Coronary-subclavian steal syndrome: A case series and review of the literature

Abstract

Objective

To report a case series of three patients with symptomatic coronary-subclavian steal syndrome (CSSS) and to review the literature on published case series.

Methods

We retrospectively reviewed three cases of CSSS patients treated with open and endovascular surgery at a single center over a period of three decades (1996–2024). A comprehensive review of case series involving more than three patients was also performed.

Results

The first patient was a 65-year-old male with a 12-year history of coronary artery bypass grafting (CABG), presenting with unstable angina. Coronary angiography revealed a patent left internal mammary artery (LIMA) graft with retrograde flow through the left subclavian artery (LSA) and occlusion at the LSA ostium. He underwent a successful carotid-subclavian bypass, which significantly improved his symptoms. He died 6 years later from heart failure. The second patient was a 73-year-old woman with a 15-year history of CABG and balloon angioplasty of the grafts. She presented with dyspnea, stable angina, and progressive functional decline. Critical stenosis in the LSA was identified, and her symptoms resolved after successful stent placement. She died 6 years later from progressive heart failure. The third patient was a 75-year-old woman with diabetes, hypertension, and heart failure, who also had a history of CABG. She presented with worsening dyspnea, orthopnea, and edema. Imaging revealed occlusion of the circumflex artery graft and severe LSA stenosis. Successful stenting of the LSA alleviated her symptoms and restored normal blood flow from the LIMA graft. She was discharged after 2 days and remains well at the six-month follow-up.

Conclusion

CSSS should be considered in the differential diagnosis of patients with a history of CABG who present with angina or heart failure. Prompt treatment can lead to significant symptom improvement.

Keywords

Coronary-subclavian steal syndrome coronary-subclavian steal subclavian steal syndrome CABG

Introduction

Coronary-subclavian steal syndrome (CSSS) was described as a complication of coronary artery bypass grafting (CABG) involving the left internal mammary artery (LIMA), which is the preferred conduit for myocardial revascularization due to its superior patency compared to other grafts.¹ During CABG, the proximal end of the LIMA is left intact in the left subclavian artery (LSA), while the distal end is anastomosed to the target coronary artery. CSSS occurs due to retrograde blood flow through the LIMA graft, often as a result of proximal LSA stenosis or occlusion. This condition can lead to various cardiac symptoms, including angina, acute coronary syndrome, heart failure, and arrhythmias. Furthermore, symptoms tend to worsen with activity involving the left upper extremity.² Less commonly, other etiologies such as arteritis and upper extremity arteriovenous fistulas have also been reported to cause compromise of LSA flow and result in CSSS.^3,4 The syndrome’s name reflects its similarity to the physiology behind vertebral-subclavian steal syndrome, which causes vertebrobasilar insufficiency⁵

While CSSS has traditionally been regarded as an uncommon complication of CABG, the increasing use of LIMA grafts and the improvement in life expectancy are expected to elevate its prevalence⁶ Therefore, it is crucial to be aware of this condition and manage it appropriately. The aim of the present study was to report a case series of patients with CSSS and to review the literature on published case series.

Case 1

A 65-year-old male patient with a history of hypertension, dyslipidemia, and a 12-year history of coronary artery bypass grafting (CABG), including a left internal mammary artery (LIMA) anastomosis to the left anterior descending artery (LAD) and saphenous vein grafts to the circumflex artery and the posterior descending artery (PDA), was hospitalized due to chest pain, and dyspnea, secondary to unstable angina. An echocardiogram revealed a left ventricular ejection fraction (LVEF) of 30%, and coronary angiography showed occlusion of the saphenous vein grafts. A retrograde subclavian angiography trough the brachial artery showed complete patency of the LIMA graft to the distal LAD, with retrograde flow to the LSA. Additionally, a complete occlusion at the LSA ostium was noted. (Figure 1) A carotid-subclavian bypass was planned for restoring normal blood flow to the LIMA graft and the left upper extremity. Following exposure of the arteries, a 6 mm PTFE graft was sewn to the carotid artery in a terminal-lateral fashion with a continuous polypropylene suture. The graft was then passed beneath the sternocleidomastoid muscle to the subclavian artery, where a termino-lateral anastomosis was completed. The patient’s postoperative course was uneventful, and he was discharged on the fifth postoperative day. Two months later, the patient experienced severe dyspnea. A subsequent angiography confirmed a patent carotid-subclavian bypass, a patent LIMA-LAD anastomosis and the already known complete occlusion of the two previous bypasses to the PDA and the circumflex artery. Two new venous bypasses were performed: one to another portion of the circumflex artery and one to the distal portion of the DPA beyond the previous anastomosis. The procedures were completed without complications. Five years later, the patient experienced a recurrent episode of progressive dyspnea and chest pain. Myocardial infarction was ruled out, but atrial flutter was detected on the electrocardiogram. Ablation of the cavo-tricuspid isthmus and the right atrial appendage was performed. Six months after this procedure, an echocardiogram showed a further decrease in LVEF to 25%. The patient subsequently died 1 year later due to heart failure progression.

Figure 1.

Angiography from 1996. White arrow showing complete occlusion at the ostium of the left subclavian artery.

Case 2

A 73-year-old female with a history of diabetes mellitus, dyslipidemia, smoking, PAD, hypertension, and three-vessel coronary artery disease (CAD), who underwent CABG 15 years ago with LIMA graft to the LAD and saphenous vein grafts to the right coronary artery and circumflex artery. She presented to the outpatient clinic with dyspnea and chest pain on moderate exertion. Physical examination revealed a left supraclavicular bruit and diminished left radial and ulnar pulses. Pulse volume recording (PVR) showed a significant difference in blood pressure between the arms: 135 mmHg in the right arm and 83 mmHg in the left arm (Figure 2(a)).

Figure 2.

(a) Preoperative pulse volume recording showing a blood pressure difference between arms (right: 135 mmHg, left: 83 mmHg). (b) Retrograde flow in the left internal mammary graft to the left subclavian artery. (c) Severe stenosis in the left subclavian artery. (d) Patent stent in the left subclavian artery. (e) Postoperative pulse volume recording demonstrating improved pressure in the left arm (141 mmHg). (f) 5-year postoperative angio CT scan. White arrow head shows patency of the subclavian artery stent, and white arrow shows a patent left internal mammary anastomosis to the left anterior descending artery.

Echocardiogram showed a left ventricular ejection fraction (LVEF) of 50%. A stress test with myocardial perfusion imaging (MPI) indicated 15%–18% ischemia in the anterior wall. Coronary angiography revealed that all three bypass grafts were patent but showed retrograde blood flow through the LIMA into the LSA (Figure 2(b)). Also, 80% stenosis in the LSA proximal to the LIMA ostium was seen (Figure 2(c)). A diagnosis of coronary-subclavian steal syndrome was made and endovascular intervention was planned. Using a right femoral access and a 6 Fr × 90 cm Rabee ® (Cook Medical, Bloomington, IN, USA) introducer sheath, a 7 mm × 30 mm Precise PRO RX ® (Cordis Co., Miami, FL, USA) stent was successfully deployed at the ostium of the LSA, followed by post-dilatation with a 6 mm × 30 mm balloon (Figure 2(d)). Complete resolution of the stenosis was achieved. Postoperatively, the patient’s course was uneventful, with a new PVR showing improvement in segmental curves and pressures (Figure 2(e)). The patient was discharged on postoperative day 3. Two years after the intervention the patient underwent a femoral-femoral bypass due to aortoiliac oclussive disease. A CT scan done 5 years after intervention showed a patent LSA stent and LIMA graft (Figure 2(f)). She was followed for 6 years without further coronary syndromes, and with LVEF of 35%. She passed away at the age of 79 due to progressive heart failure.

Case 3

A 75-year-old female with a history of diabetes mellitus, hypertension, dyslipidemia, chronic renal failure, PAD, and CAD, which had been treated with CABG 6 years ago with a LIMA graft to the LAD, and saphenous vein grafts to the circumflex artery and the PDA, presented with a one-month history of progressive dyspnea, orthopnea, and lower extremity edema. She denied chest pain. She sought emergency care due to worsening dyspnea. Upon examination, crackling sounds were noted in the lung bases. Chest X-ray showed bilateral lung edema, and the electrocardiogram revealed a left axis deviation and a left anterior fascicular block without signs of ischemia. High sensitivity cardiac troponins were normal. An echocardiogram and a nuclear stress test showed a LVEF of 47% and ischemia of 14%, respectively. The patient was diagnosed with new-onset heart failure. A CT angiogram was ordered, which revealed a patent LIMA-LAD anastomosis alongside an occluded LSA at its ostium (Figure 3(a)).

Figure 3.

(A) Preoperative CT scan. White arrow shows left subclavian artery occlusion secondary to atherosclerotic plaque. (B) Angiography. White arrow reveals retrograde flow from the left internal mammary artery graft to the left subclavian artery. (C) White arrow showing patency of the left internal mammary artery anastomosis to anterior descending artery. (D) Six-month postoperative CT scan. White arrow shows a patent stent in the left subclavian artery. (E) CT scan reconstruction. White arrow head showing a patent stent in the subclavian artery. White arrow shows patent left internal mammary anastomosis to the left anterior descending artery.

Coronary angiography confirmed reversed blood flow through the LIMA graft to the distal LSA (Figures 3(b), and 3(c)). A PVR showed diminished curves and pulses in the left arm compared to the right arm.

Initially, a right percutaneous femoral access was attempted, but due to difficulty crossing the occlusion at the LSA, a left brachial access was required for successful passage. After several attempts, using the femoral access with a 6 Fr × 90 cm Rabee ® (Cook Medical, Bloomington, IN, USA) introducer sheath, a through-and-through wire technique was employed using a 0.014 guidewire and a microcatheter. Predilatation of the occlusion was performed with a 4 mm × 40 mm Admiral Xtreme ® (Medtronic, Minneapolis, MN, USA) balloon. Subsequently, a Protégé GPS ® (Medtronic, Minneapolis, MN, USA) 9 mm × 40 mm self-expanding stent was deployed at the ostium of the LSA, with 1–2 mm protrusion into the aortic arch. Post-dilation was carried out with a 7 mm × 20 mm Admiral Xtreme ® (Medtronic, Minneapolis, MN, USA) balloon. The final angiogram showed adequate patency of the LSA stent without dissection and resolution of the reversed blood flow from the LIMA graft. The postoperative course was uneventful, and she was discharged on postoperative day 2. At the 6-month follow-up, the patient was doing well, with compensated heart failure and no cardiac symptoms. Six month postoperative angio CT scan showed a patent LSA stent and LIMA graft (Figures 3(d), and 3(e)).

Table 1 displays a summary of the three cases.

Table 1.

Summary of patients’ characteristics, treatment, and outcomes.

Year of CABG	Year of CSSS diagnosis	Age/Gender	Comorbidities	Symptoms	Graft involved	Treatment	Follow-up
1984	1996	65/Male	DLP, HTA	Dyspnea and chest pain	LIMA-LAD	Carotid-subclavian bypass with PTFE	Died after 5 years of heart failure
1996	2011	73/Female	DM, DLP, HTA, Smoking, PAD	Dyspnea and chest pain	LIMA-LAD	Precise PRO RX® (Cordis Co., Miami, FL, USA) 7 mm × 30 mm stent in LSA	Died after 6 years of heart failure
2018	2024	75/Female	DM, DLP, HTA, Smoking, PAD, CRF	Progressive dyspnea, orthopnea, and lower extremity edema	LIMA-LAD	Protégé GPS ® (Medtronic, Minneapolis, MN, USA) 9 mm × 40 mm stent in LSA	Alive, 6 months postoperative

CABG: coronary artery bypass grafting, CSSS: coronary subclavian steal syndrome, CRF: chronic renal failure, DLP: dyslipidemia, DM: diabetes mellitus, HTA: hypertension, LAD: left anterior descending artery, LIMA: left internal mammary artery, LSA: left subclavian artery, PAD: peripheral arterial disease.

Discussion

CSSS is an uncommon manifestation of subclavian artery stenosis occurring in patients who have undergone CABG with internal mammary artery. It usually affects the LSA but may involve also the right, if the right internal mammary artery was used. Myocardial hypoperfusion results due to retrograde blood flow through the patent LIMA graft, which compensates for the perfusion to the left upper extremity.⁷ This can lead to a variety of symptoms such as chronic angina, ischemic heart failure, ventricular arrhythmias or acute coronary syndromes. Symptoms are usually worsened with activity involving the left upper extremity.⁸ English et al.⁹ reported a prevalence of 1.5% for LSA stenosis in the general population, with an increased prevalence of 11.5% observed in patients with PAD. In contrast, the prevalence of significant LSA stenosis in patients undergoing CABG ranged from 0.2% to 6.8%.^10,11

Notably, two of our three patients in the present study had PAD, and one of them underwent surgical intervention for severe aorto-iliac oclussive disease.

There is no established time frame for the development of CSSS following CABG. Westerband et al.¹² reported a mean interval of 14 years (range: 2–31 years) between CABG and the onset of CSSS in their study of 14 patients. Similarly, Wenkel et al.¹³ observed an average time frame of 86 months (range: 2–213 months) from revascularization surgery to the development of CSSS in their study of 9 patients. Similarly, our three patients presented CSSS after a mid-long term follow up period. When CSSS emerges several years after CABG surgery, it is often due to progression of occlusive disease in the proximal LSA. Conversely, if CSSS presents within the first year after CABG, it suggests that pre-existing LSA stenosis was present but not identified at the time of the initial surgery.⁶

Physical examination has a high predictive value for diagnosing LSA stenosis. A blood pressure difference of more than 20 mmHg between the arms or the presence of a supraclavicular bruit should raise suspicion of LSA stenosis.⁶ Various non-invasive imaging modalities can confirm the diagnosis, including duplex ultrasound, CT angiography, and MRI. The latter techniques are often considered superior because they provide a more detailed view of the anatomy, including plaque morphology and surrounding tissue.⁶ Coronary angiography remains the gold standard for confirming CSSS, as it allows retrograde flow visualization through the LIMA during native coronary angiography.¹⁴ There has always been some debate on whether to perform routine angiography for detecting LSA stenosis before CABG, but due to the low incidence (0.44%) of CSSS after CABG, physical examination remains the most commonly used screening method.^5,15 If the physical examination is positive, prompt evaluation with duplex scanning or angiography is mandatory.¹²

Treatment for symptomatic CSSS includes open and endovascular surgery. The 2011 guidelines from the European Society of Cardiology and the American Heart Association recommend endovascular treatment as the first-choice therapy for treating LSA stenosis. Endovascular therapy is preferred due to its proven long-term efficacy and patency, as well as its lower morbidity rates.¹⁶ Additionally, patients with CSSS are often high-risk individuals who may have anterior wall myocardial ischemia, making open surgery particularly risky for them, although a bypass is still an option.⁶ Che et al.¹ published the largest single-center series of patients with CSSS treated using an endovascular approach, reporting a technical success rate of 97.3%. Similarly, Faggioli et al.² reported on 10 patients with CSSS treated endovascularly, achieving a technical success rate of 90%. In the largest series of patients undergoing LSA stent placement before CABG surgery, involving 167 patients. Balloon-expandable stents were placed in 97% of these patients, making them the preferred choice as they provide a more precise position and higher radial force, which is advantageous for the proximal and ostial lesions often seen in LSA stenosis.¹⁷

On the other hand, Paty et al.¹⁸ performed bypass using PTFE conduits, achieving 100% patency at a mean follow-up of 43 months. Similarly, in a more recent study, Wenkel et al.¹³ reported on 9 patients with CSSS who underwent primary treatment with carotid-subclavian bypass using a prosthetic graft, achieving a patency rate of 100% at a mean follow-up of 79.9 months. Table 2 shows a complete summary of published case series of patients with CSSS, including patient characteristics, time frame between CABG and CSSS, treatment and outcomes.

Table 2.

Review of case series with more than 3 patients with coronary-steal syndrome.

Author and year	N	Age (median, range) or (mean, SD)	Comorbidities	Years of prior CABG (median, range) or (mean, SD	Open surgery N	Endovascular treatment N	Complications <30 days postoperative	Follow-up (median, range) or (mean, SD)	Mortality <30 days postoperative
Bryan F. et al. 1995²⁴	5	65 (56–68)	HTA (60%), DM (40%), COPD (20%), PAD (40%), Smoking (20%)	Mean: 7.8 y	4	1	No	20 m (12 m to 25 m)	0 (0%)
Bryan F. et al. 1995²⁴	5	65 (56–68)	HTA (60%), DM (40%), COPD (20%), PAD (40%), Smoking (20%)	Range: (1 m–18 y)	4	1	No	20 m (12 m to 25 m)	0 (0%)
Marques K. et al. 1996²⁰	31	68 (49–80)	NA	Mean: 1.6 y	0	31	6/31 (19.3%)	3.1y (0.1y–7.0y)	2 (6%)
							−4 LSA dissection
							−1 Brachial AV fistula
							−1 Transient hemianopsia
Angle J. et al. 2003¹⁸	21	62 (49–76)	NA	NA	0	21	4/21 (19%):	27 m (4 m–68 m)	2 (9.5%)
							−1 Angina
							−1 Femoral Hematoma
							−1 Pseudoaneurysm
							−1 Aphasia
Paty P. et al. 2003¹⁸	10	62 (47–78)	DLP (90%), Smoking (60%), DM (20%)	Mean: 46 m	10	0	1/10 (10%)	43m (3m–102 m)	0 (0%)
Paty P. et al. 2003¹⁸	10	62 (47–78)	DLP (90%), Smoking (60%), DM (20%)	Range: (3–146 m)	10	0	−1 lymph leak	43m (3m–102 m)	0 (0%)
Westerband A. et al. 2003¹²	14	69 (49–80)	HTA (71.4%), PAD (35.7%), DM (35.7%), CRF (14.2%), Smoking (50%)	Mean: 14 y (2 y–31 y)	1	13	No	33.6 m (6–51 m)	0 (0%)
Costa S. et al. 2007⁸	3	73 (67–77)	HTA (66.6%), DM (33.3%), Smoking (33.3%), CRF (33.3%)	2 y, 11 y, 3rd unknown	2	1	No	NA, NA, 56m	0 (0%)
Kilic I. et al. 2013²⁵	3	69,59,51	HTA (100%), DM (66%), DLP (100%), Smoking (33%), PAD (33%)	3 y, 3 y, 5 y	0	3	No	Na, Na, 6 m	0 (0%)
Almeida B. et al. 2014²⁶	16	67.2 (53–81)	HTA (100%), DM (43.7%), CRF (6.2%), Smoking (31.2%)	Not Mentioned	0	16	2/16 (12.5%)	12 m	2 (12.5%)
							−1 hematoma
							−1 pseudoaneurysm
Faggioli G. et al. 2014²	10	72 ( 63–85)	HTA (100%), DM (60%), DLP (100%), Smoking (30%), COPD (30%), CRF (30%).	Mean: 9 y ± 8.4 y	4	6	2/10 (20%)	14.4 m ± 8.7 m	0 (0%)
							−1 SA dissection and LIMA occlusion
							−1 Brachial Hematoma
Marc M. et al. 2015²⁷	3	58,59,51	DM (33%), PAD (66%), CPOD (33%) and CRF (66%),	6 y, 17 y, 19y	0	3	No	Na, Na, 6 m	0 (0%)
Che W. et al. 2017¹	37	65±6	DM (35%), HTA (57%), Smoking (68%), HTA (57%), DLP (70%)	Median: 5.2 y	1	36	5/37 (8.0%)	44 m±32 m	0 (0%)
				Median: 5.2 y			−1 Transient ischemic attack
				Range: (1.3 m - 17.8 y).			−1 IMA dissection
							−2 LSA dissection
							−1 Puncture Site Hematoma
De Roeck F. et al. 2019²⁸	4	77 (84, 77, 69, 85, 70)	HTA (20%), DM (20%) PAD (20%), CRF (20%)	1 y, 9 y, 10 y, 22 y	0	3	1/4 (25%)	NA	1 (25%)
De Roeck F. et al. 2019²⁸	4	77 (84, 77, 69, 85, 70)	HTA (20%), DM (20%) PAD (20%), CRF (20%)	1 y, 9 y, 10 y, 22 y	0	3	−1 Tonic Clonic Seizures	NA	1 (25%)
Real C. et al. 2021²⁹	3	61, 72, 76	HTA (33.3%), DLP (33.3%), DM (33.3%), CRF (33.3%)	5 m, 12 m, 36 m	0	3	No	5 m, 6 m, 10 m	0 (0%)
Wenkel M. et al. 2024¹³	9	69.1 (51–81)	HTA (100%), Smoking (100), DLP (88.9%), PAD (44.4%), COPD (44.4%), DM (33.3%), CRF (33.3%)	Mean: 86 m ± 65.7 m	9	0	No	69 m (12 m–188 m	0 (0%)

CABG: coronary artery bypass grafting, CRF: chronic renal failure, DLP: dyslipidemia, DM: diabetes mellitus, HTA: hypertension, M: month, NA: not available, PAD: peripheral arterial disease, Y: year.

Song et al.¹⁹ compared long-term outcomes of endovascular stenting versus extrathoracic surgical bypass for subclavian steal syndrome in patients without prior CABG. The primary patency rates at 1, 5, and 10 years were 91%, 67%, and 49% for the endovascular group, and 99%, 95%, and 89% for the open surgery group (p = .001). Although this study demonstrates a greater benefit with open surgery, the results cannot be directly extrapolated to patients with CSSS due to the high risk these patients carry, largely attributable to baseline cardiopathies.

Regarding asymptomatic patients, treating LSA stenosis before CABG might be beneficial for avoiding future complications. Che et al.¹⁷ treated asymptomatic patients scheduled for CABG who had LSA stenosis of over 80%. In other series by Westerband et al.¹² and Marques et al.,²⁰ asymptomatic patients with LSA stenosis of over 50% and over 70%, respectively, as determined by angiography, were treated prophylactically with PTA before CABG surgery.

Complications after LSA stenting for the treatment of CSSS are extremely rare; however, there have been some cases of LIMA dissection, angina pectoris, STEMI with ventricular fibrillation, and transient ischemic attack (TIA).^1,21,22 In a series of 12 patients with vertebral-subclavian steal syndrome treated with LSA angioplasty, a protective delay in flow reversal post-PTA was observed, suggesting a mechanism against cerebral embolism.²³ Similarly, it is hypothesized that this also applies to coronary artery embolisms in CSSS, due to the protection provided by the delayed reversal of blood flow from the LIMA graft.¹

In conclusion, we present three cases of patients with CSSS who were successfully treated with open and endovascular surgery. The optimal treatment for CSSS remains uncertain, as there are currently no studies comparing different treatment modalities for this syndrome, since the existing literature comprises only case reports and case series. A thorough review of the literature on case series involving CSSS patients is also presented. Further research comparing different approaches is needed to determine the most effective treatment modality for patients with CSSS.

Footnotes

Acknowledgments

Gonzalo Perez and Francisco Vergara

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Ethical statement

ORCID iDs

Mauricio Gonzalez-Urquijo

Francisco Valdes

Michel Bergoeing

Leopoldo Marine

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. Coronary-subclavian steal syndrome, an easily overlooked entity in interventional cardiology. Cathet Cardiovasc Interv 2020; 96(3): 614–619. DOI: 10.1002/ccd.28362.

29.

Real

Vivas

Martínez

, et al. Endovascular treatment of coronary subclavian steal syndrome: a case series highlighting the diagnostic usefulness of a multimodality imaging approach. Eur Heart J Case Rep 2021; 5(3): ytab056. DOI: 10.1093/ehjcr/ytab056.