
一位 66 岁女性因正细胞正色素性贫血（血红蛋白水平 8.6 g/dL）就诊，寻求进一步评估和治疗。外周血涂片显示破碎红细胞。患者因收缩期杂音、心电图异常和红细胞破碎而被转至心内科。经胸超声心动图显示肥厚型心肌病，室间隔厚度明显增加至 24mm，且室壁运动呈高动力性，导致左心室流出道严重梗阻（压力阶差 200mmHg）。还可见因二尖瓣前叶收缩期前向运动导致的二尖瓣反流。贫血的原因被认为是由于左心室流出道梗阻和二尖瓣反流导致的机械性血管内溶血性贫血。给予患者阿替洛尔和 Ia 类抗心律失常药物西苯唑啉治疗以缓解流出道梗阻，压力阶差降低至 70mmHg。治疗 3 个月后，她的血红蛋白水平升至 11.4g/dL，未再进行贫血的额外治疗。
