An unusual complication during alcohol septal ablation: severe left anterior descending artery vasospasm causing cardiac arrest: a case report and review of the literature

Abstract

Abstract Background Septal reduction therapy can be considered along the lines of hypertrophic obstructive cardiomyopathy patients who have drug-refractory symptoms. This can be applied either surgical myectomy or either alcohol septal ablation (ASA). Alcohol septal ablation has been performed successfully since the first announcement of ASA in 1995. Case summary We present a case report of coronary artery vasospasm that occurred in the left anterior descending artery (LAD) during ASA. We performed ASA via first septal artery. Two cubic centimetre of 99% ethanol was slowly injected and 10 min later balloon was withdrawn. Then the patient felt severe chest pain; his systolic blood pressure went down quickly and fibrillated. We started the cardiopulmonary resuscitation (CPR). After CPR, the rhythm was achieved total 4 min later cardiac arrest but blood pressure was low. Emergent coronary angiography showed that coronary spasm caused severe occlusion in the LAD segment just after the first septal artery and impaired coronary flow nearly totally in the LAD just after septal artery. At that time, we decided to implant a stent due to the patient’s serious condition and a 3.5 × 18 mm drug-eluting stent was implanted. We performed control angiography to patient 3 days later of the procedure and LAD flow was TIMI 3. Discussion The causes of LAD occlusion are alcohol leakage, dissection, and vasospasm. It is important to detect the correct reason for appropriate treatment. Alcohol leakage impairs and causes coronary flow disruption; this can cause ventricular wall motion abnormalities. In our case, there was severe spasm in the LAD coronary artery and LAD flow was severely impaired. On echocardiogram, there was no myocardial wall motion abnormality. So alcohol leakage was ruled out. Left anterior descending artery image was not typical dissection. As a result of these findings, we concluded that the cause of LAD occlusion was coronary artery vasospasm.