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Ann Thorac Surg 2006;82:1702-1703
© 2006 The Society of Thoracic Surgeons
Department of Cardiothoracic Surgery, The Royal Melbourne Hospital, PO Box 2135, Parkville, Victoria 3052, 3050, Australia
(Email: alistair.royse{at}mh.org.au).
The article by Madssen and colleagues [1] examines a most important question. Cardiologists and interventional radiologists seek to reduce the morbidity of femoral arterial puncture and possibly to reduce the dislodgement of aortic arch atheroma during their procedures by cannulating the radial artery prior to coronary angiography or other procedures. After all, the radial artery is easily accessible, and allows for simple compression bandaging and rapid mobilization of the patient. The question is whether this may compromise subsequent use of the same radial artery as a conduit for coronary artery bypass surgery.
In this study these authors found that at 1 year post-angiography, the right radial artery which was cannulated was significantly smaller than the noncannulated left radial artery by a small degree, yet the response to ischemic or nitroglycerin induced vasodilation remained the same for both left and right sides. Patients with multiple radial artery cannulations were excluded. The site of this imaging was proximal to the side of cannulation for angiography and represents the distal segment of the radial artery that would be used in the coronary bypass graft. These results are both encouraging and of some concern.
At 1 year after angiography, there seemed to have been complete recovery of the endothelial function of the radial artery. Wide individual variation may have reflected multiple causes including some calcification within the radial artery that was not documented in the study. This is encouraging for the cardiac surgeon for it represents normal radial artery vascular function proximal to the puncture site, validating use of the radial artery as a conduit after this approach to angiography.
However, it would be expected that the radial artery of the dominant hand would be up to 6% larger than the nondominant side. These authors found that the right radial artery representing the dominant side was significantly smaller than the nondominant side, suggesting that scar formation at the site of radial artery puncture had caused some degree of stenosis with some degree of reduced flow, and therefore a reduced size of the radial artery proximal to the puncture site. Provided that this puncture site was excluded from use in the bypass conduit, then no difficulty would be expected with its use as a conduit. The problem with this rationale arises when numerous passages of the needle are required to cannulate the radial artery resulting in: greater scarring of the vessel, proximal puncture site, dissection for some distance within the wall of the radial artery at the time of angiography, prolonged compression causing occlusion of the radial artery, or repeated radial artery punctures resulting from repeated coronary angiograms or other interventional vascular procedures in time. It would be expected under these circumstances that occlusion, or a greater degree of scarring or damage to the radial artery over a longer distance would likely ensue. These may potentially damage the radial artery sufficiently to contraindicate radial artery use as a conduit.
To return to the central question: How much trauma to the radial artery can be sustained before the radial artery is no longer suitable as a conduit for coronary artery bypass surgery? This article would suggest that a single distally sited radial artery puncture for coronary angiography induces some damage that should not preclude the use of the radial artery as a conduit. In this regard, this article is of significant value. It remains to be seen whether "routine" radial artery based coronary angiography or coronary interventions would damage the radial artery sufficiently to preclude it for subsequent coronary artery bypass surgery as a conduit.
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