UpToDate
Official reprint from UpToDate®
www.uptodate.com ©2016 UpToDate®

Quantitative coronary angiography: Clinical applications

Author
Morton J Kern, MD, MSCAI, FAHA, FACC
Section Editor
Donald Cutlip, MD
Deputy Editor
Gordon M Saperia, MD, FACC

INTRODUCTION

A reduction in the coronary artery luminal cross-sectional diameter, estimated by visual inspection of the radiocontrast lumenogram during angiography, has been utilized to formulate predictions about clinical presentations and stress-induced reductions in coronary blood flow. Anatomic and physiologic approaches to coronary artery disease are complementary and at times will yield contradictory results. (See "Clinical use of coronary artery pressure flow measurements".) As a result, quantitative approaches to the angiographic evaluation of coronary anatomy are occasionally employed in some laboratories.

There are a number of clinical applications for quantitative coronary arteriography (QCA) including predicting restenosis after angioplasty, comparing the results of different interventional techniques, and evaluating the natural history of coronary artery disease. These issues will be reviewed here, beginning with the limitations of visual and QCA, while the technical aspects of QCA are discussed separately. (See "Quantitative coronary angiography: Technical issues".)

LIMITATIONS OF VISUAL CORONARY ARTERIOGRAPHY

The rationale for performing quantitative coronary arteriography (QCA) is based upon the limitations of visual coronary arteriography. The greatest advantage of QCA is its theoretical freedom from observer influences and bias, minimizing significant potential intraobserver and interobserver variability [1-3]. In prospective studies, the potential for observer error with visual analysis from a coronary angiogram has been estimated to exceed 35 percent [1].

The extent of the variability is related in part to the severity of the lesion under scrutiny; lesser degrees of variation are reported for stenoses that represent either less than 20 percent or more than 80 percent of the vessel diameter [4]. Visual analysis generally leads to overestimation of severe stenoses, and to underestimation of more modest degrees of luminal narrowing [5].

There is also significant discordance between visual estimates of luminal narrowing and the functional significance of stenosis [6]. The functional significance of coronary stenotic lesions is governed not only by degree of stenosis, but also by such features as the shape, length, and eccentricity of the lesion, collateral routes of perfusion, and vasomotor tone among others [7-10]. These physical constraints and resultant flow characteristics contribute to the disparity between the angiographic and corresponding physiologic assessment of disease severity [11].

       

Subscribers log in here

To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information or to purchase a personal subscription, click below on the option that best describes you:
Literature review current through: Nov 2016. | This topic last updated: Mon Nov 30 00:00:00 GMT+00:00 2015.
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2016 UpToDate, Inc.
References
Top
  1. DeRouen TA, Murray JA, Owen W. Variability in the analysis of coronary arteriograms. Circulation 1977; 55:324.
  2. Goldberg RK, Kleiman NS, Minor ST, et al. Comparison of quantitative coronary angiography to visual estimates of lesion severity pre and post PTCA. Am Heart J 1990; 119:178.
  3. Zir LM. Observer variability in coronary angiography. Int J Cardiol 1983; 3:171.
  4. Shub C, Vlietstra RE, Smith HC, et al. The unpredictable progression of symptomatic coronary artery disease: a serial clinical-angiographic analysis. Mayo Clin Proc 1981; 56:155.
  5. Fleming RM, Kirkeeide RL, Smalling RW, Gould KL. Patterns in visual interpretation of coronary arteriograms as detected by quantitative coronary arteriography. J Am Coll Cardiol 1991; 18:945.
  6. White CW, Wright CB, Doty DB, et al. Does visual interpretation of the coronary arteriogram predict the physiologic importance of a coronary stenosis? N Engl J Med 1984; 310:819.
  7. Vlodaver Z, Neufeld HN, Edwards JE. Pathology of coronary disease. Semin Roentgenol 1972; 7:376.
  8. Epstein SE, Cannon RO 3rd, Watson RM, et al. Dynamic coronary obstruction as a cause of angina pectoris: implications regarding therapy. Am J Cardiol 1985; 55:61B.
  9. Feldman RL, Nichols WW, Pepine CJ, Conti CR. Hemodynamic significance of the length of a coronary arterial narrowing. Am J Cardiol 1978; 41:865.
  10. Feldman RL, Nichols WW, Pepine CJ, et al. The coronary hemodynamics of left main and branch coronary stenoses. The effects of reduction in stenosis diameter, stenosis length, and number of stenoses. J Thorac Cardiovasc Surg 1979; 77:377.
  11. Gould KL. Percent coronary stenosis: battered gold standard, pernicious relic or clinical practicality? J Am Coll Cardiol 1988; 11:886.
  12. Stiel GM, Stiel LS, Schofer J, et al. Impact of compensatory enlargement of atherosclerotic coronary arteries on angiographic assessment of coronary artery disease. Circulation 1989; 80:1603.
  13. Umans VA, Robert A, Foley D, et al. Clinical, histologic and quantitative angiographic predictors of restenosis after directional coronary atherectomy: a multivariate analysis of the renarrowing process and late outcome. J Am Coll Cardiol 1994; 23:49.
  14. Reiber JH, Serruys PW, Kooijman CJ, et al. Assessment of short-, medium-, and long-term variations in arterial dimensions from computer-assisted quantitation of coronary cineangiograms. Circulation 1985; 71:280.
  15. Vas R, Eigler N, Miyazono C, et al. Digital quantification eliminates intraobserver and interobserver variability in the evaluation of coronary artery stenosis. Am J Cardiol 1985; 56:718.
  16. Zir LM, Miller SW, Dinsmore RE, et al. Interobserver variability in coronary angiography. Circulation 1976; 53:627.
  17. Gould KL, Kelley KO. Physiological significance of coronary flow velocity and changing stenosis geometry during coronary vasodilation in awake dogs. Circ Res 1982; 50:695.
  18. Gould KL, Kelley KO, Bolson EL. Experimental validation of quantitative coronary arteriography for determining pressure-flow characteristics of coronary stenosis. Circulation 1982; 66:930.
  19. Wilson RF, Marcus ML, White CW. Prediction of the physiologic significance of coronary arterial lesions by quantitative lesion geometry in patients with limited coronary artery disease. Circulation 1987; 75:723.
  20. Zijlstra F, van Ommeren J, Reiber JH, Serruys PW. Does the quantitative assessment of coronary artery dimensions predict the physiologic significance of a coronary stenosis? Circulation 1987; 75:1154.
  21. McPherson DD, Hiratzka LF, Lamberth WC, et al. Delineation of the extent of coronary atherosclerosis by high-frequency epicardial echocardiography. N Engl J Med 1987; 316:304.
  22. Arnett EN, Isner JM, Redwood DR, et al. Coronary artery narrowing in coronary heart disease: comparison of cineangiographic and necropsy findings. Ann Intern Med 1979; 91:350.
  23. Dietz WA, Tobis JM, Isner JM. Failure of angiography to accurately depict the extent of coronary artery narrowing in three fatal cases of percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1992; 19:1261.
  24. Nissen SE, Gurley JC, Grines CL, et al. Intravascular ultrasound assessment of lumen size and wall morphology in normal subjects and patients with coronary artery disease. Circulation 1991; 84:1087.
  25. Ambrose JA. Prognostic implications of lesion irregularity on coronary angiography. J Am Coll Cardiol 1991; 18:675.
  26. Haase J, Ozaki Y, Di Mario C, et al. Can intracoronary ultrasound correctly assess the luminal dimensions of coronary artery lesions? A comparison with quantitative angiography. Eur Heart J 1995; 16:112.
  27. Lesperance J, Hudon G, White CW, et al. Comparison by quantitative angiographic assessment of coronary stenoses of one view showing the severest narrowing to two orthogonal views. Am J Cardiol 1989; 64:462.
  28. Sanz ML, Mancini J, LeFree MT, et al. Variability of quantitative digital subtraction coronary angiography before and after percutaneous transluminal coronary angioplasty. Am J Cardiol 1987; 60:55.
  29. Tobis J, Nalcioglu O, Johnston WD, et al. Videodensitometric determination of minimum coronary artery luminal diameter before and after angioplasty. Am J Cardiol 1987; 59:38.
  30. Katritsis D, Lythall DA, Cooper IC, et al. Assessment of coronary angioplasty: comparison of visual assessment, hand-held caliper measurement and automated digital quantitation. Cathet Cardiovasc Diagn 1988; 15:237.
  31. Herrington DM, Siebes M, Walford GD. Sources of error in quantitative coronary angiography. Cathet Cardiovasc Diagn 1993; 29:314.
  32. Kirkeeide RL, Gould KL, Parsel L. Assessment of coronary stenoses by myocardial perfusion imaging during pharmacologic coronary vasodilation. VII. Validation of coronary flow reserve as a single integrated functional measure of stenosis severity reflecting all its geometric dimensions. J Am Coll Cardiol 1986; 7:103.
  33. Klocke FJ. Measurements of coronary blood flow and degree of stenosis: current clinical implications and continuing uncertainties. J Am Coll Cardiol 1983; 1:31.
  34. Zijlstra F, Fioretti P, Reiber JH, Serruys PW. Which cineangiographically assessed anatomic variable correlates best with functional measurements of stenosis severity? A comparison of quantitative analysis of the coronary cineangiogram with measured coronary flow reserve and exercise/redistribution thallium-201 scintigraphy. J Am Coll Cardiol 1988; 12:686.
  35. Gould KL, Kirkeeide RL, Buchi M. Coronary flow reserve as a physiologic measure of stenosis severity. J Am Coll Cardiol 1990; 15:459.
  36. Wijns W, Serruys PW, Reiber JH, et al. Quantitative angiography of the left anterior descending coronary artery: correlations with pressure gradient and results of exercise thallium scintigraphy. Circulation 1985; 71:273.
  37. Harrison DG, White CW, Hiratzka LF, et al. The value of lesion cross-sectional area determined by quantitative coronary angiography in assessing the physiologic significance of proximal left anterior descending coronary arterial stenoses. Circulation 1984; 69:1111.
  38. Tron C, Kern MJ, Donohue TJ, et al. Comparison of quantitative angiographically derived and measured translesion pressure and flow velocity in coronary artery disease. Am J Cardiol 1995; 75:111.
  39. Bartúnek J, Sys SU, Heyndrickx GR, et al. Quantitative coronary angiography in predicting functional significance of stenoses in an unselected patient cohort. J Am Coll Cardiol 1995; 26:328.
  40. Serruys PW, Foley DP, Kirkeeide RL, King SB 3rd. Restenosis revisited: insights provided by quantitative coronary angiography. Am Heart J 1993; 126:1243.
  41. Foley DP, Bonnier H, Jackson G, et al. Prevention of restenosis after coronary balloon angioplasty: rationale and design of the Fluvastatin Angioplasty Restenosis (FLARE) Trial. The FLARE Study Group. Am J Cardiol 1994; 73:50D.
  42. Foley JB, Penn IM, Brown RI, et al. Safety, success, and restenosis after elective coronary implantation of the Palmaz-Schatz stent in 100 patients at a single center. Am Heart J 1993; 125:686.
  43. Ellis SG, Savage M, Fischman D, et al. Restenosis after placement of Palmaz-Schatz stents in native coronary arteries. Initial results of a multicenter experience. Circulation 1992; 86:1836.
  44. Strikwerda S, Montauban van Swijndregt E, Foley DP, et al. Immediate and late outcome of excimer laser and balloon coronary angioplasty: a quantitative angiographic comparison based on matched lesions. J Am Coll Cardiol 1995; 26:939.
  45. Strikwerda S, van Swijndregt EM, Melkert R, Serruys PW. Quantitative angiographic comparison of elastic recoil after coronary excimer laser-assisted balloon angioplasty and balloon angioplasty alone. J Am Coll Cardiol 1995; 25:378.
  46. Pomerantsev EV, Kobayashi Y, Fitzgerald PJ, et al. Coronary stents: In vitro aspects of an angiographic and ultrasound quantification with in vivo correlation. Circulation 1998; 98:1495.
  47. Rensing BJ, Hermans WR, Strauss BH, Serruys PW. Regional differences in elastic recoil after percutaneous transluminal coronary angioplasty: a quantitative angiographic study. J Am Coll Cardiol 1991; 17:34B.
  48. Rensing BJ, Hermans WR, Vos J, et al. Luminal narrowing after percutaneous transluminal coronary angioplasty. A study of clinical, procedural, and lesional factors related to long-term angiographic outcome. Coronary Artery Restenosis Prevention on Repeated Thromboxane Antagonism (CARPORT) Study Group. Circulation 1993; 88:975.
  49. Serruys PW, Luijten HE, Beatt KJ, et al. Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon. A quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. Circulation 1988; 77:361.
  50. Kalbfleisch SJ, McGillem MJ, Simon SB, et al. Automated quantitation of indexes of coronary lesion complexity. Comparison between patients with stable and unstable angina. Circulation 1990; 82:439.
  51. Topol EJ, Leya F, Pinkerton CA, et al. A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease. The CAVEAT Study Group. N Engl J Med 1993; 329:221.
  52. Holmes DR Jr, Topol EJ, Califf RM, et al. A multicenter, randomized trial of coronary angioplasty versus directional atherectomy for patients with saphenous vein bypass graft lesions. CAVEAT-II Investigators. Circulation 1995; 91:1966.
  53. Kuntz RE, Gibson CM, Nobuyoshi M, Baim DS. Generalized model of restenosis after conventional balloon angioplasty, stenting and directional atherectomy. J Am Coll Cardiol 1993; 21:15.
  54. Sandor T, Als AV, Paulin S. Cine-densitometric measurement of coronary arterial stenoses. Cathet Cardiovasc Diagn 1979; 5:229.
  55. Terres W, Tatsis E, Pfalzer B, et al. Rapid angiographic progression of coronary artery disease in patients with elevated lipoprotein(a). Circulation 1995; 91:948.
  56. Mack WJ, Xiang M, Selzer RH, Hodis HN. Serial quantitative coronary angiography and coronary events. Am Heart J 2000; 139:993.
  57. Treasure CB, Klein JL, Weintraub WS, et al. Beneficial effects of cholesterol-lowering therapy on the coronary endothelium in patients with coronary artery disease. N Engl J Med 1995; 332:481.
  58. Quinn TG, Alderman EL, McMillan A, Haskell W. Development of new coronary atherosclerotic lesions during a 4-year multifactor risk reduction program: the Stanford Coronary Risk Intervention Project (SCRIP). J Am Coll Cardiol 1994; 24:900.
  59. Stone PH, Gibson CM, Pasternak RC, et al. Natural history of coronary atherosclerosis using quantitative angiography in men, and implications for clinical trials of coronary regression. The Harvard Atherosclerosis Reversibility Project Study Group. Am J Cardiol 1993; 71:766.
  60. Hodis HN, Mack WJ, LaBree L, et al. Serial coronary angiographic evidence that antioxidant vitamin intake reduces progression of coronary artery atherosclerosis. JAMA 1995; 273:1849.
  61. Effect of simvastatin on coronary atheroma: the Multicentre Anti-Atheroma Study (MAAS). Lancet 1994; 344:633.
  62. Superko HR, Krauss RM. Coronary artery disease regression. Convincing evidence for the benefit of aggressive lipoprotein management. Circulation 1994; 90:1056.