Ann Thorac Surg 2000;69:1040-1041
© 2000 The Society of Thoracic Surgeons
ORIGINAL ARTICLES: CARDIOVASCULAR
Invited commentary
Oz M. Shapira, MDa
a Department of Cardiothoracic Surgery, Boston Medical Center, 88 East Newton St, Boston, MA 02118, USA
e-mail: oshapira{at}bu.edu
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Introduction
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 Introduction
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The radial artery is an attractive arterial conduit for coronary artery bypass grafting (CABG) for several reasons. First, it is easy to harvest in parallel with the internal mammary artery. In addition, there is often sufficient length to allow grafting of any target vessel. Finally, the radial artery caliber is well matched to that of most coronary arteries, and its thick muscular wall affords easy surgical handling. Recent studies also suggest improved inherent physiologic properties of the radial artery, similar to those of the internal mammary artery. Thus, single and bilateral radial arteries are increasingly used as the second arterial conduit of choice (after the internal mammary artery) with encouraging early and midterm results.
The major disadvantage of the radial artery is its propensity for vasospasm documented both clinically, and in studies using organ-chamber methodology. Enhanced reactivity of the radial artery to norepinephrine, serotonin, angiotensin II, and endothelin I compared with internal mammary artery has been documented in vitro and is confirmed in this study by Bond and colleagues. Clinical and angiographic (eg, the "string" sign) evidence of radial artery spasm are well recognized. Thus, most surgeons (although not all) emphasize the necessity for pharmacologic intervention to prevent vasospasm when these conduits are used. The calcium channel antagonist diltiazem has been empirically selected by most surgeons.
However, diltiazem does not completely eliminate graft spasm. Short- and midterm angiographic studies performed in patients undergoing CABG and treated with diltiazem documented radial artery graft spasm in 1% to 9.7%. Also, use of diltiazem may be associated with negative inotropic and chronotropic side effects, a distinct disadvantage after CABG. Therefore, the empiric selection of diltiazem as the agent of choice has been recently challenged.
In their paper, Bond and colleagues, using organ-chamber methodology, compared the efficacy of diltiazem with that of two other calcium antagonists in preventing norepinephrine- and endothelin-induced radial artery spasm. They found diltiazem to be much less effective compared with nifedipine and amlodipine. The results of this study confirm previous reports from our laboratory and others documenting that diltiazem is a very weak radial artery vasodilator. Although nifedipine and amlodipine are more vascular selective, the potential for undesirable myocardial depression and conduction side effects still exists. An alternative agent is nitroglycerin. Nitroglycerin lacks the above-mentioned side effects, and has been shown to be very effective in preventing radial artery spasm. Because vascular responses to vasoactive agents in vivo may be utterly different than those observed in vitro, one should be cautious in implementing these laboratory observations in clinical practice. Undoubtedly, the data provided by Bond and others clearly justify a placebo-controlled prospective randomized clinical trial to determine whether antispasmodic treatment is at all better than placebo, and to identify the agent of choice for prevention of radial artery graft spasm.
Related Article
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Differential effects of calcium channel antagonists in the amelioration of radial artery vasospasm
- Brian R. Bond, James L. Zellner, B. Hugh Dorman, Marlina M. Multani, John M. Kratz, Arthur J. Crumbley, III, Fred A. Crawford, Jr, and Francis G. Spinale
Ann. Thorac. Surg. 2000 69: 1035-1040.
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