What is the Role of Angiogenesis Markers in Cardiac Allograft Vasculopathy Following Heart Transplantation

Purpose Cardiac allograft vasculopathy (CAV) remains a major limiting factor in long-term survival post heart transplantation (HT). However the pathophysiology of CAV remains illusive. The aim of this study was to investigate if angiogenesis as assessed by peripheral blood biomarkers is associated with the presence of CAV. Methods 49 consecutive patients ≥ 2 years post-HT were prospectively enrolled in the study and stratified by time post-transplantation (<4 and ≥ 4 years post transplant) and CAV status (no CAV including Stanford Class 1 and 2 vs. angiographic CAV and Stanford Class ≥ 2). Peripheral blood protein expression angiogenesis markers including angiopoetin-2, vascular endothelial growth factor A, C and D and endoglin were measured using a multiplex immunoassay system. Results Of 49 patients enrolled in the study, 27 had CAV. Patients with CAV had a trend for a lower LVEF (55.6 ± 14.8% vs 63.1 ±5.8% p 0.08) but no other significant differences including age and immunosuppressive regimen were found between the groups. Peripheral blood angiogenesis factors were similar when patients were stratified by presence of CAV or severity of CAV. Moreover angiogenesis factors did not differ with stratification by time post HT. Conclusion Peripheral blood markers of angiogenesis did not change with duration of time post HT or the presence of CAV. Further studies are needed to evaluate a potential role of angiogenesis in the development of CAV. Cardiac allograft vasculopathy (CAV) remains a major limiting factor in long-term survival post heart transplantation (HT). However the pathophysiology of CAV remains illusive. The aim of this study was to investigate if angiogenesis as assessed by peripheral blood biomarkers is associated with the presence of CAV. 49 consecutive patients ≥ 2 years post-HT were prospectively enrolled in the study and stratified by time post-transplantation (<4 and ≥ 4 years post transplant) and CAV status (no CAV including Stanford Class 1 and 2 vs. angiographic CAV and Stanford Class ≥ 2). Peripheral blood protein expression angiogenesis markers including angiopoetin-2, vascular endothelial growth factor A, C and D and endoglin were measured using a multiplex immunoassay system. Of 49 patients enrolled in the study, 27 had CAV. Patients with CAV had a trend for a lower LVEF (55.6 ± 14.8% vs 63.1 ±5.8% p 0.08) but no other significant differences including age and immunosuppressive regimen were found between the groups. Peripheral blood angiogenesis factors were similar when patients were stratified by presence of CAV or severity of CAV. Moreover angiogenesis factors did not differ with stratification by time post HT. Peripheral blood markers of angiogenesis did not change with duration of time post HT or the presence of CAV. Further studies are needed to evaluate a potential role of angiogenesis in the development of CAV.