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Ann Thorac Surg 2001;72:816
© 2001 The Society of Thoracic Surgeons

Invited commentary

Guo-Wei He, MD, PhDa,b

a Department of Surgery, The Chinese University of Hong Kong, Hong Kong SAR, China
b Provincial Hospital, Department of Cardiac Surgery, Anhui Heart Institute, Provincial Hospital, Anhui Medical University, Hefei, China

e-mail: gwhe{at}cuhk.edu.hk

The use of arterial grafts in coronary artery bypass grafting is widely accepted and the internal mammary artery (IMA) has been the primary major arterial graft. Arterial grafts are small to mid-sized conduit arteries. A major concern of arterial grafting is perioperative vasospasm in the graft [1, 2]. Although the results of IMA grafting are excellent, and this artery is used in the daily practice of most cardiac surgeons around the world, vasospasm is encountered in IMA grafts, as in other arterial grafts such as the radial artery and the gastroepiploic artery. Vasospasm of arterial grafts has been studied for many years and methods to overcome spasm have been developed. These include: (1) avoidance of the most spastic part of the IMA (the very distal section [3]); (2) pharmacological methods: spray of vasodilators on the IMA pedicle or intraluminal injection of vasodilators [4]; and (3) mechanical dilatation of the IMA graft with/without additional pharmacological methods.

Vasospasm in arterial grafts is clearly related to endothelial function. Our most recent studies show differences in the release of nitric oxide and endothelium-derived hyperpolarizing factor between the IMA and the saphenous vein [5]. Development of vasospasm in an arterial graft is clearly related to damage to endothelial function. When endothelial function is damaged, such as occurs with inadequate preparation of the graft, the graft has a tendency to go into vasospasm; therefore, preservation of endothelium during preparation of the IMA is important.

With regard to preservation of endothelial function in general, pharmacological methods should be better than mechanical dilatation. This is because any mechanical dilatation of the graft in diameter of only 1 mm to 2 mm diameter inevitably damages the intima and its single-layered endothelium to some extent by contact with the mechanical dilator. Although the authors demonstrated that endothelium-dependent relaxation is preserved after long balloon dilatation, this does not exclude the damage to the endothelium by mechanical dilatation due to the fact that endothelium-dependent relaxation may reach 100% when only a percentage of endothelial cells is functioning. Evidence of mechanical damage to the endothelium is shown by the authors’ own data in that the percentage of intact endothelium by silver nitrate staining is significantly less after long balloon dilatation, compared with control (see Figure 6A in the article by Jeanmart and associates). Therefore, strictly speaking, the so-called "atraumatic" device in this article is still traumatic. Moreover, although endothelium-dependent relaxation is preserved, the long-term influence of damage to the endothelium on graft patency is unknown and needs to be studied.

On the other hand, pharmacological methods have proved to be effective in dilatation of arterial grafts. In my practice, particularly in small-sized patients such as in some Chinese women, the diameter of the IMA is between 1 mm to 1.5 mm. When dissected from the chest wall, the initial flow can be very low, even immeasurable. However, after treatment with vasodilators such as VG solution (verapamil + nitroglycerin) [4]— either sprayed on the pedicle or injected intraluminally (the tip of a 24 gauge needle only inserted into the IMA for 0.5 cm)— 20 to 30 minutes later, with a pump pressure of 60 to 70 mm Hg, flow increases tremendously and usually becomes ejecting. I have no need for any mechanical dilators that are inserted into an IMA graft for either "short" or "long" distances as the authors used in this study.

I would therefore recommend caution regarding the mechanical dilatation of arterial grafts. Such use should be limited to a small number of patients in whom the surgeon cannot overcome vasospasm by other means. In my own opinion, such situations are rare.

References

  1. He G.-W. Arterial grafts for coronary surgery: vasospasm and patency rate. J Thorac Cardiovasc Surg 2001;121:431-433.[Free Full Text]
  2. He G.-W. Arterial grafts for coronary artery bypass: biological characteristics, functional classification, and clinical choice. Ann Thorac Surg 1999;67:277-284.[Abstract/Free Full Text]
  3. He G.-W. Contractility of the human internal mammary artery at the distal section increases towards the end. Emphasis on not using the end of the artery for grafting. J Thorac Cardiovasc Surg 1993;106:406-411.[Abstract]
  4. He G.-W., Rosenfeldt F.L., Angus J.A., Buxton B.F. Pharmacological dilatation of internal mammary artery during surgery. J Thorac Cardiovasc Surg 1994;107:1440-1444.[Abstract/Free Full Text]
  5. Liu Z.-G., Ge Z.-D., He G.-W. Difference in hyperpolarization between human internal mammary artery and saphenous vein. Circulation 2000;102(Suppl III):III296-III301.[Abstract/Free Full Text]

Related Article

Arterial balloon catheter: a new atraumatic device for dilating arterial grafts
Hugues Jeanmart, Louis P. Perrault, Nathalie Desjardins, Olivier Chavanon, Michel Carrier, and James D. Fonger
Ann. Thorac. Surg. 2001 72: 810-815. [Abstract] [Full Text] [PDF]




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