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Ann Thorac Surg 1995;60:1810-1812
© 1995 The Society of Thoracic Surgeons
National Defence Medical Centre and University of Ottawa Heart Institute, Ottawa, Ontario, Canada
Accepted for publication June 17, 1995.
| Abstract |
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| Introduction |
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``The complex hemodynamic situation created by uniting the fate of the arm and the myocardium makes scrupulous evaluation essential.'' A. Hedley Brown [1]
In 1961, Reivich and associates [2] described cerebral ischemia due to flow reversal in a vertebral artery arising beyond subclavian stenosis. An editorial [3] felicitously named this ``the subclavian steal.'' Collateral inflow from other subclavian branches was predictable, but not clinically significant until the internal mammary (internal thoracic) arteries (IMAs) were used as coronary bypass grafts from the early 1970s. In 1974, Harjola and Valle [4] reported ``delay in the flow'' of contrast medium in an IMA beyond subclavian stenosis, which they corrected by carotid--subclavian artery grafting. In 1977, however, Brown [1] reported true coronary subclavian steal in a patient who died at the end of a coronary bypass procedure using both IMAs; retrograde coronary to subclavian flow was measured by flowmeter at 100 mL/min but incorrectly ascribed to probe reversal. Brown believed that this patient died because coronary subclavian steal was not overcome by inflow through native channels and the other grafts, found patent at autopsy. Other examples of coronary subclavian steal have been described; in 1977, Tyras and Barner [5] reported 2 cases (0.44%) in 450 patients having IMA--coronary artery grafting. Angina may result but, as in our case of recurring coronary steal, the iatrogenic myocardial perfusion deficit may be silent. Stenosis of the brachiocephalic trunk, producing ``innominate grand larceny,'' requires transthoracic endarterectomy; this is not usually done for subclavian obstruction, which is most commonly treated by carotid--subclavian artery grafting, preferably with a synthetic conduit. Percutaneous transluminal subclavian angioplasty has been described [6], and more recently [7], directional atherectomy.
A 43-year-old Royal Canadian Air Force Navigator, whose legs were badly burned in a 1957 aircraft accident, was referred for new electrocardiographic abnormalities, having no cardiac discomfort then, nor at any time since. Arm blood pressures (BPs) were equal. Treadmill exercise test (TMT) produced ventricular tachycardia and electrocardiographic ischemia. Left ventriculogram was normal. Important proximal stenoses in the anterior descending coronary artery (ADCA) and in its major diagonal branch, other coronary vessels being unremarkable, made us consider coronary bypass, despite lack of symptoms [8]. Because burn scars would preclude saphenous vein use, coronary angiography included selective demonstration of large IMAs; there were no subclavian pressure gradients.
In 1973, the right IMA (RIMA) was grafted to the diagonal branch and the left IMA (LIMA) to the ADCA, with excellent angiographic results then and a year later. In 1984, after he had discontinued antiplatelet therapy, the patient's exercise tolerance was diminished and his TMT again was positive. The BP difference between the arms was 60 mm Hg. The ADCA stenosis was unchanged but the diagonal branch was occluded above its graft and there was new nonobstructive disease in other coronary vessels; the RIMA was excellent but contrast medium coursing down the ADCA flowed rapidly up the LIMA (Fig 1
) and into the left subclavian artery, opacifying it beyond the proximal occlusion (Fig 2
). Selective right vertebral artery angiography showed a large high-flow vessel, sending equal streams to normal basilar and large left vertebral arteries; LIMA inflow produced turbulent dilution of this retrograde flow into the left subclavian artery (Fig 3
). Nonobstructive disease was seen in both common and external carotid arteries. An 8-mm GoreTex (W. L. Gore & Assoc, Flagstaff, AZ) common carotid--subclavian artery graft (CSG) was placed with excellent angiographic results. Arm BPs were the same but a supraclavicular thrill and bruit have been noted since; TMT was negative.
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At reoperation, organized clot and fresh distal thrombus had produced a slit lumen. A new 8-mm Gore-Tex graft was placed, and no postoperative angiography was performed.
In 1989, worsening claudication led to aorta--bifemoral grafting. Interarm BP difference was 30 mm Hg; the TMT again was positive. The ADCA was unchanged but other coronary stenoses increased to about 25%. The RIMA was clean with high flow, but there was no LIMA flow either way at rest. The CSG was irregular with 20% proximal and 50% distal stenoses. The left vertebral artery flow was sluggish antegrade, and there was increasing carotid disease. After much discussion, we replaced the GoreTex at a second reoperation with a 12-mm Hemashield CSG graft (Meadox Medicals, Oakland, NJ); thrombus/atherosclerosis had reduced the lumen to less than 50%. No postoperative angiogram was performed. Long-term warfarin anticoagulant therapy was started and aspirin administration continued.
In 1992, the patient was asymptomatic and the arm BPs were the same, but the TMT was positive. There was increasing ADCA calcification, but the stenosis was unchanged. The CSG was smooth but there was 80% narrowing of the proximal left subclavian artery at the anastomosis heel. The LIMA was smaller with low flow, and the RIMA was excellent. No intervention was performed.
In 1994, arm BPs were the same but the TMT was still positive. There was minimal left ventricular anterior hypokinesis and increasing nonobstructive coronary disease, but the ADCA was unchanged. The CSG was regular, but the distal anastomosis heel stenosis was now 90%. Left vertebral artery flow was normal, but LIMA flow was slow, probably because of ostial compromise. To correct critically low ADCA flow, we performed percutaneous transluminal angioplasty and stent placement, which reduced the stenosis of the lumen to 10%: old problem (happily static for two decades)-new solution. The TMT was now negative.
At the 1995 follow-up, the patient was asymptomatic; medical therapy continued. Medicine being no less hazardous than surgery, anticoagulant therapy was complicated by gastrointestinal bleeding of unknown cause (international normalized ratio, 2.4) requiring transfusion of 5 units; there was no recurrence. Arm BPs were equal; there were a supraclavicular thrill and loud bruit as before.
| Comment |
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| Acknowledgments |
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We acknowledge, with pleasure, the assistance of Lucie Morin-Brock in preparing the manuscript.
| Footnotes |
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| References |
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