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Transcatheter aortic valve implantation (TAVI) has shown favorable outcomes in patients with severe symptomatic aortic valve stenosis who are at high surgical risk or inappropriate for open heart surgery. However, concerns exist over treating patients who have porcelain aorta and familial hypercholesterolemia, due to the potential complications of aortic root and aortic annulus. In this case report, we present a patient with familial hypercholesterolemia, symptomatic severe aortic stenosis, previous coronary artery bypass grafting and porcelain aorta, who was successfully treated with TAVI using a CoreValve.

Methods: A 63-year-old-woman was admitted to the emergency department with complaints of palpitation, breathlessness and dizziness. At the admission she was conscious and her systolic blood pressure was 80mmhg. At the ECG there was sustained ventricular tachycardia (Figure 1). In the ED, because of hemodynamic impairment, defibrillation with 30 j was performed and sinus rhythm was restored. After 600mg loading dose of amiodorone, intravenous maintenance therapy was continued. At the same hour two non-sustained ventricular tachycardia attacks happened. Her biochemical parameters demonstrated a potasium concentration of 2.8mmol/L, creatinine 0.8mg/dl (0.72–1.25) and sodium 137mmol/L (136–145). Transthoracic echocardiography was performed and ejection fraction was found 60% and other measurements were normal. 60mEq/L potassium replacement was given to the patient and the control potassium was 3.7mmol/L. The patient had been using amlodipine 10mg, indapamide 1.5mg and acetylsalicylic acid 100mg per day for ten years because of hypertension. The patient was complaining from intermittent chest pain so coronary angiography was performed and normal coronary arterial anatomy was observed. It was thought that VT had occurred because of hypokalemia induced by indapamide so indapamide treatment was stopped. The K was 4.5mmol/L after one week follow up. The patient was followed-up in the coronary care unit and was discharged on the eighth day of admission without any VT attacks. Conclusions: Clinicians should keep in mind that the antihypertensive drug indapamine can cause life threatening ventricular tachycardias because of its hypokalemia side effect. Therefore we emphasize that serum potassium and ECG must be carefully monitored during indapamide therapy.