Key result
Cardiac allograft vasculopathy affects ~30% of heart transplant recipients by 5 years, driving late mortality.
Cardiac allograft vasculopathy remains a major limitation to long-term survival after heart transplantation, highlighting the need for improved early surveillance techniques and preventive therapies such as mTOR inhibitors.
Cardiac allograft vasculopathy (CAV) remains the Achilles' heel of long-term survival after heart transplantation. Almost one-third of patients develop CAV by 5 years post-transplant and 1 in 8 deaths beyond a year are due to CAV. Abnormal vascular fibroproliferation in CAV occurs as a result of coronary endothelial inflammation, injury, and dysfunction triggered by immune and nonimmune insults. Surveillance methods for CAV have significant limitations, particularly for detecting early disease. Areas of investigation include myocardial and coronary blood flow quantification, and intracoronary imaging to detect early changes in the vessel wall and high-risk plaques. Treatment approaches continue to evolve, but prevention remains the focus. Newer mammalian target of rapamycin inhibitors can significantly delay the progression of CAV; however, their optimal use remains to be established. Further investigation is needed to understand the complex pathophysiology of CAV, improve surveillance techniques, and develop therapies to prevent and slow disease progression.
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Chih et al. (2016) conducted a review in Cardiac allograft vasculopathy (CAV). Cardiac allograft vasculopathy develops in almost one-third of patients by 5 years post-transplant and accounts for 1 in 8 deaths beyond a year.
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