Cardiac allograft vasculopathy: A review

Abstract

Cardiac allograft vasculopathy (CAV) is a complex disease that remains a significant cause of morbidity and mortality after orthotopic heart transplantation (OHT). Originating as a result of inflammatory response, the development and progression of CAV is attributed to endothelial dysfunction, cellular infiltration, and a wide-range of genetic and patient factors. The detection of CAV remains a diagnostic challenge, as symptoms can be variable or absent. While coronary angiography remains the initial test of choice for the diagnosis and surveillance of CAV, intravascular imaging (either by ultrasound or optical coherence tomography) and physiologic assessments are useful adjuncts in the cardiac catheterization laboratory. Positron emission tomography, computed tomographic, and magnetic resonance imaging may have a role increasing the time interval between invasive screening tests for prognosis. Medical management should include a statin, vasodilator, and tailored immunosuppressive regimen that maximally decrease allograft rejection and CAV progression while causing minimal side effects. Patients that are less responsive to pharmacotherapy should be considered for invasive management with percutaneous coronary intervention. Although surgical revascularization is a poor option, repeat OHT is the only definitive treatment option but given its morbidity should be reserved for a highly selected patient population. K E Y W O R D Scardiac allograft vasculopathy, heart transplantation, percutaneous coronary intervention

Clinical characteristics and in hospital outcomes of heart transplant recipients undergoing percutaneous coronary intervention: Insights from the National Inpatient Sample

“…however, current literature supports the role of immunologic and nonimmunologic mechanisms. 2 The prevalence and severity of CAV have progressively increased over time. It has been reported to develop as early as 1-year posttransplant in 9% of patients.…”

Combined abdominal heterotopic heart and aorta transplant model in mice

“…However, chronic allograft injury leading to graft failure and CAV remains a major obstacle to the long-term allograft survival [1,2,4]. Although the exact etiology remains unclear, multifactorial mechanisms including both immunological and non-immunological components contribute to the development of chronic allograft rejection [5,6]. In the heart, chronic allograft rejection presents as CAV, and is characterized as an accelerated form of atherosclerosis which occurs in the arteries of the transplanted heart [5,6].…”

“…Although the exact etiology remains unclear, multifactorial mechanisms including both immunological and non-immunological components contribute to the development of chronic allograft rejection [5,6]. In the heart, chronic allograft rejection presents as CAV, and is characterized as an accelerated form of atherosclerosis which occurs in the arteries of the transplanted heart [5,6]. CAV is initiated by a combination of ischemia/reperfusion injury and alloimmune injury which results in endothelial dysfunction [5,6].…”

“…In the heart, chronic allograft rejection presents as CAV, and is characterized as an accelerated form of atherosclerosis which occurs in the arteries of the transplanted heart [5,6]. CAV is initiated by a combination of ischemia/reperfusion injury and alloimmune injury which results in endothelial dysfunction [5,6]. This leads to a progressive fibroproliferative disease with intimal smooth muscle cell proliferation leading to progressive vessel occlusion, thrombotic events and eventual graft failure [5,6].…”

“…CAV is initiated by a combination of ischemia/reperfusion injury and alloimmune injury which results in endothelial dysfunction [5,6]. This leads to a progressive fibroproliferative disease with intimal smooth muscle cell proliferation leading to progressive vessel occlusion, thrombotic events and eventual graft failure [5,6]. Allograft vasculopathy (AV) can also occur in a number of solid organ transplant settings (i.e.…”