CORRESPONDENCE: LETTER TO THE EDITOR
Limitations of Angiographic Predictors of Bypass Graft Patency
Morton J. Kern, MD, FSCAI, FAHA, FACC*
* Professor of Medicine, Associate Chief Cardiology, Director Clinical Affairs, University of California, Irvine, Building 53, Route 81, Room 100, 101 The City Drive, Orange, California 92868-4080 (Email: mkern{at}uci.edu).
I compliment the work of Glineur et al. (1) on advancing our appreciation of the physiologic predictors of 6-month patency rates of bypass grafts to the right coronary artery. The patency of the gastroepiploic artery (GEA) had a significant association with minimal luminal diameter (MLD) and percent diameter stenosis, angiographic features that did not affect saphenous vein graft patency rates as much. A larger MLD (>1.4 mm) and the percent diameter stenosis (<55% narrowing) predicted GEA graft closure. The accompanying editorial by Sabik and Blackstone (2) expertly reviewed the evidence for competitive flow and coronary artery bypass graft patency, explaining some of the factors in play for the outcomes reported by Glineur et al. (1).
Although competitive flow between native and grafted coronary vessels has been known to surgeons for many years as a cause of graft failure (3–5), the prediction of graft patency on the basis of the physiology of competitive flow should not be judged by angiography alone. The numerous studies on intracoronary pressure and intravascular ultrasound imaging reinforce the failure of the angiogram to provide important physiologic and true anatomic information, especially for intermediately severe stenoses (6,7). Using angiography as a surrogate for physiologic activity is often erroneous and, at this time, is an imprecise technique when addressing physiologic mechanisms as described by Sabik et al. (5) and others (3,4). The competing flow potential of the native artery with vein graft flow can be directly measured by coronary pressure or Doppler flow in patients in the cardiac catheterization laboratory (6,8).
The measurement of hyperemic translesional pressure ratio, called fractional flow reserve (FFR) (8,9), has been applied to study the fate of coronary bypass grafts with striking results. Confirming the relevance of the physiologic stenosis severity and graft patency, Botman et al. (10) report the 1-year follow-up of 164 patients undergoing coronary bypass grafts. All vessels grafted had FFR measured beforehand with the pressure sensor angioplasty guidewire in the catheterization laboratory. At 1 year, 9% of grafts on functionally significant lesions were occluded, whereas 21% of grafts on functionally nonsignificant lesions were occluded. A significant graft occlusion rate was observed for grafted vessels with near normal physiology (FFR >0.80, normal = 1.0). The angiographic percent diameter narrowings displayed a similar but less precise correlation with graft failure. The findings from Botman et al. (10) again emphasize what is generally appreciated but unmeasured: that is, the physiologic impact of intermediately severe stenosis remains unknown by angiography.
Whereas the angiographic descriptor of MLD provided by Glineur et al. (1) is an advance over measurements of stenosis diameter (even if using a quantitative angiographic imaging system), the precise pressure across stenosis can be obtained often without difficulty by most interventional cardiologists. Certainly, severe narrowings and total occlusions do not need such direct measurements, but the physiologic assessment of intermediate lesions can assist selection of the appropriate bypass graft should the surgeon have an interest in this approach (11).
Sabik and Blackstone (2) note that using only maximal coronary artery stenosis would not adjust for coronary artery size, whereas MLD does this to a larger extent. However, neither MLD of the reference lumen diameter nor percent lumen diameter narrowing truly reflects competitive flow physiology. Although I recognize this might not be possible in many clinical settings, I believe angiographic parameters cannot and should not be used as a surrogate for coronary flow.
Finally, recent data by Sant'Anna et al. (12) challenge our assumptions regarding whether angiographic 3-vessel disease is truly physiological 3-vessel disease. Of the 250 patients undergoing angiography, when the 27% of patients with angiographic 3-vessel disease had FFR measured in all 3 of these vessels, only 9% were found to have physiologically significant 3-vessel coronary disease. Had bypass grafting been performed, a considerable incidence of graft failure would be expected at follow-up. Fortunately, in this setting graft failure is often clinically silent with the consequences of graft closure across nonsignificant lesions reverting to the native vessel, which remains patent and functional (unless the lesion progresses).
Whereas the debate about the use of the GEA graft continues, a critical question before the surgery for those vessels with intermediately severe stenoses should be answered by direct physiologic measurements: is a graft on this particular vessel going to be of any use if the physiology is nearly normal (13)?
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Footnotes
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Please note: Dr. Kern is a speaker for Radi Medical and Volcano Therapeutics, 2 companies that manufacture the pressure guidewire used in the physiologic assessment of coronary artery disease.
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References
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1. Glineur D, D'hoore W, El Khoury G, et al. Angiographic predictors of 6-month patency of bypass grafts implanted to the right coronary artery J Am Coll Cardiol 2008;51:120-125.[Abstract/Free Full Text]2. Sabik JF, Blackstone EH. Coronary artery bypass graft patency and competitive flow J Am Coll Cardiol 2008;51:126-128.[Free Full Text] 3. Hashimoto H, Isshiki T, Ikari Y, et al. Effects of competitive blood flow on arterial graft patency and diameter. Medium-term postoperative follow-up. J Thoracic Cardiovasc Surg 1996;111:399-407.[Abstract/Free Full Text] 4. Tedoriya T, Kawasuji M, Sakakibara N, Ueyama K, Watanabe Y. Pressure characteristics in arterial grafts for coronary bypass surgery Cardiovasc Surg 1995;3:381-385.[CrossRef][Medline] 5. Sabik III JF, Lytle BW, Blackstone EH, Khan M, Houghtaling PL, Cosgrove DM. Does competitive flow reduce internal thoracic artery graft patency? Ann Thorac Surg 2003;76:1460-1466. 6. Kern MJ, Lerman A, Bech JW, et al. Physiological assessment of coronary artery disease in the cardiac catheterization laboratory: a scientific statement from the American Heart Association Committee on Diagnostic and Interventional Cardiac Catheterization, Council on Clinical Cardiology Circulation 2006;114;:1321-1341.[Abstract/Free Full Text] 7. Topol EJ, Nissen SE. Our preoccupation with coronary luminology. The dissociation between clinical and angiographic findings in ischemic heart disease. Circulation 1995;92:2333-2342.[Abstract/Free Full Text] 8. Pijls NHJ, Van Gelder B, Van der Voort P, et al. Fractional flow reserve: a useful index to evaluate the influence of an epicardial coronary stenosis on myocardial blood flow Circulation 1995;92:318-319.[Web of Science] 9. Pijls NHJ, de Bruyne B, Peels K, et al. Measurement of fractional flow reserve to assess the functional severity of coronary-artery stenoses N Engl J Med 1996;334:1703-1708.[Abstract/Free Full Text] 10. Botman CJ, Schonberger J, Koolen S, et al. Does stenosis severity of native vessels influence bypass graft patency? A prospective fractional flow reserve-guided study Ann Thorac Surg 2007;83:2093-2097.[Abstract/Free Full Text] 11. Botman KJ, Pijls N, Bech JW, et al. Percutaneous coronary intervention or bypass surgery in multivessel disease? A tailored approach based on coronary pressure measurement Catheter Cardiovasc Interv 2004;63:184-191.[CrossRef][Web of Science][Medline] 12. Sant'Anna FM, Silva EER, Batista LA, Venture FM, Barrozo CAM, Pijls NHJ. Influence of routine assessment of fractional flow reserve on decision making during coronary interventions Am J Cardiol 2007;99:504-508.[CrossRef][Web of Science][Medline] 13. Pijls NHJ, Van Schaardenburgh P, Manoharan G, et al. Percutaneous coronary intervention of functionally non-significant stenoses: 5 year follow-up of the Defer Study J Am Coll Cardiol 2007;49:2105-2111.[Abstract/Free Full Text]
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