Cardiac allograft vasculopathy (CAV) is an accelerated form of coronary artery disease that affects vessels of transplanted hearts,
and is characterised by diffuse intimal hyperplasia and luminal narrowing in the allograft arteries,
epicardial vessels and microcirculation1.
Post-transplant CAV occurs in up to 47% of patients depending on the time since transplant (8% within 1 year,
30% within 5 years,
47% within ten years) according to the International Society of Heart and Lung Transplantation registry (ISHLT)3.
CAV is a significant cause of mortality.
The proportion of deaths caused by CAV is 10% between 1 and 3 years post-transplant,
with other causes including acute rejection,
graft failure,
multi-organ failure,
infection,
renal failure,
and malignancy3.
It is a different process to ordinary coronary artery disease and the pathophysiology is believed to be immune-related representing a form of chronic allograft rejection2. Inflammatory activation leads to endothelial damage and altered vascular permeability,
which leads to vascular smooth muscle proliferation and cytokine release,
leading to progressive luminal narrowing2.
CAV can be managed by altering immunosuppression and performing percutaneous coronary intervention,
however,
definitive management is repeat transplantation2.
Donor risk factors for CAV include increasing age,
male sex,
hypertension.
Recipient risk factors include early severe rejection an increased number of rejection episodes,
CMV infection,
insulin resistance,
hypertension,
hyperlipidemia and higher BMI.
Smoking will accelerate progression2.
CAV is often asymptomatic due to denervation, therefore awareness and screening is key. The ISHLT Working Group recommends angiography as the standard test for routine screening of patients.
Intravascular ultrasound (IVUS) assesses all layers of the vessel wall as well as the lumen2.
IVUS is more sensitive in quantifying the total plaque burden when compared to angiography alone,
as it measures intimal thickening,
which can underestimate the extent of disease on the basis of luminal narrowing alone4.
CT is a useful non-invasive tool to evaluate,
grade and monitor CAV with high specificity and sensitivity.
CT is less costly and less resource intensive than conventional angiography.
CT can also provide information on the cardiac chambers and function in one single test.
Coronary CT angiograms (CCTAs) are generally performed on high number multislice multidetector CTs. CCTAs are performed with iodinated contrast with bolus tracking in the left atrium after non-contrast imaging. Prospective gating is attempted,
however,
due to cardiac denervation,
beta-blockers which are administered as standard to decrease heart rate often have little effect,
necessitating retrospective scanning and increasing the dose. Image quality is paramount,
given that the vessels affected most by motion are also those most affected by CAV (distal segments and side branches)4.
Studies comparing CCTA with angiography in the detection of significant stenoses demonstrate sensitivity of 70-86%,
specificity of 92-99%,
positive predictive value of 81-89% and negative predictive value of 77-99%2.
The dose implication must be considered.
In our institution (MMUH Radiology directorate,
Radiology Dept.
2013-2017) the dose of a prospective CCTA is 5.7mSv (1.4 years background radiation or 260CXRs),
while a retrospective CCTA dose is almost double that at 11.2mSv. In comparison,
invasive angiography has an average dose of approximately 5–6 mSv.
Given that post-cardiac transplantation patients have a high lifetime burden of radiation with multiple radiographs,
CTs and angiograms, dose is an important consideration.
Additionally,
the prolonged use of immunosuppression increases their lifetime cancer risk.
Normal CCTA has a good negative predictive value in outruling CAV and generally correlates well with formal angiography.
CT is also useful in detecting other abnormalities such as pulmonary findings (lung cancer,
interstitial lung disease etc).