REVIEWS
Myocardial Thievery: The Coronary-Subclavian
Steal Syndrome
Thomas J. Takach, MD, George J. Reul, MD, Denton A. Cooley, MD,
J. Michael Duncan, MD, James J. Livesay, MD, David A. Ott, MD, and
Igor D. Gregoric, MD
Department of Cardiovascular Surgery, The Texas Heart Institute at St. Lukes Episcopal Hospital, Houston, Texas
Coronary-subclavian steal syndrome entails the reversal
of blood flow in a previously constructed internal mam-
mary artery coronary conduit, which produces myocar-
dial ischemia. The most frequent cause of the syndrome
is atherosclerotic disease in the ipsilateral, proximal
subclavian artery. Although coronary-subclavian steal
was initially reported to be rare, the increasing documen-
tation of this phenomenon and its potentially cata-
strophic consequences in recent series suggests that the
incidence of the problem has been underreported and
C oronary-subclavian steal (CSS) was once believed to
be rare, but the increasing documentation of this
phenomenon and its potentially catastrophic conse-
quences suggests that the incidence of CSS has been
underreported and that its clinical impact has been
REVIEWS
underestimated. In this study, we review the causes and
background of CSS; methods of preventing, diagnosing,
and treating it; and the potential influence of various
treatment regimens on long-term survival and the like-
lihood of late adverse events in patients with CSS
syndrome.
Patients and Methods
The Ovid and PubMed search engines were used to
search the National Library of Medicines Medline data-
base for published English-language case reports and
series in which CSS is described. Search terms used to
identify these studies included coronary-subclavian
steal and coronary-subclavian steal syndrome; ath-
erosclerosis combined with innominate artery, com-
mon carotid artery, subclavian artery, or great ves-
sels; and brachiocephalic combined with vessels,
atherosclerosis, bypass, endovascular procedure,
transposition, stenosis, imaging, or concomitant
coronary artery disease. All case series found were
included in the review; reports of individual cases were
included if they were unique in terms of clinical presen-
tation, diagnosis, management, or outcome.
Address correspondence to Dr Cooley, Department of Cardiovascular
Surgery, The Texas Heart Institute, PO Box 20345, Houston, TX 77225;
e-mail: dcooley@heart.thi.tmc.edu.
2006 by The Society of Thoracic Surgeons
Published by Elsevier Inc
that its clinical impact has been underestimated. We
review the causes and background of coronary-subcla-
vian steal; methods of preventing, diagnosing, and treat-
ing it; and the potential influence of various treatment
regimens on long-term survival and the likelihood of late
adverse events in patients with coronary-subclavian steal
syndrome.
(Ann Thorac Surg 2006;81:386 92)
2006 by The Society of Thoracic Surgeons
Background
Coronary-subclavian steal syndrome is defined as a
reversal of flow in a previously constructed internal
mammary artery (IMA) coronary conduit, producing
myocardial ischemia. Typically, CSS syndrome is
caused by proximal subclavian artery stenosis in pa-
tients with an ipsilateral IMA coronary conduit. The
anatomic findings, physiologic alterations, and patho-
logic consequences were initially described by Harjola
and Valle [1] in 1974. In their report on a patient who
presented with angina after an otherwise successful
coronary artery bypass grafting (CABG) procedure, the
authors stated that the anatomic, physiologic, and
clinical associations among their findings represented
a distinct clinical entity. Within 3 years, others applied
the name coronary-subclavian steal syndrome to the
process after recognizing the similarities between the
pathologic mechanisms of this syndrome and those of
the previously recognized vertebral-subclavian steal
syndrome that produces vertebrobasilar insufficiency
[2, 3].
As initially described more than 30 years ago, proximal
subclavian artery stenosis, which is the most common
cause of CSS, is usually caused by atherosclerotic disease
[13]. However, several other pathologic processes can
also compromise the subclavian artery flow to cause CSS,
including Takayasus arteritis [4, 5], radiation arteritis [6],
and giant cell arteritis [7]. Furthermore, absence of a
proximal subclavian artery stenosis does not preclude
the occurrence of CSS; the reversal of IMA coronary
conduit flow and the subsequent myocardial ischemia
that comprise the CSS syndrome have been reported to
occur in association with an upper-extremity hemodial-
ysis fistula [8 10] and an anomalous connection of the
0003-4975/06/$32.00
doi:10.1016/j.athoracsur.2005.05.071
Ann Thorac Surg REVIEW TAKACH ET AL 387
2006;81:386 92 CORONARY-SUBCLAVIAN STEAL SYNDROME

Table 1. Selected Series: Coronary-Subclavian Steal

Recurrent
Coronary-Subclavian Mean
Institution Year No. Treatment Method Steal (N) Follow-up Reference

Texas Heart Institute 2005 32 PTA: 27; bypass: 5 1 3.2 y [20]

a
Charleston Area Medical Center 2004 27 PTA: 27 3.1 y [26]
Arizona Heart Institute 2003 9 PTA: 9 2 2.4 y [16]
Albany Medical College 2003 10 Bypass:10 0 3.5 y [47]
University of Virginia 2003 18 PTA: 18 2 2.3 y [25]
Sheba Medical Center (Israel) 2002 7 PTA: 7 0 1.4 y [27]
University of Florida 2001 4 Bypass: 3 0 none [32]
University Hospitals Homburg/Saar (Germany) 2001 2 PTA: 2 0 none [29]
b
Polyclinique Essey-les-Nancy (France) 1999 6 PTA: 6 4.3 y [30]
c
Mayo Clinic 1998 27 PTA: 27 1.2 y [23]
St. Antonius Hospital (Netherlands) 1996 10 PTA: 10 1 3.1 y [33]
WDIF Foundation (Milwaukee) 1995 6 PTA: 6 0 none [31]
University of Connecticut 1995 4 PTA: 4 0 3.3 y [28]
Emory University 1995 5 Bypass: 4 0 1.7 y [19]
a
Recurrence not reported for coronary-subclavian steal subgroup alone. Total recurrence (all brachiocephalic vessels) 14.6% (13 of 89); mean follow-up,
3.1 years. b
Recurrence not reported for coronary-subclavian steal subgroup alone. Total recurrence (all brachiocephalic vessels) 15.5% (16 of 103);
c
mean follow-up, 4.3 years. Recurrence not reported for coronary-subclavian steal subgroup alone. Total subclavian artery failure (initial failure plus
recurrent stenosis) 10.6% (7 of 66); mean follow-up, 1.2 years.

PTA percutaneous transluminal angioplasty; WDIF William Dorros-Isadore Feuer (Interventional Cardiovascular Disease Foundation, Ltd.).

left subclavian artery to the pulmonary artery in d-
transposition of the great arteries [11].
Presentation
Although CSS has significant consequences, its clinical
of an ipsilateral IMA coronary conduit or to recognize the
progression of brachiocephalic disease after placement of
an ipsilateral IMA coronary conduit may lead to the
development of CSS and myocardial ischemia [24]. Initial
reports detailing the causes and clinical manifestations of

impact was not fully appreciated until recently. Initial
reports suggested that most patients with primary and
recurrent CSS experience angina [1216]. However, re-
cent reports of CSS cases increasingly note silent
ischemia [17], congestive heart failure [16, 18 20], isch-
emic cardiomyopathy [20, 21], and myocardial infarction
[22, 23] as presenting cardiac symptoms. Therefore, it is
likely that early cases of the most severe manifestations
of CSS syndrome went unrecognized, leading to an
underappreciation of both the incidence and the poten-
tial clinical impact of CSS [20]. In patients with known
coronary artery disease and a history of coronary revas-
cularization, sudden death or myocardial infarction is
likely to be attributed to the more commonly occurring
progressive, native-vessel coronary artery disease rather
than to unrecognized or progressive great vessel disease
that can produce ischemia. Sullivan and colleagues [23]
recently reported that of their 27 patients with CSS, 16
(59.3%) presented with stable angina and 11 (40.7%)
presented with unstable coronary syndromes, including
4 acute myocardial infarctions.
Incidence
Although an early study by Brown [2] suggested that the
incidence of significant brachiocephalic disease in pa-
tients who undergo elective CABG is 0.5% to 2.0%, a
more recent study reports that the incidence of concom-
itant disease is 0.1% to 0.2% [20]. Nonetheless, failure to
identify significant subclavian disease before placement
REVIEWS
CSS described the problem as rare [3, 24]. However,
several recent reports involving larger numbers of pa-
tients show that CSS is more common than was initially
appreciated (Table 1). These findings suggest that in a
busy cardiothoracic program, approximately 2 to 4 cases
per year may be found [16, 19, 20, 23, 2533].
Several factors contributed to an early underestimation
of the incidence of CSS. These factors included the less
frequent general use of IMA conduits during the time
period that followed the recognition of CSS as a distinct
clinical entity, the initial lack of development and subse-
quent low availability of noninvasive methods for diag-
nosis of concomitant brachiocephalic disease, the failure
to apply effective diagnostic methods, a limited aware-
ness of the problem, the lack of effective preoperative
screening for concomitant brachiocephalic disease before
CABG, and a tendency to attribute the most severe
manifestations of CSS syndrome to other causes. The
documentation of larger numbers of patients with CSS
during the last 10 years (Table 1) reflects an increased
awareness of the problem and the application of more
effective diagnostic methods.
Screening and Diagnosis
The identification of anatomic findings that may lead to
CSS, the physiologic alterations of early CSS, and the
pathologic changes of CSS syndrome will significantly
influence the management and outcome of patients in
several clinical settings. These include patients about to
 388 REVIEW TAKACH ET AL
CORONARY-SUBCLAVIAN STEAL SYNDROME
Fig 1. Brachiocephalic disease symptoms. Common carotid artery
disease may compromise flow or produce emboli that affect the ante-
rior cerebral circulation, producing neurologic symptoms. Subclavian
artery disease may affect any of the following: the posterior cerebral
circulation by vertebral-subclavian steal, producing vertebrobasilar
insufficiency; the coronary circulation by coronary-subclavian steal,
producing coronary insufficiency; or the distal brachial circulation,
producing either extremity insufficiency or microembolization. In-
nominate artery disease, if present, may affect either the right sub-
clavian artery circulation or the right common carotid artery circula-
tion, or both. (CHF congestive heart failure; MI myocardial
infarction; TIAs transient ischemic attacks.)
REVIEWS
undergo elective CABG, patients who develop clinical
symptoms after CABG, and patients who have been
treated previously for known CSS.
In patients about to have elective coronary revascular-
ization, significant subclavian or innominate artery dis-
ease is most easily recognized if an upper extremity
blood pressure differential is detected [34]. However,
such a differential is not always found in these patients,
because 31% of patients with brachiocephalic disease
also have significant multivessel disease that may affect
pressures in both upper extremities [35]. Alternative
screening methods that may produce more useful infor-
mation include ultrasonic duplex scanning before and
after arm exercise, and direct angiography, which can be
performed during evaluation of the coronary arteries [36,
37]. In this setting, angiography can be performed with
minimal risk and is the most efficient diagnostic tool.
Although angiography is invasive and involves the ad-
ministration of potentially nephrotoxic and allergenic
contrast material, these disadvantages and risks are ei-
ther eliminated or significantly reduced if the procedure
is performed concomitantly with cineangiography of the
coronary vessels. Furthermore, angiography provides the
definitive anatomic information required for surgical
intervention.
The current practice at several institutions, including
ours, is to screen the proximal subclavian artery in all
patients undergoing cineangiography of the coronary
Ann Thorac Surg
2006;81:386 92
arteries [20, 36] and to perform arch aortography and
four-vessel cerebral angiography if significant subclavian
artery disease is found. This practice has enabled us to
identify several patients with great vessel disease before
they underwent elective CABG [20, 38]. It has also en-
abled us to document in several patients the progression
of brachiocephalic atherosclerosis from a nonsignificant
disease to a radiologically and clinically significant one
that causes CSS after an otherwise successful coronary
revascularization.
Angiography also produces the most efficient screen-
ing and diagnostic information for symptomatic patients
who have had previous CABG or a prior intervention for
known CSS. The use of angiography in such patients
adds minimal risk when performed concomitantly with
cineangiography, which is needed to rule out progressive
native vessel coronary artery disease or inadequate con-
duit flow in these patients.
In the evaluation of asymptomatic patients after inter-
vention for known CSS, noninvasive imaging using the
method of Grosveld and colleagues [37] provides reliable
screening information. Ultrasonic duplex scanning of the
brachiocephalic and vertebral vessels, as well as hemo-
dynamic measurements and neurologic examinations,
are performed before and after exercise to differentiate
hemodynamically significant lesions from nonsignificant
ones. Extremity exercise is standardized (1.5 W/sec for 5
min) by means of an ergonomic apparatus. An examina-
tion is considered positive if any of the following are
detected: (1) new or recurrent vertebrobasilar, hemi-
spheric, or coronary (related to CSS syndrome) symp-
toms or signs; (2) a decrease of 0.15 or more in the blood
pressure index of the ipsilateral arm compared with the
contralateral arm; (3) reversal of flow in the ipsilateral
vertebral or carotid artery; or (4) common carotid artery
evaluation indicating a marked serial increase in velocity
( 130 cm/s), a marked serial decrease in the ratio of
blood flow velocity in the internal carotid artery to that in
the common carotid artery. Although neck exposure is
limited, direct visualization of occlusive or ulcerated
proximal plaque is occasionally possible. Before ultra-
sound technology was incorporated, screening and fol-
low-up examinations of these patients relied solely on
hemodynamic and clinical evaluation. A positive exami-
nation leads to aortic arch and four-vessel cerebral an-
giography in each case.
Noninvasive imaging techniques, including high reso-
lution, multi-slice computed tomographic scanning and
magnetic resonance angiography, have shown promise
in some recent studies when used to screen for and
diagnose brachiocephalic disease [5, 10]. Although the
applicability of these techniques is limited by their cost
and availability, each method is noninvasive and may
provide a dynamic picture if used in combination with
duplex assessment of intraluminal velocity [39]. In addi-
tion, contrast-enhanced, color-coded, real-time sonogra-
phy is currently being assessed and has been shown to
clinically differentiate blood flow direction [40].
Ann Thorac Surg
2006;81:386 92
Brachiocephalic Manifestations
Although patients with CSS syndrome may have a broad
spectrum of symptoms related to myocardial ischemia,
the same great vessel disease that causes CSS may also
produce concomitant symptoms unrelated to the heart
(Fig 1). Proximal subclavian artery disease may also affect
the posterior cerebral circulation, the ipsilateral brachial
circulation, or both. Therefore, compromise of subclavian
artery flow may cause the simultaneous occurrence of
CSS and vertebral-subclavian steal, producing posterior
cerebral insufficiency and vertebrobasilar symptoms [41
45]. This same distribution of disease may also compro-
mise distal flow, resulting in brachial insufficiency and
extremity claudication, or produce emboli, resulting in
signs of extremity microembolization [46].
The finding of concomitant, multivessel brachioce-
phalic disease is common [35]. Significant atherosclerotic
disease in the common carotid artery, innominate artery,
or contralateral subclavian artery may produce concom-
itant symptoms related to the respective circulations
supplied by those vessels. Common carotid artery dis-
ease may compromise blood flow or produce emboli that
affect the anterior cerebral circulation, resulting in neu-
rologic symptoms. Innominate artery disease, if present,
may affect the right subclavian artery circulation, the
right common carotid artery circulation, or both [14, 38].
If any of the previously mentioned patterns of neuro-
logic change occur after coronary revascularization
(whether or not the patient has cardiac symptoms), the
clinician should consider the possibility that CSS is
present. Detection of CSS at this early stage would
enable intervention before the potential onset of isch-
emic symptoms. Although symptoms may appear early if
an IMA conduit was constructed in the presence of
unrecognized, ipsilateral brachiocephalic disease, they
more commonly appear years after surgery as the bra-
chiocephalic disease progresses from mild to severe.
Bryan and colleagues [19] report that among 5 patients
with post-CABG CSS syndrome, mean time from surgery
to the report of symptoms was 7.8 years (range, 1 month
to 18 years). Similarly, Elian and associates [27] report
that symptoms associated with CSS began an average of
5.8 years (range, 1.7 to 10.5 years) after CABG in the 7
patients in their series.
Management
Although CSS primarily affects the heart and produces
heart-related symptoms, CSS can be treated effectively
with noncardiac interventions. Successful correction of
CSS with relief of symptoms has been accomplished by
aorta-subclavian bypass [20, 38]; carotid-subclavian by-
pass [19, 47, 48]; axillo-axillary bypass [49]; transposition
of the IMA [50]; and percutaneous transluminal angio-
plasty with stenting [16, 25, 26, 28, 51, 52], laser ablation
[53], rotational thrombectomy [54], or atherectomy [55] of
the subclavian artery. Although subclavian stenosis has
been found to recur after several types of intervention
[16, 17, 20, 25, 56 58], the excellent long-term patency
after bypass remains the standard to which the outcomes
REVIEW TAKACH ET AL 389
CORONARY-SUBCLAVIAN STEAL SYNDROME
of all other procedures are compared. Multiple studies
have shown that a 10-year actuarial patency of more than
90% with acceptably low morbidity and mortality can be
achieved by using either direct reconstruction methods
that preserve aortic inflow when multiple great vessels
are involved [21, 41, 59, 60] or extra-anatomic, cervical
bypass for single-vessel brachiocephalic disease [61 63].
Excellent results have been achieved using Dacron (He-
mashield; Meadox Medicals, Inc, Oakland, NJ) or poly-
tetrafluoroethylene conduits [21, 59 63].
As a less invasive alternative to operative bypass,
endovascular interventions for the treatment of recurrent
and primary CSS are being evaluated at several institu-
tions [16, 23, 25, 26, 62]. Early results have shown accept-
able operative and early patency, although midterm
patency rates are somewhat lower than those associated
with operative bypass [23, 26, 62]. Endovascular interven-
tion offers tangible benefits regarding cost, level of inva-
siveness, and subjective patient satisfaction [62]. For
these techniques, however, we do not know yet the
long-term durability, patterns of failure, efficacy as an
adjunct to CABG, anticoagulation requirements, efficacy
as treatment for complex (multivessel) disease, or long-
term cost. Until these additional questions are answered,
the precise indications for endovascular intervention
versus operative reconstruction as treatment for brachio-
cephalic disease remain unsettled. Long-term results will
provide further insight into the advantages and disad-
vantages of the endovascular approach and provide fur-
ther direction regarding optimal management of primary
and recurrent CSS.
REVIEWS
Little is known about the natural history of untreated
or medically managed CSS. However, Bryan and col-
leagues [19] report observational and medical manage-
ment of one patient who refused percutaneous or inva-
sive intervention for CSS. This patient expired less than
12 months after the initial diagnosis.
Clearly, if preoperative testing shows significant sub-
clavian artery disease ipsilateral to a planned IMA coro-
nary artery conduit, CSS may be avoided by using
all-vein coronary conduits. This approach to treating
patients with coronary artery disease and concomitant
brachiocephalic disease is used at several institutions [64]
and is associated with acceptably low operative morbid-
ity, low operative mortality, and excellent long-term
brachiocephalic graft patency in patients receiving con-
comitant reconstruction. Nonetheless, the use of all-vein
conduits in such patients has become controversial [16,
20, 25, 65], because a recent study showed that patients
who undergo concomitant brachiocephalic reconstruc-
tion and CABG using all-vein conduits have a poor
10-year actuarial freedom from death and adverse car-
diac events [20]. Although choosing not to use the IMA as
a coronary conduit effectively eliminates the possibility of
CSS, it also denies the patient the proven benefits of IMA
conduit use, which include increased long-term survival
and a reduced incidence of adverse cardiac events [66].
The demonstrated safety of concomitant brachiocephalic
reconstruction and CABG and the excellent long-term
patency of the brachiocephalic vessels after reconstruc-
 390 REVIEW TAKACH ET AL
CORONARY-SUBCLAVIAN STEAL SYNDROME
tion have led several groups to initiate studies of con-
comitant ipsilateral subclavian artery reconstruction and
CABG with use of IMA coronary conduits in patients
whose concomitant disease is recognized preoperatively.
The investigators hope to improve long-term survival
and decrease the incidence of late, adverse cardiac events
after surgery [16, 20, 25, 65].
Although the lack of an IMA conduit in patients having
concomitant brachiocephalic reconstruction and CABG
may increase the likelihood of late, adverse cardiac
events, it is likely that these late events are influenced by
several factors, including the systemic distribution of
atherosclerosis. Therefore, lifestyle change and risk-
factor modification are aggressively encouraged in these
patients. Long-term rates of adverse events and survival
continue to be closely followed in these patients to
determine whether this management approach improves
outcome.
As an alternative to the use of either all-vein conduits
or an IMA conduit after brachiocephalic reconstruction
in patients with concomitant disease, the use of free IMA
grafts or radial artery conduits may be considered. How-
ever, the specific long-term outcomes associated with
these conduits and their relative impact on freedom from
late, adverse cardiac events compared with that of IMA
grafts have not been definitively established. Decisions
about the operative approach, technique, and staging to
be used with an individual patient must ultimately be
based on the institutions experience, the patients par-
ticular risk factors, and the severity of the disease.
We currently do not use endovascular treatment for
REVIEWS
brachiocephalic disease in conjunction with CABG, be-
cause the open surgical treatment of brachiocephalic
disease has proven safe and durable at our institution,
and the need for CABG negates the advantages of angio-
plasty and stenting that relate to cost, level of invasive-
ness, and need for anesthesia. However, we do use the
endovascular technique in patients who have CSS after
CABG. These patients are followed as part of an ongoing
study that maintains strict follow-up with serial duplex
examinations before and after exercise [37].
Follow-Up
Close follow-up is essential for all patients who receive
brachiocephalic reconstruction as treatment for CSS syn-
drome. The wide spectrum of symptoms and modes of
presentation that may accompany recurrent disease, the
unproven long-term utility of specific intervention types,
and the possibility that a catastrophic outcome may be
the initial mode of presentation warrant serial clinical
and noninvasive examinations [34, 67]. Performing serial
duplex examinations before and after arm exercise has
been reported to effectively diagnose recurrent brachio-
cephalic disease [37, 68]. Although this diagnostic
method requires a trained technician, it has the advan-
tages of high sensitivity and specificity, noninvasiveness,
and low cost [37, 68, 69]. Other direct and indirect
methods that have been used to establish the diagnosis of
recurrent CSS include arch aortography, cerebral angiog-
raphy [25], and sestamibi imaging [70].
Ann Thorac Surg
2006;81:386 92
Comment
In summary, CSS syndrome is a distinct clinical entity
that may have profound consequences for the survival
and lifestyle of the individual patient. Increased aware-
ness of the problem and screening for brachiocephalic
disease in patients with coronary artery disease will help
to decrease the incidence of CSS. Preoperative angio-
graphic screening limited to brachiocephalic vessels
proximal to a potential IMA conduit is an effective
screening method for concomitant disease and adds little
risk when performed concomitantly with cineangiogra-
phy of the coronary vessels. However, the most appro-
priate way to manage concomitant brachiocephalic dis-
ease and coronary artery disease is unsettled. Studies are
currently ongoing in which the IMA is used as a coronary
conduit after brachiocephalic reconstruction of the ipsi-
lateral subclavian artery in patients with concomitant
disease. Patients who have CSS syndrome after CABG
have been successfully treated with both operative by-
pass and endovascular techniques. Close follow-up is
essential after treatment of CSS syndrome in order to
decrease the likelihood of adverse and catastrophic
events that may be associated with recurrent disease.
Stephen N. Palmer, PhD, ELS, provided editorial support; Wil-
liam M. Andrews, MA, CMI, provided medical illustrations.
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