Ann Thorac Surg 2006;81:2154
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Invited commentary
Anders Franco-Cereceda, MD, PhD
Department of Thoracic Surgery, Karolinska University Hospital, Stockholm, 171 76 Sweden
(Email: andfra{at}mbox.ki.se).
The use of the radial artery as a graft for coronary revascularization was already introduced in the 1970s, but shortly thereafter it was abandoned due to a high rate of graft failure. This was partly due to the inability to recognize radial artery spasm, but it was also due to lack of proper pharmacological tools to prevent this. Because it was later noted that radial grafts were indeed patent in patients long after their surgery, the radial artery was reassessed and its role as an alternative arterial graft was re-established. Although the patency rate is debatable, several studies now suggest that by using drugs such as calcium channel blockers and nitroglycerin to prevent spasms, 10-year radial artery graft patency may reach 90% and greater, making the radial artery a valuable addition in arterial grafting.
In their interesting article, Arshad and coworkers [1] have addressed the differences in vascular reactivity between the radial artery and internal mammary artery in an attempt to establish a molecular basis for the regulation of vasomotor tone in the radial artery. The relative production of vasoconstrictor agents (ie, thromboxane is enhanced in the radial artery compared with vasodilator autocoids or prostacyclin). This is not the case for the internal mammary artery. Moreover, the release of thromboxane suppresses nitric oxide-mediated vasodilatation through inhibition of soluble guanylate cyclase activity. The findings may have important clinical implications because we know that circulating thromboxane is elevated in coronary artery disease and released after cardiac surgery. In addition, the results help explain the relative role of endogenous (acetylcholine, prostanoids) and exogenous (nitroglycerin, phosphodiesterase inhibitors) vasodilators in prevention of graft spasm. By their study, Arshad and coworkers [1] provide us with not only a suggested mechanism by which radial artery spasm is explained, but more importantly, a suggested pharmacologic target to prevent this.
 |
References
|
|---|
- Arshad M, Vijay V, Floyd BC, et al. Thromboxane receptor stimulation suppresses guanylate cyclase-mediated relaxation of radial arteries Ann Thorac Surg 2006;812147–1754..
Top
References