Although females with MYBPC3 mutations showed later onset of the disease, female patients were more symptomatic at diagnosis and had more frequent heart failure events once they had developed hypertrophy.
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.
An elderly woman was admitted to our hospital for evaluation of an abdominal aortic aneurysm (AAA) and we decided to treat her AAA with endovascular aneurysm repair. Her renal function became worse after the operation and a renogram suggested flow disturbance of her right renal artery. We performed angiography and checked her right renal artery using intravascular ultrasound. The ultrasound revealed thrombus formation and severe stenosis caused by the stent graft. We performed percutaneous transluminal renal angioplasty at the ostium of her right renal artery. After this procedure, her renal function rapidly improved.
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