Journal of Cardiovascular Echography

LETTER TO EDITOR
Year
: 2019  |  Volume : 29  |  Issue : 2  |  Page : 86--87

High-risk NSTEMI due to subclavian artery atherothrombosis in a prior coronary artery bypass graft patient


Michele Coceani1, Francesco Sbrana2, Marco Ciardetti1, Beatrice Dal Pino2, Cataldo Palmieri1, Sergio Berti1, Alberto Giannoni3, Michele Emdin4, Tiziana Sampietro2,  
1 Division of Interventional Cardiology, Fondazione Toscana Gabriele Monasterio, Pisa and Massa, Pisa, Italy
2 Lipoapheresis and Inherited Dyslipidemias Center, Fondazione Toscana Gabriele Monasterio, Pisa, Italy
3 Division of Cardiology and Cardiovascular Medicine, Fondazione Toscana Gabriele Monasterio, Pisa, Italy
4 Division of Cardiology and Cardiovascular Medicine, Fondazione Toscana Gabriele Monasterio; Institute of Life Sciences, Scuola Superiore Sant'Anna, Pisa, Italy

Correspondence Address:
Francesco Sbrana
Fondazione Toscana Gabriele Monasterio, Via Moruzzi 1, 56124, Pisa
Italy




How to cite this article:
Coceani M, Sbrana F, Ciardetti M, Pino BD, Palmieri C, Berti S, Giannoni A, Emdin M, Sampietro T. High-risk NSTEMI due to subclavian artery atherothrombosis in a prior coronary artery bypass graft patient.J Cardiovasc Echography 2019;29:86-87


How to cite this URL:
Coceani M, Sbrana F, Ciardetti M, Pino BD, Palmieri C, Berti S, Giannoni A, Emdin M, Sampietro T. High-risk NSTEMI due to subclavian artery atherothrombosis in a prior coronary artery bypass graft patient. J Cardiovasc Echography [serial online] 2019 [cited 2020 Nov 30 ];29:86-87
Available from: https://www.jcecho.org/text.asp?2019/29/2/86/263015


Full Text



Dear Sir,

A 78-year-old female with a history of familial hypercholesterolemia, chronic renal disease secondary to nephroangiosclerosis, and anemia came to our attention for acute coronary syndrome characterized by diffuse ST-segment depression on 12-lead electrocardiogram [Figure 1]a. No other coronary risk factors were present. Three years earlier, she had been diagnosed with stable angina and had undergone the left internal mammary artery to the left anterior descending artery bypass grafting (at that time, tendon xanthomas were present and low-density lipoproteins cholesterol was 248 mg/dl in the absence of lipid-lowering therapy). Before surgery, invasive angiography had shown subocclusive stenoses of both coronary artery ostia [Figure 1]b,[Figure 1]c and [Supplementary Videos 1, 2], the origin of the left subclavian artery [Supplementary Video 3], and of the juxtarenal abdominal aorta [Figure 1]d and [Supplementary Video 4]. Indeed, bypass surgery had been preceded by subclavian artery stenting; the right coronary artery had not been revascularized either surgically, because of porcelain aorta, or percutaneously after surgery, given the absence of residual ischemia at stress echocardiography.{Figure 1}

After admission, she was symptomatic for the chest pain; the right and left arterial brachial pressures were 150/80 and 110/60 mmHg, respectively. Baseline high-sensitivity troponin was 31.2 ng/L and reached a peak value of 755.4 ng/L, which was compatible with the diagnosis of acute myocardial infarction. Invasive angiography was repeated through the left radial artery which confirmed 2-vessel coronary artery disease, and also revealed a stenosis of the subclavian artery between the stent which had been previously implanted and the origin of the left internal mammary artery, which was patent [Figure 1]e and [Supplementary Video 5]. Because of an anomalous left radial artery with an associated vasospasm [Supplementary Video 6], a guiding catheter could not be advanced. For this reason, a second arterial access was obtained through the right femoral artery. A long supportive sheath (Super Arrow-Flex, Teleflex) was then placed across the subocclusion of the abdominal aorta [Supplementary Video 7], and a Judkins left diagnostic catheter was advanced through the sheath for contrast injection into the subclavian artery. From the left radial artery, a 0.035-inch hydrophilic guidewire was positioned in the descending aorta, and subsequently, the stenosis of the subclavian artery was dilated with a 5 mm × 40 mm balloon [Armada, Abbott Vascular, [Figure 1]f. Finally, an 8 mm × 27 mm stent (Express LD, Boston Scientific) was deployed, partially overlapped with the previous stent [Figure 1]g and Supplementary Video 8]. Angiographic outcome was satisfactory [Figure 1]h, and the electrocardiogram rapidly improved. During the postprocedural period, the patient remained asymptomatic for angina but developed contrast-induced nephropathy which required two dialysis sessions. She was eventually discharged home 12 days after the initial procedure and is still doing well.

Subclavian “steal” phenomenon is caused by proximal subclavian artery steno-occlusive disease which leads to retrograde blood flow in the ipsilateral vertebral artery. Symptoms due to compromised vertebrobasilar and brachial blood flows characterize the subclavian steal syndrome and include paroxysmal vertigo, drop attacks, and arm claudication.[1] Coronary-subclavian artery steal syndrome is a rare complication of coronary artery bypass grafting surgery and is secondary to retrograde flow from the left internal mammary artery to the left subclavian artery in the presence of a proximal stenosis of the latter.[2] Significant left subclavian artery stenosis in patients referred for coronary bypass surgery has a prevalence that varies from 0.2%–6.8%,[3] but progression of atherosclerosis may occur even after cardiac surgery. Coronary-subclavian steal syndrome typically presents with stable angina, but acute coronary syndrome in patients with previous coronary artery bypass graft has been described.[3],[4],[5] Percutaneous coronary intervention represents first-line therapy for these patients, whereas vascular bypass surgery is reserved for high-risk cases (such as those with chronic total occlusion of the subclavian artery).[6] Although in the past, coronary-subclavian steal syndrome was thought to be relatively rare, the more frequent description of this phenomenon in recent years suggests that its clinical impact has been underestimated.[2] Compared to previous reports, in the present case, the interventional cardiologists were faced with several technical challenges (such as arterial access difficulties and diffuse calcified atherosclerosis) which complicated the placement of the stent in the left subclavian artery.[MULTIMEDIA:1][MULTIMEDIA:2][MULTIMEDIA:3][MULTIMEDIA:4][MULTIMEDIA:5][MULTIMEDIA:6][MULTIMEDIA:7][MULTIMEDIA:8]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Osiro S, Zurada A, Gielecki J, Shoja MM, Tubbs RS, Loukas M. Areview of subclavian steal syndrome with clinical correlation. Med Sci Monit 2012;18:RA57-63.
2Takach TJ, Reul GJ, Cooley DA, Duncan JM, Livesay JJ, Ott DA, et al. Myocardial thievery: The coronary-subclavian steal syndrome. Ann Thorac Surg 2006;81:386-92.
3Uzunlar B, Karabulut A, Dogan Z. Non-ST elevation myocardial infarction triggered by subclavian steal syndrome. Int J Angiol 2016;25:e37-e38.
4Dimas B, Lindsey JB, Banerjee S, Brilakis ES. ST-segment elevation acute myocardial infarction due to severe hypotension and proximal left subclavian artery stenosis in a prior coronary artery bypass graft patient. Cardiovasc Revasc Med 2009;10:191-4.
5Cresti A, Misuraca L, Pieraccini M, Calabria P, Sinesi L, Picchi A, et al. An unexpected culprit lesion: Subclavian artery stenosis. G Ital Cardiol (Rome) 2015;16:574-7.
6Linni K, Ugurluoglu A, Mader N, Hitzl W, Magometschnigg H, Hölzenbein TJ. Endovascular management versus surgery for proximal subclavian artery lesions. Ann Vasc Surg 2008;22:769-75.