Endovascular Treatment of Coronary Subclavian Steal Syndrome

Abstract

We present a case of coronary subclavian steal syndrome due to severely calcified left subclavian artery and prior patent left internal mammary artery (LIMA) to distal left anterior descending artery (LAD). Our patient underwent percutaneous treatment of subclavian stenosis with the AngioSculpt balloon PTA (AngioScore, Inc.) and stenting. This is the first report describing the use of AngioSculpt scoring balloon in the treatment of calcified subclavian artery disease. We review the diagnostic and treatment modalities of subclavian steal syndrome and coronary subclavian steal syndrome.

VASCULAR DISEASE MANAGEMENT 2011;8(12):E207–E210

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Case report

A 77-year-old male with a history of coronary artery disease and unstable angina had an emergent single vessel bypass (left internal mammary artery [LIMA] to distal left anterior descending artery [LAD]) performed after a failed attempt at percutaneous transluminal coronary angioplasty (PTCA) of the native LAD artery in 1990. He subsequently underwent PTCA of the right coronary artery (RCA) in 1994. He presented in October 2010 to our institution with symptoms of recurrent exertional angina. His medical regimen included aspirin, clopidogrel, metoprolol, lisinopril, atorvastatin, hydrochlorothiazide, amlodipine, and sublingual nitroglycerin as needed. His blood pressure was 130/70 mm Hg (right arm) and 100/60 mm Hg (left arm). He developed substernal chest discomfort with minimal exertion with mild radiation of pressure down his left arm, limiting him to <3 blocks of ambulation. The discomfort was relieved with rest and nitroglycerin. An exercise nuclear stress test revealed >2 mm of downsloping ST-segment depressions and reversible defects in the mid to distal inferior wall and apex. He was then referred for coronary angiography.

Cardiac catheterization revealed 1) severe obstructive, calcified disease in the proximal and mid RCA; 2) moderate disease in the left circumflex artery; 3) an occluded native LAD artery with a patent LIMA to distal LAD artery; and 4) a nearly occluded, very heavily calcified lesion in the proximal left subclavian artery prior to the takeoff of the left vertebral artery and the LIMA graft (Figure 1). Reversal of flow from the left vertebral artery was noted, providing angiographic evidence for subclavian steal syndrome (SSS).

The RCA was initially treated successfully with rotational atherectomy and drug-eluting stenting of the proximal and mid lesions. The patient’s chest discomfort briefly improved after discharge, but then recurred 3 weeks later with chest pain being exacerbated by left upper extremity exercise. The patient was also noted to experience symptoms of left arm claudication. Given the recurrent symptoms of exertional angina and prior angiographic evidence of SSS, a concomitant diagnosis of coronary subclavian steal syndrome (CSSS) was considered likely. We subsequently chose an endovascular approach to treat the left subclavian artery stenosis.

A 6 Fr, 65 cm sheath (Terumo Corporation, Tokyo, Japan) was used to engage the origin of the left subclavian artery via the right femoral artery. Unfractionated heparin anticoagulation was used during the procedure. A V18 Control Wire guidewire (Boston Scientific) crossed the severely calcified, eccentric lesion in the subclavian artery. An AngioSculpt 4 x 40 mm scoring balloon catheter (AngioScore) was used for predilatation given the calcific burden of the lesion (12 atm, 40 seconds) (Figure 2). The V18 guidewire was then exchanged for a Supra Core 0.035 guidewire (Abbott Vascular) over which a subsequent predilatation was performed with a 5 x 40 mm FoxCross balloon (Abbott) (9 atm, 30 seconds). An Express LD 8 x 27 mm balloon-expandable stent (Boston Scientific) was deployed (10 atm, 20 seconds) (Figure 3) and postdilatation was performed with a 9 x 20 mm Admiral Xtreme balloon (Invatec, Medtronic, 9 atm, 20 seconds). An excellent angiographic result was achieved (Figure 4) with minimal residual left subclavian stenosis and no gradient across the lesion. In addition, at the end of the procedure there was angiographic evidence of antegrade left vertebral artery flow and more brisk filling of the LIMA. The patient’s symptoms of angina and left upper extremity claudication resolved and he remained symptom-free at his 6-month follow-up interview.

Pathophysiology and Clinical Characteristics

SSS is commonly present in patients with hemodynamically significant proximal subclavian artery stenosis (SAS) and refers to the phenomenon of flow reversal from the ipsilateral vertebral artery via shunting of blood to adequately perfuse the lower pressure system of the subclavian artery distal to the stenosis. This phenomenon was first described in 1965 by Toole et al in 2 patients with symptoms of cerebral ischemia.¹ The same mechanism and pathophysiology explains the CSSS in patients with prior coronary artery bypass graft (CABG) surgery utilizing the internal mammary artery, where the reversal of flow from the internal mammary artery (IMA) to the subclavian artery produces myocardial ischemia and angina particularly during upper extremity exercise.²

The most common cause of SSS is atherosclerosis. Rare conditions may also cause SSS such as:

• Takayasu arteritis;
• Compression of the subclavian artery in the thoracic outlet syndrome; or 
• Postoperatively after repair of aortic coarctation or tetralogy of Fallot with a Blalock-Taussig anastomosis.^3-5

In most cases, SSS is asymptomatic. When symptomatic, patients present with upper extremity symptoms, such as arm pain/discomfort and paresthesia, or neurological symptoms including dizziness, blurry vision, and syncope, particularly after ipsilateral upper extremity exercise. On physical examination there is often a significant difference in the systolic arterial pressure and the peripheral pulses between the affected and the normal arm. A supraclavicular or cervical bruit may be appreciated.^6-7 The diagnosis of this syndrome is usually made noninvasively with Doppler studies, magnetic resonance angiography, or computed tomography angiography. Invasive subclavian and cerebral angiography may be necessary to confirm the diagnosis and to identify additional extracranial or intracranial vascular disease. Interestingly, angiographic evidence of reversal of flow in the ipsilateral vertebral artery is demonstrated in only a minority of patients with subclavian stenosis.^8-9

SSS does not predict future cerebrovascular events, but has been associated with an increased incidence of transient ischemic attacks, usually due to concomitant carotid disease.¹⁰ Patients with SSS are also at increased risk for concomitant CAD, and as a result, SSS has been associated with an increase in future cardiovascular and all-cause mortality.¹¹

Treatment Options

Lifestyle modifications including a low-fat diet and smoking cessation should be implemented in all patients with SSS due to atherosclerosis. In addition, aggressive medical therapy for diabetes, hyperlipidemia, hypertension, and antiplatelet therapy have led to a reduction in long-term cardiovascular events.¹² Surgical or percutaneous treatment is usually reserved for patients with disabling symptoms despite lifestyle modifications and maximal medical therapy.

The 2 invasive treatment options include an endovascular approach with percutaneous transluminal angioplasty (PTA) and stent placement in the subclavian artery or surgical bypass with either carotid-subclavian or axillary-axillary bypass. These procedures have high technical success rates and excellent long-term patency rates. This type of revascularization needs to be individualized based on the lesion morphology and clinical comorbidities.

The initial surgical treatment of subclavian stenosis was performed by direct transthoracic approach.¹³ Subsequently, extrathoracic carotid-subclavian bypass was performed and found to be associated with lower morbidity and mortality rates and durable relief of symptoms. The carotid-subclavian bypass has been shown to have postoperative relief of symptoms in >90% of patients and 5-year patency rates up to 100%. The perioperative mortality rates range from 0% to 18% in different series.^14-17 Complications include Horner’s syndrome, phrenic and recurrent laryngeal nerve palsy, and injury to the thoracic duct.¹⁸ There is also an increased risk of stroke (0.9%) associated with clamping of the carotid artery during the procedure.¹⁹ The postoperative use of antiplatelet agents have been shown to increase the graft patency rates.²⁰

The endovascular approach with PTA and stent placement in the subclavian artery also has high success rates (80%-100%) with close to 0% periprocedural mortality. Most complications are attributed to distal embolization and occur in 3%-6% of cases. Long-term patency is 94%-97% at 20 months.^21-24 The lower periprocedural complication rates compared to surgery make the endovascular approach an attractive option, especially for patients at high surgical risk. On the other hand, heavily calcified lesions, lesions involving vertebral artery, or a totally occluded subclavian artery may render the percutaneous route more challenging and increase the risk of complications.

To our knowledge, this is the first report describing the use of AngioSculpt scoring balloon in the treatment of subclavian artery disease. The AngioSculpt balloon was chosen in this case due to the severely calcified nature of the subclavian lesion. The semi-compliant balloon is designed with a flexible, nitinol scoring element and 3 or 4 rectangular spiral struts needed to score the target lesion. Therefore, scoring balloon use allows us to concentrate uniform radial forces along the edges of the nitinol element, potentially improving the ability to “score” the calcified plaque, while minimizing the risk of perforation.

References

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From the New York Presbyterian Hospital, Weill Cornell Medical College, New York, New York.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. The authors report no conflicts of interest regarding the content herein.
Manuscript submitted August 10, 2011, provisional acceptance given August 15, 2011, final version accepted September 29, 2011.
Corresponding author: Dr. Dmitriy N. Feldman, MD, New York Presbyterian Hospital, Weill Cornell Medical College, Greenberg Division of Cardiology, 520 East 70th Street, New York, NY 10021. Email: dnf9001@med.cornell.edu