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Ann Thorac Surg 2007;83:515-516
© 2007 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Invited commentary

Louis P. Perrault, MD, PhD, Arnaud Mommerot, MD

Department of Surgery, Montreal Heart Institute, 5000 Belanger St, Montreal, Quebec, H1T1C8 Canada

(Email: louis.perrault{at}icm-mhi.org).

Arterial conduits are increasingly used for coronary artery bypass grafting surgery (CABG). Their superior long-term patency rate, compared with venous grafts, make them the conduits of choice for myocardial revascularization. However, both radial arteries (RAs) and internal mammary arteries (IMAs) are prone to a dreaded complication, the vasospasm. In vitro studies help to elucidate the pathophysiological mechanisms involved and may improve the perioperative management of these grafts to prevent occurrence of such adverse events. In this article, Rabbani and associates [1] address the basis of the regulation of IMA and RA contraction by extracellular and intracellular calcium, and by cyclic AMP (cAMP). They demonstrate that the contraction elicited by thromboxane A2 (TXA2), and by the {alpha}-adrenoreceptor agonist, phenylephrine (both released during CABG with cardiopulmonary bypass) have different mechanisms. Although the TXA2 analog, U46619, induces contraction through combined extracellular calcium influx and intracellular calcium release, phenylephrine induces contraction mainly through an extracellular calcium influx. These data suggest that calcium channel blockers may not be useful in preventing TXA2-induced vasospasm. On the other hand, the cAMP signaling pathway does not seem to be affected by TXA2. Thus, pharmacological agents maintaining a high cAMP level, either by increasing its production or by preventing its degradation, are likely to be useful in this situation.

This study brings new insights to the pathophysiology of arterial graft spasm in the perioperative period and suggests an interest for certain pharmacological drug classes in preventing graft contraction elicited by endogenous TXA2 release, including phosphodiesterase III inhibitors (such as milrinone) or adenylate cyclase activators (such as forskolin) used here. Although this type of in vitro study gives insight into the operative mechanisms shortly after graft implantation, further work (both bench and clinical) should address the optimal long-term drug management of the RA as a graft conduit.


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  1. Rabbani G, Vijay V, Sarabu MR, Gupte SA. Regulation of human internal mammary and radial artery contraction by extra- and intra-cellular Ca2+ and by cAMP Ann Thorac Surg 2007;83:510-516.[Abstract/Free Full Text]

Related Article

Regulation of Human Internal Mammary and Radial Artery Contraction by Extracellular and Intracellular Calcium Channels and Cyclic Adenosine 3', 5' Monophosphate
Golam Rabbani, Venkataramana Vijay, Mohan R. Sarabu, and Sachin A. Gupte
Ann. Thorac. Surg. 2007 83: 510-515. [Abstract] [Full Text] [PDF]



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