Case Report and Brief Review

Anterolateral Myocardial Infarction Induced by Coronary-
Subclavian-Vertebral Steal Syndrome Successfully Treated with

*Reji Pappy, MD, §Thomachan Kalapura, MD, MRCP, §Thomas A. Hennebry, MB, BCh BAO, MD
*Reji Pappy, MD, §Thomachan Kalapura, MD, MRCP, §Thomas A. Hennebry, MB, BCh BAO, MD

Coronary-subclavian-steal syndrome (CSSS) is a known cause of myocardial infarction. This entity has been observed in individuals who present with angina. However, this case is unique because this is the first reported patient presenting not only with angina, but also with an anterolateral non-STsegment elevation myocardial infarction (NSTEMI) from CSSS, and at the same time experiencing dizziness from vertebral subclavian steal (VSS), an entity together called coronarysubclavian- vertebral steal syndrome (CSVSS). This patient had angiographic evidence of retrograde blood flow (“steal”) through both the left internal mammary artery (LIMA) graft and the left vertebral artery due to occlusion of the proximal left subclavian artery. The “steal” from the LIMA graft lead to the NSTEMI. Stenting of only the subclavian artery, without any intervention in the coronary arterial tree, led to restoration of antegrade blood flow through the LIMA graft and left vertebral artery, which resulted in complete resolution of the cardiac and neurological symptoms experienced by the patient and to normalization of the observed electrocardiographic (ECG) changes.

Patients with CSVSS have been reported to concomitantly present with symptoms and signs of vertebrobasilar insufficiency from retrograde blood flow in the vertebral artery (blurry vision, nausea, vertigo, syncope, ataxia, dysarthria, diplopia, headache, focal seizures, confusion, and rarely, stroke) and symptoms and signs of coronary insufficiency (“silent” ischemia, angina, congestive heart failure, or myocardial infarction) from retrograde blood flow in the LIMA graft, both of which are due to proximal subclavian artery stenosis. Signs and symptoms of subclavian stenosis or occlusion include weakness, paresthesias, coldness and intermittent claudication of the ipsilateral exercising arm, weak radial or ulnar pulses, supraclavicular bruits, blood pressure differences in the upper extremities of usually > 20 mmHg and extremity microembolization.

Case Description. A 49-year-old Caucasian female with a history of two-vessel coronary artery bypass grafting (CABG) in 1999 (left internal mammary artery graft to the left anterior descending artery and saphenous venous graft to the 1st diagonal artery), hypertension, peripheral vascular disease, hyperlipidemia and tobacco use presented in April 2005 with a 3-year history of left arm claudication, tingling and numbness at rest and on arm exercise and vertigo when ambulating. In addition, she had experienced angina during the previous 2–3 days. On physical examination, there was a systolic blood pressure difference in the bilateral upper extremities of 60 mmHg (left < right). An ECG revealed deep, symmetric T-wave inversions in V2–V6, I and aVL (Figure 1). Her creatine clearance was normal, and cardiac injury markers were elevated with a troponin 1 of 2.31, which subsequently normalized after intervention. Doppler studies revealed patent bilateral vertebral and carotid arteries. An echocardiogram revealed hypokinesis of the anterolateral wall and severe hypokinesis of the apex. This presentation was consistent with an anterolateral NSTEMI.

The patient was referred for cardiac catheterization, where adigital subtraction arch aortogram revealed a 100% ostial left subclavian artery occlusion (Figure 2). There was also retrograde blood flow in the left vertebral and LIMA (Figure 3), which was consistent with CSVSS. An 8 Fr multipurpose catheter was used for engagement of the left subclavian stump, then with the use of a J-ed angled Glidewire® (Terumo Corporation, Somerset, New Jersey) and a QuickCross Spectranetics sheath (Spectranetics Corporation, Colorado Springs, Colorado), the lesion was crossed. After confirmation of location in the distal lumen by contrast injection, the proximal subclavian artery was dilated to 12 atm using a 6 x 40 mm Agiltrac balloon (Abbott Laboratories, Abbott Park, Illinois), and subsequently, a 7 x 28 mm and a 7 x 18 mm Omnilink® stent (Guidant Corporation, Indianapolis, Indiana) were deployed. After successful treatment with balloon angioplasty and stenting of the left subclavian artery, there was no residual pressure gradient across the proximal subclavian artery (Figure 4), and moreover, there was restoration of antegrade blood flow in the left vertebral and left internal mammary arteries (Figure 4) without evidence of competitive flow.

This patient had sustained resolution of left arm claudication, vertebrobasilar dizziness and angina after stenting of the subclavian artery without any intervention done in the coronary arterial tree. At almost 2-year follow up, the subclavian artery remains patent.

Discussion. CSSS was first described in 1974. Since then the incidence of CSSS has gradually increased as the LIMA has become the conduit of choice for CABG. CSSS is observed in 0.5% to 1.1% of those with prior CABG.1 CSSS has been implicated in causing angina in the past, however, only twice has CSSS been reported as leading to an NSTEMI (both in older men) without any report of concomitant VSS.2 Our review of the literature indicates that this is the first case report of a patient presenting with anterolateral NSTEMI and dizziness with subsequent evidence of CSVSS.

The pathophysiology of CSSS parallels that of VSSS. In VSSS, the subclavian artery stenosis is located proximal to the origin of the vertebral artery. Symptoms of vertebrobasilar insufficiency can occur when there is reversal of blood flow (“steal”) in the ipsilateral vertebral artery due to vasodilation, which causes low resistance in the vascular bed supplying the ipsilateral exercising upper extremity. Likewise, in CSSS, the subclavianartery stenosis is located proximal to the origin of the internal mammary artery. Angina pectoris or myocardial infarction can occur when there is reversal of blood flow (“steal”) in the internal mammary artery due to vasodilation and the resulting low resistance in the vascular bed supplying the ipsilateral exercising upper extremity.

Other reported causes of coronary steal leading to angina pectoris include patients with LITA-PA (left internal thoracic artery-pulmonary artery) fistulae,3 coronary artery fistulae,4 left upper extremity arteriovenous fistulae on hemodialysis,5 and a LIMA side branch “stealing” blood flow to the LAD post-CABG.6

Atherosclerotic disease is the most common cause implicated in subclavian stenosis. Other entities associated with subclavian occlusion or stenosis include fibromuscular dysplasia, radiation arteritis, Takayasu’s disease, giant-cell arteritis, Behçet’s disease, tumor encasement, thromboembolism, trauma and dissecting aortic arch aneurysm.

Diagnostic modalities that have been used to detect subclavian arterial disease prior to placement of a LIMA graft include arteriography (gold standard), duplex ultrasonography before and after arm exercise, computed tomography angiography and the combination of magnetic resonance imaging and magnetic resonance angiography.7,8 It is imperative to screen every patient for subclavian stenosis with at least bilateral upper extremity blood pressure evaluation and subclavian auscultation when considering using the LIMA as a bypass vessel. Currently, there are several institutions that screen the proximal subclavian artery in all patients undergoing cineangiography of the coronary arteries and then perform an arch aortogram and 4-vessel cerebral angiography if significant subclavian artery disease is found.9–12

Methods that have been reportedly used to treat either CSS or VSS due to subclavian stenosis or occlusion include carotid-subclavian bypass, aorto-subclavian bypass, axilloaxillary artery bypass, transposition of the IMA (internal mammary artery), laser ablation, directional atherectomy, subclavian endarterectomy and angioplasty with or without stenting of the subclavian artery.13,14

With angioplasty and stenting, the initial success rate in stenotic lesions is 98–100%; however, the treatment of total occlusions is more difficult, with acute technical success of 46–84%.15 Long-term durability has been demonstrated with reports of primary patency at 5 years in subclavian artery angioplasty alone of 67%, and with stenting, it is approximately 76%.16,17 In carotid-subclavian bypass, the 5-year bypass graft patency rate is 58–78%.18

Complications of endovascular treatment of subclavian artery stenosis occur in 5–14% of cases and are usually less fatal and not as prolonged as complications of surgical treatment that occur in 5–20% of cases with a 5% mortality rate.18–21 In the contemporary era, stenting for subclavian artery occlusion has favorable immediate and late clinical outcomes and is associated with low morbidity, short hospitalization and a high rate of success.19–21

Further investigation is reasonable to establish cost-effective criteria in selecting patients who would benefit from pre-CABG screening for subclavian artery stenosis, to select patients who would benefit from distal embolization protection devices during angioplasty or stenting, and to identify factors that can be modified to prevent subclavian artery restenosis.



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