Coronary-Subclavian Steal Syndrome: Percutaneous Approach

Coronary subclavian steal syndrome is a rare ischemic cause in patients after myocardial revascularization surgery. Subclavian artery stenosis or compression proximal to the internal mammary artery graft is the underlying cause. The authors present a clinical case of a patient with previous history of non-ST elevation myocardial infarction, triple coronary bypass, and effort angina since the surgery, with a positive ischemic test. Coronary angiography revealed a significant stenosis of the left subclavian artery, proximal to the internal mammary graft. 1. Introduction The coronary subclavian steal syndrome (CSSS) was first described in 1974 and is caused by retrograde or insufficient blood flow through the internal mammary artery graft, with subsequent myocardial ischemia. Proximal atherosclerotic stenosis of the ipsilateral subclavian artery is the most frequent cause [1]. Although most cases of angina after coronary bypass graft surgery (CABG) are due to native-vessel or graft atherosclerotic disease progression, this syndrome should not be disregarded [2]. The traditional approach for this problem is surgical revascularization of the subclavian artery with a bypass graft, but percutaneous transluminal subclavian artery angioplasty has emerged as an effective alternative to surgery and it is now a widely accepted method of treating symptomatic subclavian steal syndrome. 2. Case Report The authors present the case report of a 69-year-old male patient with several cardiovascular risk factors (hypertension, hyperlipidaemia, and previous smoking) and history of coronary artery bypass grafting (CABG) 6 years before when the left internal mammary artery (LIMA) was grafted to the left anterior descending artery (LAD), saphenous vein conduit was grafted to posterior descendent artery and left radial artery grafted to the intermediary branch. No medical imaging of the aortic arch and its branches was performed before cardiac surgery. He had recurrence of angina following the surgery (CCS class II) mainly when exerting the upper limbs. His therapy was adjusted and remained only mildly symptomatic until 2011 when he was referred to for coronary angiography because of gradually worsening exertional angina with no response to medical therapy. There were no neurological or claudication complaints. Physical examination only showed an II/VI systolic murmur. Basal EKG and blood analysis were unremarkable. On the transthoracic echocardiogram, there was only mild aortic sclerosis and good global and segmental systolic left ventricle function. He had a positive exercise