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The Subclavian Steal Syndrome Vincent A. Piccone, Jr. and Harry H. LeVeen Ann Thorac Surg 1970;9:51-75 DOI: 10.1016/S0003-4975(10)66110-3

The online version of this article, along with updated information and services, is located on the World Wide Web at: http://ats.ctsnetjournals.org

The Annals of Thoracic Surgery is the official journal of The Society of Thoracic Surgeons and the Southern Thoracic Surgical Association. Copyright 1970 by The Society of Thoracic Surgeons. Print ISSN: 0003-4975; eISSN: 1552-6259.

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COLLECTIVE REVIEW

The Subclavian Steal SyndromeVincent A. Piccone, Jr., M.D., and Harry H. LeVeen, M.D.he subclavian steal syndrome is characterized by cerebral ischemic attacks caused by reversal of blood flow through the vertebral artery consequent to arterial obstruction proximal to the origin of the vertebral artery (Fig. 1). While not a separate disease entity, the subclavian steal syndrome relates cerebral ischemia to a remote vascular lesion which is surgically correctable and more frequent than was anticipated.HISTORY

T

T h e anastomotic channels supplying the subclavian artery beyond a proximal occlusion were well described by the anatomists [54]. Detailed collateral pathways are found in Tagariellos work with dogs and cadavers [94]. Contorni [141 demonstrated the vertebral-basilar-vertebral collateral artery flow with angiograms in human subjects for the first time in 1960. Contrast medium injected into the contralateral brachial artery of an asymptomatic patient with an absent left radial pulse flowed up the right vertebral artery, down the left vertebral artery, and onward to the left subclavian artery just distal to the occlusion. Rob [79], Toole [981, and Fields [29] discussed the siphon of the vertebral collateral artery at the third Princeton Conference on Cerebrovascular Diseases in January, 1961. Thus, while the necessity for brachiad flow in the vertebral collateral artery was recognized, the causal relationship between cerebral ischemic attacks and occlusion of the proximal subclavian artery remained obscure until later in 1961. Then Reivich and associates [78], in several case reports and animal experiments, clearly associated cerebral ischemic attacks with the reversed vertebral flow described by Contorni. At the same time, an editorial in the NewFrom the Departments of Surgery, College of Medicine, State University of New York Downstate Medical Center and Veterans Administration Hospital, Brooklyn, N.Y. Address reprint requests to Dr. Piccone, Department of Surgery, leterans Administration Hospital, Brooklyn, N.Y. 11209.

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PICCONE AND LEVEEN

F I G . 1. Occlusion of the subclavian artery proximal to the vertebral artery causes shunting of blood from the cerebral circulation through the vertebral artery and into the subclavian artery.

England Joul-nal of Medicine [30] endowed the literature with the descriptive term subclavian steal. This nomenclature provoked lively competition typified by such names as brain drain [59], grand larceny of the vertebral for large steals [24], subclavian snitch for small steal [44],and brachial-basilar insufficiency [68]. T h e original, subclavian steal, has endured and has become the accepted name.ANATOMY

T h e anatomical basis for the subclavian steal syndrome is founded in collateral circulation which sustains flow in the subclavian artery after52THE ANNALS OF THORACIC SURGERY

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COLLECTIVE REVIEW:

Subclavian Steal Syndrome

occlusion of the proximal portion. T h e collateral pathways [6, 55, 59, 67, 68, 711 (Fig. 2) include the following:1 . external carotid artery to occipital artery to muscular branches of vertebral artery 2. external carotid artery to superior thyroid artery to inferior thyroid artery to thyrocervical trunk 3. superior epigastric artery, intercostal artery, and contralateral internal mammary artery to ipsilateral internal mammary artery

iimF I G . 2. T h e collateral circulation maintains flow in the subclauian artery aftei occlusion of the proximal portion. T h e m a i n pathways include contralateral uertebial arteries (a) and basilar arteries (b) t o ipsilateral uertebral arteries (c); external carotid artery (d) to superior thyroid artery (e) t o inferior thyroid artery ( f ) to thyrocervical trunk (g); external carotid artery (d) to occipital artery (h) to mttsciilar branches of uertebral arteries (i); aorta to posterior intercostal arteries (j) to sztpwioi intercostal arteries (k) to costocervical trunk (1); and superior epigastrzc arteyy (m) and anterior intercostal arteries (n) t o contralateral internal mammary to urteiy (0) ipsilateral internal mammary artery (p).VOL.

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PICCONE AND LEVEEN

4. aorta and posterior intercostal arteries to superior intercostalartery to costocervical trunk 5 . contralateral vertebral and basilar artery to vertebral artery

The unique and most essential of these collateral routes in terms of flow is the vertebral artery, which is usually the only sizable collateral [71]. Rapid retrograde flow consequent to proximal occlusion of the inflow vessel presupposes large collateral arteries with high pressures and high inflow capabilities. The basilar artery from the circle of Willis and the contralateral vertebral artery do provide this unusually high inflow capability (Fig. 3). The size of the basilar artery is comparable to the vertebral arteries and connects directly with each. The posterior communicating branches of the internal carotid arteries are also vessels of substantial size. High flows are thus directed into a low pressure system with almost no resistance in the shunt. Interruption of the subclavian artery proximal to the vertebral artery thus poses little threat of ischemia to the upper limb but diverts significant amounts of blood from the brain.HEMODYNAMICS

The hemodynamic changes in the subclavian steal syndrome have been studied experimentally in dogs and monkeys and are now well documented in man. Occlusive disease proximal to the origin of theA n t e r i o r communicating

Posterior

aSuperior cerebr

rior c e r e b r a l

Anterior spinal

F I G . 3 . Circle of Willis and uertebral-basilar axis, showing the large inflow urssels that make the subclauian steal possible.

54

THE ANNALS OF THORACIC SURGERY

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vertebral artery reduces the pressure in the subclavian artery distal to the obstruction. When the pressure at the subclavian end of the vertebral artery drops below the basilar artery pressure, the vertebral artery flow is reversed. Diversion of basilar artery blood can be of such magnitude that symptoms of cerebral ischemia ensue. Reivich and associates [78] used an electromagnetic flowmeter to show that a subclavian pressure 10% less than systemic arterial pressure would reverse flow in the vertebral artery. Sammartino and Toole [82] demonstrated reversal of flow in the vertebral artery immediately after establishment of a systemic-subclavian pressure differential exceeding 2 1 to 40 mm. Hg. A 50% reduction in the lumen of the subclavian or innominate artery is necessary to produce the critical pressure gradient of 10% 1173. Berger and associates [4] found that a 65 mm. Hg pressure differential across the stenotic lesion produced a reversed flow of 29 ml. per minute in a patient with a subclavian steal syndrome. Significant stenotic lesions of the subclavian artery without the steal phenomenon were noted by Gonzalez and associates [36], who suggested that the degree of participation of the vertebral artery as a collateral may be variable and depends, among other things, upon the inflow from the other collateral pathways. Regional hemodynamic changes have been measured in monkeys by multiple electromagnetic flowmeters. T h e reversed flow through the vertebral artery was greater than the normal forward flow [39]. When vertebral flow was reversed, flow in the contralateral vertebral artery and both carotid arteries showed marked compensatory increases, but the total cerebral flow, measured by summation of flowmeter readings and internal jugular vein drainage, was slightly decreased. When the posterior communicating branches of the middle cerebral artery were occluded, the compensatory increase in internal carotid flow was almost abolished, thus demonstrating the major role of these vessels in the collateral circuit [39]. Quantitative measurements in man show similar changes in cerebral hemodynamics. Hardesty and associates [40, 411 measured flow in the carotid and vertebral arteries of patients undergoing radical neck dissection. T h e average internal carotid artery flow was 370 ml. per minute, and the average vertebral artery flow was 45 ml. per minute (1 1% of the total cerebral artery flow). T h e total cerebral artery flow in patients under anesthesia was 830 ml. per minute. Kety and Schmidt [49] obtained a figure of 750 ml. per minute. Hardesty et al. [41] occluded the subclavian artery proximal to the origin of the vertebral artery and found a retrograde flow through the vertebral artery of 25 to 98 ml. per minute and a compensatory increase of 25 to 60 ml. per minute through the internal carotid artery. Reversed vertebral flow only partially compensates for the normalVOL.

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PICCONE AND LEVEEN