Ann Thorac Surg 2009;87:634-636. doi:10.1016/j.athoracsur.2008.07.016
© 2009 The Society of Thoracic Surgeons
Case Reports
Massive Alterations of the Left Internal Thoracic Artery Late After Repair for Aortic Coarctation
Brigitte R. Osswald, MD*,
Stefan Knipp, MD,
Ingo Wiese,
Heinz G. Jakob, MD, PhD
Department for Thoracic and Cardiovascular Surgery, University of Essen, Essen, Germany
Accepted for publication July 9, 2008.
* Address correspondence to Dr Osswald, Department of Thoracic and Cardiovascular Surgery, University of Essen, Hufelandstr. 55, Essen, 45147, Germany (Email: brigitte.osswald{at}uk-essen.de).
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Abstract
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Adhesions or unattended injury are known but are seldom reasons to prevent withdrawing the use of the left internal thoracic artery during coronary artery bypass grafting. The patient in this case report was a 68-year-old man, who had undergone repair for aortic coarctation 34 years prior to coronary artery bypass grafting. After left internal thoracic artery harvesting, a no-flow situation of the graft was present. Transection of the graft revealed massive atherosclerotic alterations. To avoid unnecessary left internal thoracic artery harvesting, preoperative imaging in terms of a left internal thoracic artery angiography during coronary angiography is mandatory. The fact of finding massive alterations decades after pressure reduction indicates that relief from shear stress is not necessarily combined with remodeling of vascular alterations.
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Introduction
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Arterial revascularization represents the gold standard for coronary artery bypass grafting coronary artery bypass grafting. Structural alterations of the left internal thoracic artery (LITA) due to thoracic trauma, radiation, or massive atherosclerosis are extremely rare. This is the first report on massive structural alterations of the LITA decades after longstanding aortic coarctation. The aim of our case report is to focus on the necessity to perform LITA, imaging especially in patients with history of aortic coarctation.
A 68-year-old man was admitted to the hospital presenting with an acute coronary syndrome. Coronary angiography confirmed left main disease and high-degree proximal stenoses of the left coronary system, and an already impaired left ventricular function classified as an ischemic cardiomyopathy with left ventricular dilation (20 mm Hg at rest and 24 mm Hg after exercise). Acute symptoms persisted for 3 hours and primarily improved by administration of intravenous nitroglycerin and heparin. For 4 weeks he suffered from recurrent episodes of typical angina. Cardiovascular risk factors included smoking (40 pack-years), an elevated cholesterol level, and hypertension, which was already being treated by angiotensin-converting enzyme inhibitors and β-blockers. Thirty-four years ago the patient underwent repair for aortic coarctation. In 2001, he had prostate cancer that was successfully treated.
The preoperative cardiac troponin I level was 0.03/nL. Because of recurrent unstable angina, despite intravenous medication, an emergent on-pump coronary artery bypass grafting was immediately performed. Due to his hemodynamically stable condition at the beginning of the surgical procedure, the left LITA was harvested. Because of the emergency, there was no preoperative thoracic roentgenogram or imaging of the LITA done during coronary angiography. Furthermore, a preoperative evaluation of the cuff arm pressures was not taken from both arms, but postoperatively identical arm cuff pressures were approved. During preparation of the LITA, the vessel presented massive adhesions throughout the total length of the sternum. Careful preparation allowed a complete removal and preserved vessel integrity. The thickness of the thoracic artery wall was at the upper normal level (outer diameter, 
3.5 mm); furthermore, a rather stiff vessel wall and pulselessness throughout the total length of the vessel was observed. After division of the distal end, a no-flow condition occurred that could not be resolved by medical or mechanical dilation. Because we suspected a potential technical problem, the proximal part of the LITA was cut for potential use as a free graft. Injection of saline solution into the proximal end of the graft confirmed the total occlusion. Finally, the complete transection revealed multiple subtotal and total occluding plaques throughout the total LITA (Fig 1). Therefore, a saphenous vein graft was used for left anterior descending coronary artery grafting. Complete revascularization was achieved with a further sequential saphenous vein graft to the first diagonal and first marginal branch, and another saphenous vein graft to the right coronary artery. The postoperative chest roentgenogram showed the remaining typical rib notches predominantly at the left thorax (Fig 2). A clinical investigation at rest showed no difference between the upper and lower peripheral blood pressure, indicating a good surgical result late after surgical repair for aortic coarctation.
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Fig 1. Specimen of the left internal thoracic artery after complete transection presenting multiple total and subtotal atherosclerotic lesions.
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Fig 2. Postoperative chest roentgenogram indicating the remaining rib notches as a remnant of the aortic coarctation.
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Comment
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We believe that this is the first report written describing a patient undergoing emergent coronary artery bypass grafting with documented massive atherosclerotic LITA alterations. Because the repair for aortic coarctation accounts for the more often performed surgical procedures of congenital malformations, it is likely to face a relatively large number of these types of patients in the near future. Therefore, the aim of this report is to stress the advantage of LITA imaging even during emergent coronary angiography. This is especially true for patients with prior repair of coarctation, but also for patients with a history of thoracic trauma and radiation. A systematic analysis on the failure rates for "successful" LITA harvesting is lacking. Left internal thoracic artery harvesting of a structurally altered LITA is demanding, time-consuming, and in the end, an avoidable extension of the surgical procedure. Therefore, in terms of an optimal and rapid revascularization, LITA imaging during coronary angiography, as performed by many cardiologists contributes to a substantial shortening of the procedure. Although significant stenoses of the subclavian artery or LITA itself are seldom [1], the LITA with acceptable flow pattern is still associated with a malperfusion rate as high as 2.3% [2]. Failure rates of LITA 1 year after coronary artery bypass grafting are reported to be as high as 5%; however, in only 2.3% of the same patients, the LITA itself presents stenoses of at least 50% [3]. Berger and colleagues [4, 5] published a 10% rate of late arterial graft closure; they assumed chronic competition induced by a moderate coronary lesion to represent a major factor of arterial shrinkage. More recently, 1% of the patients with low flow during flow measurement (despite proven graft patency and a technical satisfactory distal anastomosis) survived only if a venous graft was immediately connected to the same target vessel. Spontaneous dissection or severe arterial vessel spasm are discussed to be responsible for early LITA failure [6]. In our patient, the "no flow" situation primarily prevented the use of the graft. However, even in cases of less extensive graft alterations the proven advantage of arterial grafting in the general population needs to be carefully weighed against the risk of substantial structural damage, especially in patients after repair of aortic coarctation.
The current models for atherogenesis focus on shear stress as one of the major pathogenetic mechanisms. In our patient, a pre-existent vessel injury at the time of repair for aortic coarctation, because of the longstanding disease (>30 years) is assumable. On the other hand, further aggravation of the lesions after relief from the longstanding high pressure and extreme blood velocity through the thoracic artery may have also occurred. Although there is no guideline or special report, therapeutic options for the severely altered arterial vascular bed, such as preventive administration of statins and the optimization of blood pressure to possibly help further minimize vascular alterations of the arterial system.
The community will shortly face a larger number of patients who underwent simple or complex repair for aortic coarctation and related cardiac malformation. The fact of observing coronary artery disease in a 68-year-old man corresponds to the mean age of such patients. However, due to the longstanding disease with high systemic blood pressure in the upper arterial system, the probability for the development of coronary artery disease or peripheral vascular disease, especially in the upper arterial system, may be increased in patients presenting with history of aortic coarctation. Nevertheless, larger surveys are necessary to ascertain the hypothesis.
In conclusion, we predict that the prevalence of adult or elderly patients with a history of repair for aortic coarctation will increase during the next few years. Although coronary artery disease represents the leading disease of the Western countries, patients after at least a longstanding aortic coarctation may be at an even higher risk, and therefore these patients require a more intense monitoring of relevant extracardiac atherosclerosis.
Imaging of both thoracic arteries in patients presenting with a history of aortic coarctation seems mandatory, even in cases of an emergency.
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References
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- Edwards WH. An unsuspected cause for recurrent angina: subclavian artery stenosis Am Surg 1995;61:1057-1060.[Medline]
- Massoudy P, Kim YY, Cetin M, et al. Internal thoracic artery malperfusion: fast decision for an additional vein graft has impact on patient outcome Ann Thorac Surg 2004;77:2061-2065.[Abstract/Free Full Text]
- Barner HB, Mudd JG, Mark AL, Ahmad N, Dickens JF. Patency of internal mammary-coronary grafts Circulation 1976;54(Suppl 6):III70-III73.[Medline]
- Berger A, Mac Carthy PA, Vanermen H, De Bruyne B. Occlusion of internal mammary grafts: a review of the potential causative factors Acta Chir Belg 2004;104:630-634.[Medline]
- Berger A, Mac Carthy PA, Siebert U, et al. Long-term patency of internal mammary artery bypass graft Circulation 2004;110(SupplII):II36-II40.[Medline]
- Jones EL, Lattouf OM, Weintraub WS. Catastrophic consequences of internal mammary artery hypoperfusion J Thorac Cardiovasc Surg 1989;98:902-907.[Abstract]
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Abstract
Introduction
