Such complex revascularization decisions are often made by the treating cardiologist in the cath lab and require careful consideration of the clinical picture, angiographic analysis and increasingly, use of invasive imaging tools such as fractional flow reserve (FFR) and intravascular ultrasound (IVUS). The interventionalist has to address three important questions that help guide revascularization: 1) does the lesion(s) need revascularization?; 2) if PCI is to be performed, should DES or BMS be used?; and 3) are the stents optimally deployed for best short- and long-term outcomes?
1. Does the lesion need revascularization?
While revascularization improves survival in a subgroup of patients — those with ST-elevation myocardial infarction, cardiogenic shock, severe left main and triple-vessel disease with depressed ventricular function — the majority of PCIs are performed for relief of anginal symptoms or treatment of inducible ischemia. Therefore, in the setting of stable syndromes, if there is doubt about the hemodynamic significance of lesions, it is incumbent on the interventionalist to ascertain this before proceeding with PCI. The best way to avoid short- and long-term stent complications is not to deploy stents unless indicated!
Even an experienced interventional cardiologist can not accurately assess the hemodynamic significance of moderate (40–70%) lesions by visual angiographic analysis.8 Furthermore, a homogeneously diseased vessel may appear angiographically normal because no segment is worse than its adjacent reference segment. These limitations of angiography are compounded in overlapped, tortuous, eccentric, calcified lesions, as well as ostial and bifurcation lesions. Additionally, significant inter- and intra-observer variability exists in the angiographic interpretation of lesion severity.9-11 Given these limitations of angiography, physiologic techniques and IVUS have emerged as important adjunctive tools. Several physiologic measures of stenosis severity have been developed: FFR, coronary flow reserve (CFR), and hyperemic stenosis resistance (HSR).
FFR was developed as a pressure index of epicardial stenosis severity and is defined as the ratio of the maximal blood flow achievable in an epicardial coronary artery with a stenosis relative to the maximal flow in the same vessel without the stenosis.12-16 A lesion with an FFR <0.75, in a patient with normal myocardium, is considered hemodynamically significant and identifies inducible ischemia with high overall accuracy (93%).16 FFR is relatively independent of loading conditions or myocardial contractility and FFR ≤ 0.78 has been shown to accurately reflect hemodynamic lesion severity even in patients with recent infarction or with elevated left ventricular mass index.17,18
Coronary flow reserve is defined as the ratio of hyperemic blood velocity to the resting blood velocity. The CFR value ≤ 2.0 predicts inducible myocardial ischemia on stress testing with good predictive accuracy (89% to 96%).8,16,19-22 However, CFR reflects both the epicardial and the microvascular resistance, therefore, conditions such as diabetes, myocardial infarction, ventricular hypertrophy, and advanced age can impair microvascular function and reduce CFR independent of the epicardial stenosis severity. To overcome this limitation, the concept of relative CFR (rCFR) was introduced. The rCFR is obtained by dividing the CFR of the “culprit” vessel by the CFR of an adjacent “normal” vessel. A rCFR <0.8 correlates with a significant epicardial stenosis as assessed by FFR.16 However, this technique requires the interrogation of an additional vessel, and both CFR and rCFR have been largely supplanted by the use of FFR for hemodynamic assessment of lesion severity.
Recently, hyperemic stenosis resistance index (HSR) has been introduced as an additional method to evaluate the physiologic significance of a coronary stenosis.23,24 It is defined as the ratio of the translesional pressure gradient and velocity at maximal hyperemia, requiring simultaneous measurements of intracoronary pressure and velocity.23,24 An HSR > 0.8mmHg/cm/sec has been shown to be predictive of reversible ischemia on stress testing and may be particularly helpful for assessing hemodynamic severity of a stenosis in patients with microvascular disease. However, there are no prospective studies evaluating the deferral of PCI based on HSR and further research is needed before HSR can be widely adopted.
Several studies have demonstrated that PCI with BMS can be safely deferred for FFR > 0.75 and CFR values greater than 2.0.16 The largest of these studies, the randomized Deferral of PTCA Versus Performance of PTCA (DEFER) trial, demonstrated that deferred PCI based on an FFR >0.75 confers no adverse prognosis compared to routine PCI using BMS.25 In fact, at five years, there was a non-significant trend toward lower rates of cardiac death and myocardial infarction in the “defer group” compared to the “perform group” (3.3 vs. 7.9%, p = 0.21).26
In addition to accurately determining the hemodynamic severity of focal lesions, FFR may be particularly useful in guiding revascularization in more complex subsets of patients such as serial stenoses, diffuse disease, ostial and bifurcation disease, and multi-vessel disease. For serial lesions or diffuse disease, a pressure pullback during intravenous (IV) adenosine infusion can be useful.16,27 Pressure loss due to focal stenosis can be differentiated by an abrupt increase in pressure during a pullback. This technique may help avoid unnecessary revascularization using longer or overlapping DES, which are known to increase the risk of both restenosis and thrombosis.2 Ostial lesions are notoriously difficult to accurately gauge angiographically and can easily be interrogated with FFR. The angiographic assessment of the ostia of side branches of bifurcation lesions after PCI is difficult.28–30 In addition, off-label use of DES in bifurcation lesions is associated with increased rates of restenosis and stent thrombosis.2 Despite severe angiographic appearance in the ostium of “jailed” bifurcations, more than 70% to 80% of these bifurcation lesions are not hemodynamically significant by FFR.31 Thus, “jailed” side-branch lesions are often not functionally significant and PCI of the side branch can often be deferred. This single stent technique with provisional stenting of the side branch only if hemodynamically significant can improve short- and long-term outcomes of bifurcation PCI. Finally, a retrospective study of multi-vessel disease indicated that an FFR-guided strategy resulted in deployment of fewer stents, lower cost and improved outcomes compared to an angiographic-guided approach.32 This approach is currently being prospectively investigated in a randomized trial.33
IVUS can also be used in the assessment of moderate coronary lesions. In one study of 51 epicardial lesions evaluated by both IVUS and FFR, a minimal lumen cross-sectional area (MLA) of <3 mm2 and a >60% area stenosis predicted a hemodynamically significant lesion compared to FFR.34 In another study of 53 lesions, a MLA of <4 mm2 and a minimal lumen diameter <1.8 mm predicted hemodynamic significance by FFR.35 However, anatomic luminal measures assessed by IVUS do not take into account lesion length, eccentricity and area of myocardium at risk by the lesion like FFR does. Furthermore, unlike FFR, IVUS-based deferral of PCI has not been prospectively evaluated in a randomized study.
2. If PCI is to be performed, should DES or BMS used?
Once a decision is made to perform PCI, a careful clinical assessment regarding long-term tolerability and/or affordability of dual anti-platelet therapy will be important in determining if DES deployment is advisable. Clearly, if such an assessment has not been performed, as in emergency procedures, particularly in elderly patients, BMS may be preferable. Once in the cath lab, the approach should be to use DES for lesions with high expected restenosis rates and BMS for low expected restenosis rates. Very large-caliber vessels with focal lesions would likely have similar restenosis rates with BMS compared with DES. This concept was supported by a study comparing BMS and DES in coronary arteries >3.5 mm in diameter.36 A cohort of 233 patients who underwent single-vessel PCI with DES in arteries >3.5 mm had similar outcomes as 233 propensity-matched patients who received BMS. At one-year follow up, major adverse cardiac events (MACE) occurred in 8.5% of the patients with DES and 7.7% of the patients with BMS (p = 0.80). Thus, patients with large vessels (>3.5 mm) represent a population with a low risk for MACE using BMS. These findings are in line with subgroup analysis of the TAXUS-IV trial, where the benefit of DES over BMS for restenosis was limited to vessels <3.0 mm.36,37 Another approach might be the use of baseline FFR in determining which lesions would have favorable outcomes with BMS. It is known from a multi-center registry of 750 patients that FFR > 0.90 after BMS deployment is associated with a low (<6%) MACE38 and conversely, FFR <0.90 is associated with high (>20%) MACE. A recent analysis of that registry indicated that baseline FFR and stent diameter could predict optimal post stent FFR and outcomes, suggesting that both baseline FFR and expected stent diameter could be used to guide the choice of BMS versus DES.39
3. How can stent deployment be optimized?
Invasive imaging tools may be very helpful in optimizing stent deployment by reducing stent thrombosis, BMS restenosis, and possibly identifying lesions that are high risk for peri-procedural distal embolization. With either BMS or DES, the most important procedure-related risks for stent thrombosis are smaller final lumen dimensions due to stent under-expansion and/or malapposition, increased stent length, persistent slow coronary flow, multiple stents, positive remodeling, dissections, geographic miss, and late stent malapposition due to thrombus resolution.2,40–43 Post-PCI IVUS can often detect malapposition, under-expansion, residual stenosis, dissections, and geographic miss. Early studies with IVUS showed that 40–70% of angiographically well-deployed stents have under-expanded regions when examined by IVUS.44-46 These findings led to the deployment of stents at higher inflation pressure to increase stent expansion and apposition.47 However, even in the era of stent deployment at high pressure, IVUS-guided trials suggest that incomplete strut apposition occurs in 4% to 22% of PCIs.48 Achieving adequate stent expansion with large post stent minimal luminal areas also reduce the risk of restenosis with BMS. While the results of randomized studies of IVUS-guided versus angiographic-guided BMS deployment are mixed, they favor IVUS guidance. In the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study, IVUS guidance led to less target vessel revascularization (8.5% versus 15.2%, p < 0.05). In the Direct Stenting vs Optimal Angioplasty (DIPOL) study, IVUS-guidance caused the operator to post-dilate the stent in 39.7% of procedures and MACE occurred less frequently with IVUS guidance (7.3% versus 16.2%, p < 0.05).49 Similarly, the Thrombocyte activity evaluation and effects of Ultrasound guidance in Long Intracoronary stent Placement (TULIP) study investigated IVUS-guided stenting in long, diffuse coronary lesions50 and found lower restenosis rates with IVUS guidance (23% versus 46%, p = 0.008). However, the REStenosis after Intravascular ultrasound STenting (RESIST) trial showed only a trend toward reduction in restenosis in the IVUS-guided group51 and the OPTimization with ICUS to reduce stent restenosis (OPTICUS) trial showed no difference between in the IVUS-guided and angiographic guided groups.52 The differences in procedural endpoints in these randomized trials and the use of various adjunctive treatment strategies make these trials difficult to compare. However, taken together, these results demonstrate that IVUS guidance of stent deployment leads to larger final vessel sizes, reduced stent under-expansion, and probably reduced restenosis rates with BMS. Accepted IVUS criteria for optimal BMS deployment include: (a) minimal stent cross-sectional area (CSA) > 7 mm2, (b) minimal stent CSA > 80% of average proximal and distal reference segments, and (c) complete stent apposition to vessel wall.53,54 A minimal stent CSA > 9 mm2 is associated with the lowest restenosis rates.45,55 While there are no published randomized studies of IVUS-guided DES deployment, IVUS guidance may be important to assure optimal stent expansion and strut apposition with DES.56 In addition to achieving larger final vessel sizes, IVUS guidance may be important in the detection of atherosclerosis plaque composition during PCI. Recent studies suggest that increased necrotic core plaque content detected by radiofrequency backscatter IVUS analysis (virtual histology) is an independent predictor of distal embolization during PCI in patients presenting with both STEMI and anginal syndromes.57,58 As distal protection devices may reduce peri-procedural embolization, it may be important to identify necrotic core content before stent deployment.59 While these data are very intriguing, this strategy of using plaque characterization to guide PCI strategy is currently unproven and warrants further study. Finally, FFR can also provide information regarding successful stent deployment. In a study with BMS, a post stent FFR > 0.94 had a concordance rate of 91% with IVUS for detecting optimally deployed stents.60 However, this finding was not confirmed in a larger study.61 At present, IVUS is more commonly used than FFR to assess for optimal stent deployment.
Fractional flow reserve and IVUS are important adjuncts to angiography and help guide PCI. These tools may help avoid unnecessary revascularizations, guide stent selection, decrease costs and optimize outcomes.
1. Lagerqvist B, James SK, Stenestrand U, et al. Long-term outcomes with drug-eluting stents versus bare-metal stents in Sweden. N Engl J Med 2007;356:1009–1019.
2. Luscher TF, Steffel J, Eberli FR, et al. Drug-eluting stent and coronary thrombosis: biological mechanisms and clinical implications. Circulation 2007;115:1051–1058.
3. Maisel WH. Unanswered questions — drug-eluting stents and the risk of late thrombosis. N Engl J Med 2007;356:981–984.
4. Finn AV, Joner M, Nakazawa G, et al. Pathological correlates of late drug-eluting stent thrombosis: strut coverage as a marker of endothelialization. Circulation 2007; 115:2435–2441.
5. Fuke S, Maekawa K, Kawamoto K, et al. Impaired endothelial vasomotor function after sirolimus-eluting stent implantation. Circ J 2007;71:220–225.
6. Maekawa K, Kawamoto K, Fuke S, et al. Images in cardiovascular medicine. Severe endothelial dysfunction after sirolimus-eluting stent implantation. Circulation 2006; 113:e850–e851.
7. Lerman A, Eeckhout E. Coronary endothelial dysfunction following sirolimus-eluting stent placement: should we worry about it? Eur Heart J 2006;27:125–126.
8. Tobis J, Azarbal B, Slavin L. Assessment of intermediate severity coronary lesions in the catheterization laboratory. J Am Coll Cardiol 2007;49:839–848.
9. Goldberg RK, Kleiman NS, Minor ST, Abukhalil J, Raizner AE. Comparison of quantitative coronary angiography to visual estimates of lesion severity pre and post PTCA. Am Heart J 1990;119:178–184.
10. Fischer JJ, Samady H, McPherson JA, et al. Comparison between visual assessment and quantitative angiography versus fractional flow reserve for native coronary narrowings of moderate severity. Am J Cardiol 2002;90:210–215.
11. DeRouen TA, Murray JA, Owen W. Variability in the analysis of coronary arteriograms. Circulation 1977;55:324–328.
12. Pijls NH, van Son JA, Kirkeeide RL, De Bruyne B, Gould KL. Experimental basis of determining maximum coronary, myocardial, and collateral blood flow by pressure measurements for assessing functional stenosis severity before and after percutaneous transluminal coronary angioplasty. Circulation 1993;87:1354–1367.
13. Pijls NH, 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.
14. Kern MJ, de Bruyne B, Pijls NH. From research to clinical practice: current role of intracoronary physiologically based decision making in the cardiac catheterization laboratory. J Am Coll Cardiol 1997;30: 613–620.
15. De Bruyne B, Pijls NH, Barbato E, et al. Intracoronary and intravenous adenosine 5'-triphosphate, adenosine, papaverine, and contrast medium to assess fractional flow reserve in humans. Circulation 2003;107: 1877–1883.
16. 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.
17. Samady H, Lepper W, Powers ER, et al. Fractional flow reserve of infarct-related arteries identifies reversible defects on noninvasive myocardial perfusion imaging early after myocardial infarction. J Am Coll Cardiol 2006;47:2187–2193.
18. Chhatriwalla AK, Ragosta M, Powers ER, et al. High left ventricular mass index does not limit the utility of fractional flow reserve for the physiologic assessment of lesion severity. J Invasive Cardiol 2006;18: 544–549.
19. Doucette JW, Corl PD, Payne HM, et al. Validation of a Doppler guide wire for intravascular measurement of coronary artery flow velocity. Circulation 1992;85: 1899–1911.
20. Gould KL, Kirkeeide RL, Buchi M. Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol 1990;15:459–474.
21. Heller LI, Cates C, Popma J, et al. Intracoronary Doppler assessment of moderate coronary artery disease: comparison with 201Tl imaging and coronary angiography. FACTS Study Group. Circulation 1997;96:484–490.
22. Labovitz AJ, Anthonis DM, Cravens TL, Kern MJ. Validation of volumetric flow measurements by means of a Doppler-tipped coronary angioplasty guide wire. Am Heart J 1993;126:1456–1461.
23. Verberne HJ, Meuwissen M, Chamuleau SA, et al. Effect of simultaneous intracoronary guidewires on the predictive accuracy of functional parameters of coronary lesion severity. Am J Physiol Heart Circ Physiol 2007;292: H2349–H2355.
24. Meuwissen M, Siebes M, Chamuleau SA, et al. Hyperemic stenosis resistance index for evaluation of functional coronary lesion severity. Circulation 2002;106: 441–446.
25. Bech GJ, De Bruyne B, Pijls NH, et al. Fractional flow reserve to determine the appropriateness of angioplasty in moderate coronary stenosis: a randomized trial. Circulation 2001;103:2928–2934.
26. Pijls NH, van Schaardenburgh P, Manoharan G, et al. Percutaneous coronary intervention of functionally nonsignificant stenosis: 5-year follow-up of the DEFER Study. J Am Coll Cardiol 2007;49: 2105–2111.
27. De Bruyne B, Pijls NH, Heyndrickx GR, Hodeige D, Kirkeeide R, Gould KL. Pressure-derived fractional flow reserve to assess serial epicardial stenoses: theoretical basis and animal validation. Circulation 2000;101:1840–1847.
28. George BS, Myler RK, Stertzer SH, et al. Balloon angioplasty of coronary bifurcation lesions: the kissing balloon technique. Cathet Cardiovasc Diagn 1986;12: 124–38.
29. Costa RA, Mintz GS, Carlier SG, et al. Bifurcation coronary lesions treated with the “crush” technique: an intravascular ultrasound analysis. J Am Coll Cardiol 2005;46:599–605.
30. Colombo A, Moses JW, Morice MC, et al. Randomized study to evaluate sirolimus-eluting stents implanted at coronary bifurcation lesions. Circulation 2004;109: 1244–1249.
31. Koo BK, Kang HJ, Youn TJ, et al. Physiologic assessment of jailed side branch lesions using fractional flow reserve. J Am Coll Cardiol 2005;46: 633–637.
32. Wongpraparut N, Yalamanchili V, Pasnoori V, et al. Thirty-month outcome after fractional flow reserve-guided versus conventional multivessel percutaneous coronary intervention. Am J Cardiol 2005;96:877–884.
33. Fearon WF, Tonino PA, De Bruyne B, Siebert U, Pijls NH. Rationale and design of the Fractional Flow Reserve versus Angiography for Multivessel Evaluation (FAME) study. Am Heart J 2007;154: 632–636.
34. Sipahi I, Nicholls SJ, Tuzcu EM. Intravascular ultrasound in the current percutaneous coronary intervention era. Cardiol Clin 2006;24:163–173, v.
35. Briguori C, Anzuini A, Airoldi F, et al. Intravascular ultrasound criteria for the assessment of the functional significance of intermediate coronary artery stenoses and comparison with fractional flow reserve. Am J Cardiol 2001;87:136–141.
36. Steinberg DH, Mishra S, Javaid A, et al. Comparison of effectiveness of bare metal stents versus drug–eluting stents in large (> or =3.5 mm) coronary arteries. Am J Cardiol 2007;99:599–602.
37. Moses JW, Leon MB, Popma JJ, et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med 2003;349: 1315–1323.
38. Pijls NH, Klauss V, Siebert U, et al. Coronary pressure measurement after stenting predicts adverse events at follow-up: a multicenter registry. Circulation 2002;105: 2950–2954.
39. Samady H, McDaniel MC, Veledar E et al. Pre-Stent Fractional Flow Reserve and Stent Diameter Predict Optimal Post Stent Fractional Flow Reserve: Implications for Selection of Drug Eluting Stents. Circulation Oct 2006; 114: II_784.
40. Kereiakes DJ, Choo JK, Young JJ, Broderick TM. Thrombosis and drug-eluting stents: a critical appraisal. Rev Cardiovasc Med 2004;5:9–15.
41. Orford JL, Lennon R, Melby S, et al. Frequency and correlates of coronary stent thrombosis in the modern era: analysis of a single center registry. J Am Coll Cardiol 2002;40:1567–1572.
42. Cheneau E, Leborgne L, Mintz GS, et al. Predictors of subacute stent thrombosis: results of a systematic intravascular ultrasound study. Circulation 2003;108: 43–47.
43. Chieffo A, Bonizzoni E, Orlic D, et al. Intraprocedural stent thrombosis during implantation of sirolimus-eluting stents. Circulation 2004;109:2732–2736.
44. Fearon WF, Yeung AC. Evaluating intermediate coronary lesions in the cardiac catheterization laboratory. Rev Cardiovasc Med 2003;4:1–7.
45. Moussa I, Di Mario C, Di Francesco L, et al. Subacute stent thrombosis and the anticoagulation controversy: changes in drug therapy, operator technique, and the impact of intravascular ultrasound. Am J Cardiol 1996;78:13–17.
46. Moussa I, Di Mario C, Reimers B, et al. Subacute stent thrombosis in the era of intravascular ultrasound-guided coronary stenting without anticoagulation: frequency, predictors and clinical outcome. J Am Coll Cardiol 1997;29:6–12.
47. Fitzgerald PJ, Oshima A, Hayase M, et al. Final results of the Can Routine Ultrasound Influence Stent Expansion (CRUISE) study. Circulation 2000;102: 523–530.
48. Tanabe K, Serruys PW, Degertekin M, et al. Incomplete stent apposition after implantation of paclitaxel-eluting stents or bare metal stents: insights from the randomized TAXUS II trial. Circulation 2005;111:900-905.
49. Gil RJ, Pawlowski T, Dudek D, et al. Comparison of angiographically guided direct stenting technique with direct stenting and optimal balloon angioplasty guided with intravascular ultrasound. The multicenter, randomized trial results. Am Heart J 2007;154:669-675.
50. Oemrawsingh PV, Mintz GS, Schalij MJ, et al. Intravascular ultrasound guidance improves angiographic and clinical outcome of stent implantation for long coronary artery stenoses: final results of a randomized comparison with angiographic guidance (TULIP Study). Circulation 2003;107: 62–67.
51. Schiele F, Meneveau N, Vuillemenot A, et al. Impact of intravascular ultrasound guidance in stent deployment on 6-month restenosis rate: a multicenter, randomized study comparing two strategies--with and without intravascular ultrasound guidance. RESIST Study Group. REStenosis after Ivus guided STenting. J Am Coll Cardiol 1998;32: 320–328.
52. Mudra H, di Mario C, de Jaegere P, et al. Randomized comparison of coronary stent implantation under ultrasound or angiographic guidance to reduce stent restenosis (OPTICUS Study). Circulation 2001;104: 1343–1349.
53. Serruys PW, Deshpande NV. Is there MUSIC in IVUS guided stenting? Is this MUSIC going to be a MUST? Multicenter Ultrasound Stenting in Coronaries Study. Eur Heart J 1998;19:1122-1124.
54. Nageh T, De Belder AJ, Thomas MR, et al. Intravascular ultrasound-guided stenting in long lesions: an insight into possible mechanisms of restenosis and comparison of angiographic and intravascular ultrasound data from the MUSIC and RENEWAL trials. J Interv Cardiol 2001;14:397-405.
55. Moussa I, Moses J, Di Mario C, et al. Does the specific intravascular ultrasound criterion used to optimize stent expansion have an impact on the probability of stent restenosis? Am J Cardiol 1999;83:1012-7.
56. Javaid A, Chu WW, Cheneau E, et al. Comparison of paclitaxel-eluting stent and sirolimus-eluting stent expansion at incremental delivery pressures. Cardiovasc Revasc Med 2006;7:208-11.
57. Kawamoto T, Okura H, Koyama Y, et al. The relationship between coronary plaque characteristics and small embolic particles during coronary stent implantation. J Am Coll Cardiol 2007;50:1635-40.
58. Kawaguchi R, Oshima S, Jingu M, et al. Usefulness of virtual histology intravascular ultrasound to predict distal embolization for ST-segment elevation myocardial infarction. J Am Coll Cardiol 2007; 50:1641–1646.
59. Kawaguchi R, Hoshizaki H, Hiratsuji T, et al. Effectiveness of distal protection with the GuardWire Plus during primary angioplasty for acute myocardial infarction. J Cardiol 2005;45:99–106.
60. Hanekamp CE, Koolen JJ, Pijls NH, Michels HR, Bonnier HJ. Comparison of quantitative coronary angiography, intravascular ultrasound, and coronary pressure measurement to assess optimum stent deployment. Circulation 1999;99: 1015–1021.
61. Fearon WF, Luna J, Samady H, et al. Fractional flow reserve compared with intravascular ultrasound guidance for optimizing stent deployment. Circulation 2001;104:1917-1922.