<unk>  <unk>  is a progressive type of coronary artery disease in people who have had a heart transplant. As the donor heart has lost its nerve supply there is typically no chest pain, and<unk>  is usually detected on routine testing. It may present with symptoms such as tiredness and breathlessness. It arises when the blood vessels supplying the transplanted heart change in structure. They gradually narrow and restrict its blood flow, subsequently leading to impairment of the heart muscle or sudden death. In addition to the same risk factors for coronary artery disease due to the build up of plaque,<unk>  is more likely to occur if the donor was older or died from explosive brain death, and if there is cytomegalovirus infection. Its mechanism involves immunological (innate and adaptive) and nonimmunological factors, with distinct features on histological samples of coronary arteries. Other major causes of death following heart transplantation include graft failure, organ rejection and infection. Diagnosis is by regular follow-up and monitoring of the transplanted heart for early signs of disease. Tests include coronary angiography, intravascular ultrasound, dobutamine stress echocardiography, positron emission tomography, computed tomographic angiography (CT angiography) and several biomarkers. Statins and aspirin are commenced early after transplantation and on detection of<unk> . Medications including sirolimus and everolimus can slow disease progression. A repeat heart transplantation may be required.<unk>  affects around half of heart transplant recipients within 10 years. It contributes to the death of 11-13% one year from heart transplantation.
Cardiac allograft vasculopathy
Graft-versus-host disease
Chronic allograft nephropathy
Transplant rejection
Cardiac amyloidosis
Extrapulmonary tuberculosis
Vasculogenic mimicry
Transplant glomerulopathy