Cardiac allograft vasculopathy screening

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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]

Overview

Cardiac allograft vasculopathy (CAV) is the leading cause of morbidity and mortality beyond the first year after heart transplantation. In most cardiac transplant centers coronary angiography currently remains the screening tool of choice for CAV. Early diagnosis is important as it may allow for alterations in medical therapy before the disease progresses to the stage where revascularization is required.

Screening

The 2010 International Society of Heart and Lung Transplant Guidelines for the care of heart transplant recipients recommend annual invasive coronary angiography as the screening tool of choice for CAV.[1] In most centers screening of graft coronary arteries for signs of CAV is usually performed six weeks after cardiac transplantation and then annually thereafter. In a retrospective study by Haddad et al it was reported that angiographic evidence of CAV increases by approximately 10% with every 2-year period after cardiac transplantation.[2] The principal advantages of coronary angiography are its wide acceptability, low cost compared with other novel imaging techniques, and ease of performance.[3] Studies have shown that coronary angiography is 80% sensitive and 96% specific in detecting CAV.[4][5]

Although coronary angiography is the preferred screening modality in many centers it lacks sensitivity in detecting early-CAV associated arterial wall changes. In early CAV due to positive arterial remodeling coronary vascular lumen is relatively preserved until negative remodeling occurs resulting in narrowing of the arterial lumen.[6] This positive remodeling is not detected by coronary angiography leading to an under-estimation of the extent of CAV.[6] Novel intracoronary imaging techniques such as intravascular ultrasound and optical coherence tomography have shown promising results in detecting these early-CAV associated coronary arterial wall changes.[7][8][9][10] Therefore supplementing these techniques to annual coronary angiography, especially in the initial years of heart transplantation may aid in identifying high-risk subjects and appropriately risk stratifying them. However, currently studies do not exist to support this strategy.

Stanford classification:

Class Intimal Thickening
Class 0 (none) No intimal thickening
Class I (trivial) Intimal thickening 0.3 mm and 180° circumference
Class II (mild) Intimal thickening 0.3 mm and >180° circumference or 0.3 to 0.5 mm and 180° circumference
Class III (moderate) Intimal thickening 0.3 to 0.5 mm and >180° circumference or intimal thickening 0.5 to 1 mm and 180° circumference
Class IV (severe) Intimal thickening >0.5 mm and >180° circumference or intimal thickening >1 mm

References

  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. 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.
  3. 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.
  4. Sharples LD, Jackson CH, Parameshwar J, Wallwork J, Large SR (2003). "Diagnostic accuracy of coronary angiography and risk factors for post-heart-transplant cardiac allograft vasculopathy". Transplantation. 76 (4): 679–82. doi:10.1097/01.TP.0000071200.37399.1D. PMID 12973108.
  5. 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.
  6. 6.0 6.1 Nissen S (2001). "Coronary angiography and intravascular ultrasound". Am J Cardiol. 87 (4A): 15A–20A. PMID 11243599.
  7. 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.
  8. 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.
  9. 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.
  10. Khandhar SJ, Yamamoto H, Teuteberg JJ, Shullo MA, Bezerra HG, Costa MA; et al. (2013). "Optical coherence tomography for characterization of cardiac allograft vasculopathy after heart transplantation (OCTCAV study)". J Heart Lung Transplant. 32 (6): 596–602. doi:10.1016/j.healun.2013.02.005. PMID 23499356.

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