Cardiac allograft vasculopathy coronary angiography

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Cardiac allograft vasculopathy Microchapters


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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]; Raviteja Guddeti, M.B.B.S. [3]


Early diagnosis of cardiac allograft vasculopathy (CAV) is of utmost importance as it allows alterations to optimal immunosuppression and risk factor modification prolonging graft survival and reducing morbidity and mortality. In most transplant centers coronary angiography is currently used to screen and diagnose transplant associated coronary artery disease.

Coronary Angiography

Previously, the diagnosis of CAV was made pathologically. However, with the advent of calcineurin-based immunosuppression post-cardiac transplant survival improved significantly and angiographic diagnosis became a standard. Currently, the International Society for Heart and Lung Transplantation (ISHLT) recommends annual invasive coronary angiography as the standard imaging technique to screen for CAV.[1] Angiographic evidence of coronary artery disease is very common after heart transplantation. In a multiinstitutional study by Constanzo et al it was demonstrated that by the end of 5 years after transplantation 42% of heart transplant subjects had angiographic evidence of graft coronary artery disease.[2]

Coronary Artery Morphology in CAV

In contrast to native coronary artery disease where there is focal, eccentric narrowing of the coronary vessels, CAV involves a more diffuse process that manifests initially as intimal thickening followed later by concentric, longitudinal lesions.[3][4][5][6] The earliest description of coronary artery morphology in CAV was given my Gao et al.[7] According to the classification by Gao et al coronary lesions were classified as Type A, discrete stenosis, tubular stenosis, multiple stenoses in the proximal, middle and distal segments of coronary arteries; Type B, diffuse concentric narrowing of the coronary arteries with onset in the mid to distal segments; and Type C, diseased vessels, diffusely irregular with loss of small branches. However the nomenclature failed to provide prognostic significance of lesion classification. In 2010 the International Society for Heart and Lung Transplantation (ISHLT) proposed a standard nomenclature for CAV by integrating coronary angiographic findings with graft function and hemodynamics.

The ISHLT recommended standard nomenclature for CAV:[8]

Classification Severity Definition¶
ISHLT CAV0 Not significant No detectable angiographic lesions
ISHLT CAV1 Mild Angiographic left main 50%, or primary vessel with maximum lesion of 70%, or any branch stenosis of 70% (including diffuse narrowing) without allograft dysfunction
ISHLT CAV2 Moderate Angiographic left main 50%; a single primary vessel 70%, or isolated branch stenosis of 70% in branches of 2 systems, without allograft dysfunction
ISHLT CAV3 Severe Angiographic left main 50%, or 2 or more primary vessels 70% stenosis, or isolated branch stenosis 70% in all 3 systems; or ISHLT CAV1 or CAV2 with allograft dysfunction (defined as left ventricular ejection fraction >45%, usually in the presence of regional wall motion abnormalities) or evidence of significant restrictive physiology

¶ A “primary vessel” denotes the proximal and middle 33% of the left anterior descending artery, the left circumflex, the ramus, and the dominant or codominant right coronary artery with the posterior descending and posterolateral branches. A “secondary branch vessel” includes the distal 33% of the primary vessels or any segment within a large septal perforator, diagonals, and obtuse marginal branches or any portion of a nondominant right coronary artery. Restrictive cardiac allograft physiology is defined as symptomatic heart failure with echocardiographic E to A velocity ratio of 2 (1.5 in children), shortened isovolumetric relaxation time (60 ms), shortened deceleration time (150 ms), or restrictive hemodynamic values (right atrial pressure 12 mm Hg, pulmonary capillary wedge pressure 25 mm Hg, cardiac index 2 l/min/m2). Adapted from the 2010 ISHLT consensus statement for recommended nomenclature of CAV


  1. Wide acceptability[8]
  2. Reduced healthcare cost compared with other novel intracoronary imaging techniques
  3. Ease of performance


  1. Lower sensitivity compared with histopathological studies, intravascular ultrasound (IVUS) and optical coherence tomography (OCT), especially in detecting early-stage CAV[9][10][11][12] Coronary angiography assesses only the arterial lumen but not the wall per se. Studies have demonstrated that early after heart transplantation disease pathology is confined to coronary arterial wall with minimal narrowing of the lumen. Therefore luminal assessment alone may lead to underestimation of the extent of disease pathology in early-CAV.[10] In a 2006 study by Stork et al in 54 heart transplant recipients it was demonstrated that the positive predictive value of coronary angiography in detecting CAV was only 44% compared with IVUS.[13]Similarly, using histologic correlations Johnson et al reported that lesions less than 25% stenosis were underestimated by coronary angiography.[14] Also, positive remodeling that occurs early in the course of atherosclerosis and that is associated with plaque vulnerability is not detected by angiography.[15][16][17]
  2. Risk of contrast nephropathy in heart transplant subjects in whom chronic renal failure is a usual comorbidity[18]


  1. Costanzo MR, Dipchand A, Starling R, Anderson A, Chan M, Desai S; et al. (2010). "The International Society of Heart and Lung Transplantation Guidelines for the care of heart transplant recipients". J Heart Lung Transplant. 29 (8): 914–56. doi:10.1016/j.healun.2010.05.034. PMID 20643330.
  2. Costanzo MR, Naftel DC, Pritzker MR, Heilman JK, Boehmer JP, Brozena SC; et al. (1998). "Heart transplant coronary artery disease detected by coronary angiography: a multiinstitutional study of preoperative donor and recipient risk factors. Cardiac Transplant Research Database". J Heart Lung Transplant. 17 (8): 744–53. PMID 9730422.
  3. Johnson DE, Gao SZ, Schroeder JS, DeCampli WM, Billingham ME (1989). "The spectrum of coronary artery pathologic findings in human cardiac allografts". J Heart Transplant. 8 (5): 349–59. PMID 2795279.
  4. Billingham ME (1989). "Graft coronary disease: the lesions and the patients". Transplant Proc. 21 (4): 3665–6. PMID 2669276.
  5. Rickenbacher PR, Pinto FJ, Chenzbraun A, Botas J, Lewis NP, Alderman EL; et al. (1995). "Incidence and severity of transplant coronary artery disease early and up to 15 years after transplantation as detected by intravascular ultrasound". J Am Coll Cardiol. 25 (1): 171–7. PMID 7798497.
  6. Haddad M, Pflugfelder PW, Guiraudon C, Novick RJ, McKenzie FN, Menkis A; et al. (2005). "Angiographic, pathologic, and clinical relationships in coronary artery disease in cardiac allografts". J Heart Lung Transplant. 24 (9): 1218–25. doi:10.1016/j.healun.2004.08.016. PMID 16143236.
  7. Gao SZ, Alderman EL, Schroeder JS, Silverman JF, Hunt SA (1988). "Accelerated coronary vascular disease in the heart transplant patient: coronary arteriographic findings". J Am Coll Cardiol. 12 (2): 334–40. PMID 3292629.
  8. 8.0 8.1 Mehra MR, Crespo-Leiro MG, Dipchand A, Ensminger SM, Hiemann NE, Kobashigawa JA; et al. (2010). "International Society for Heart and Lung Transplantation working formulation of a standardized nomenclature for cardiac allograft vasculopathy-2010". J Heart Lung Transplant. 29 (7): 717–27. doi:10.1016/j.healun.2010.05.017. PMID 20620917.
  9. Nissen S (2001). "Coronary angiography and intravascular ultrasound". Am J Cardiol. 87 (4A): 15A–20A. PMID 11243599.
  10. 10.0 10.1 St Goar FG, Pinto FJ, Alderman EL, Valantine HA, Schroeder JS, Gao SZ; et al. (1992). "Intracoronary ultrasound in cardiac transplant recipients. In vivo evidence of "angiographically silent" intimal thickening". Circulation. 85 (3): 979–87. PMID 1537134.
  11. Spes CH, Klauss V, Rieber J, Schnaack SD, Tammen AR, Uberfuhr P; et al. (1999). "Functional and morphological findings in heart transplant recipients with a normal coronary angiogram: an analysis by dobutamine stress echocardiography, intracoronary Doppler and intravascular ultrasound". J Heart Lung Transplant. 18 (5): 391–8. PMID 10363681.
  12. Tuzcu EM, Kapadia SR, Sachar R, Ziada KM, Crowe TD, Feng J; et al. (2005). "Intravascular ultrasound evidence of angiographically silent progression in coronary atherosclerosis predicts long-term morbidity and mortality after cardiac transplantation". J Am Coll Cardiol. 45 (9): 1538–42. doi:10.1016/j.jacc.2004.12.076. PMID 15862431.
  13. Störk S, Behr TM, Birk M, Uberfuhr P, Klauss V, Spes CH; et al. (2006). "Assessment of cardiac allograft vasculopathy late after heart transplantation: when is coronary angiography necessary?". J Heart Lung Transplant. 25 (9): 1103–8. doi:10.1016/j.healun.2006.05.009. PMID 16962473.
  14. Johnson DE, Alderman EL, Schroeder JS, Gao SZ, Hunt S, DeCampli WM; et al. (1991). "Transplant coronary artery disease: histopathologic correlations with angiographic morphology". J Am Coll Cardiol. 17 (2): 449–57. PMID 1991903.
  15. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ (1987). "Compensatory enlargement of human atherosclerotic coronary arteries". N Engl J Med. 316 (22): 1371–5. doi:10.1056/NEJM198705283162204. PMID 3574413.
  16. Raffel OC, Merchant FM, Tearney GJ, Chia S, Gauthier DD, Pomerantsev E; et al. (2008). "In vivo association between positive coronary artery remodelling and coronary plaque characteristics assessed by intravascular optical coherence tomography". Eur Heart J. 29 (14): 1721–8. doi:10.1093/eurheartj/ehn286. PMC 2730912. PMID 18577556.
  17. Li H, Tanaka K, Oeser B, Kobashigawa JA, Tobis JM (2006). "Vascular remodelling after cardiac transplantation: a 3-year serial intravascular ultrasound study". Eur Heart J. 27 (14): 1671–7. doi:10.1093/eurheartj/ehl097. PMID 16790471.
  18. Lindelöw B, Bergh CH, Herlitz H, Waagstein F (2000). "Predictors and evolution of renal function during 9 years following heart transplantation". J Am Soc Nephrol. 11 (5): 951–7. PMID 10770975.

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