Cardiac allograft vasculopathy intravascular ultrasound

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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

Since the early manifestations of cardiac allograft vasculopathy (CAV) are confined to the arterial wall, use of intravascular ultrasound (IVUS) makes it particularly useful in assessing graft coronary arteries early after heart transplantation. Its relatively higher sensitivity in defining arterial wall changes has shed light on important advances in the understanding of the natural history, distribution, and morphology of CAV.

Intravascular Ultrasound

Grayscale IVUS

Good tissue penetration of up to 10 mm allows accurate assessment of the arterial wall and plaque volume changes. Serial IVUS examinations starting early after heart transplantation will allow best assessment of percent change plaque volume. Evidence of CAV is found in 80% of the patients within one year of heart transplantation.[1] Similar conclusions were made by St Goar et al in a study comparing in vivo intracoronary ultrasound with angiography in cardiac transplant recipients.[2] In a 2010 study by Cale et al it was concluded that routine use of IVUS may lead to higher detection rates of sub-angiographic CAV.[3] Rapidly progressive CAV is defined as intimal thickness of ≥0.5 mm with in one year of heart transplantation.

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

Virtual Histology-IVUS

Virtual histology-intravascular ultrasound (VH-IVUS) allows in vivo characterization of different plaque morphologies [fibrous (green), fibrofatty (light green), dense calcium (white), and necrotic core (red)] by using spectral analysis of IVUS radiofrequency data.[4] Depending on the percent necrotic core and dense calcium coronary plaques can be classified into inflammatory, defined as necrotic core plus dense calcium ≥30% and non-inflammatory, defined as necrotic core plus dense calcium <30% of the total plaque volume. In a validation study of in vivo virtual histology compared with in vitro histopathology Nasu K et al demonstrated that VH-IVUS data correlated with histopathology with high accuracy.[5]

Using VH-IVUS in heart transplant recipients, Raichlin et al demonstrated that higher inflammatory burden of CAV atherosclerotic plaque burden is associated with early recurrent rejection and higher subsequent progression of CAV. This study also signifies the role of inflammation in the pathogenesis of CAV.[6] This concludes that VH-IVUS may provide supplemental information to coronary angiography in identifying at risk patients for future progression of CAV.

Advantages

  • Safe[7]
  • Relative higher sensitivity compared with coronary angiography[7] It is now considered gold standard for early diagnosis of CAV.
  • Plaque tissue characterization[6]
  • Serial IVUS examinations starting early after heart transplantation my help differentiate native atherosclerosis from CAV.

Limitation

  • IVUS is usually performed at the time of coronary angiography. This may lead to additional time of sedation and mildly increased procedural risks.
  • Ability to visualize only the proximal segments of the coronary arteries
  • Limited availability, training of personnel involved and use of specialized catheters may increase healthcare costs
  • Lower resolution compared with optical coherence tomography (OCT)

References

  1. Tuzcu EM, De Franco AC, Goormastic M, Hobbs RE, Rincon G, Bott-Silverman C; et al. (1996). "Dichotomous pattern of coronary atherosclerosis 1 to 9 years after transplantation: insights from systematic intravascular ultrasound imaging". J Am Coll Cardiol. 27 (4): 839–46. PMID 8613612.
  2. 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.
  3. Calé R, Almeida M, Rebocho MJ, Aguiar C, Sousa P, Brito J; et al. (2010). "The value of routine intracoronary ultrasound to assess coronary artery disease in cardiac allograft recipients". Rev Port Cardiol. 29 (2): 231–41. PMID 20545250.
  4. Nair A, Kuban BD, Tuzcu EM, Schoenhagen P, Nissen SE, Vince DG (2002). "Coronary plaque classification with intravascular ultrasound radiofrequency data analysis". Circulation. 106 (17): 2200–6. PMID 12390948.
  5. Nasu K, Tsuchikane E, Katoh O, Vince DG, Virmani R, Surmely JF; et al. (2006). "Accuracy of in vivo coronary plaque morphology assessment: a validation study of in vivo virtual histology compared with in vitro histopathology". J Am Coll Cardiol. 47 (12): 2405–12. doi:10.1016/j.jacc.2006.02.044. PMID 16781367.
  6. 6.0 6.1 Raichlin E, Bae JH, Kushwaha SS, Lennon RJ, Prasad A, Rihal CS; et al. (2009). "Inflammatory burden of cardiac allograft coronary atherosclerotic plaque is associated with early recurrent cellular rejection and predicts a higher risk of vasculopathy progression". J Am Coll Cardiol. 53 (15): 1279–86. doi:10.1016/j.jacc.2008.12.041. PMID 19358941.
  7. 7.0 7.1 Bocksch W, Wellnhofer E, Schartl M, Dreysse S, Klimek W, Franke R; et al. (2000). "Reproducibility of serial intravascular ultrasound measurements in patients with angiographically silent coronary artery disease after heart transplantation". Coron Artery Dis. 11 (7): 555–62. PMID 11023244.

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