The impact of splenectomy on human coronary artery atherosclerosis and vascular macrophage distribution

Background: Splenectomy can potentially impact atherosclerosis through multiple mechanisms including altered lipid homeostasis, increased coagulation, and altered macrophage recruitment to the plaque. In patients, splenectomy has been associated with increased rates of coronary artery events, while in experimental mice, splenectomy causes increased atherosclerosis but reduces systemic monocyte supply. In this study, the direct impact of splenectomy on human coronary artery atherosclerotic plaque severity and macrophage content was investigated. Methods: Coronary artery atherosclerotic plaque severity was determined at autopsy in 18 long-term (>= 10 years) splenectomy patients and 90 matched control patients. Coronary artery macrophage content was evaluated in mild atherosclerotic plaques of 11 mid-to long-term (>= 1 year) splenectomy patients and 11 matched control patients. Results: Splenectomy was associated with reduced coronary artery atherosclerosis (P = .03). The association was most pronounced for the subgroup of patients who had undergone splenectomy 20 years or more prior to death (P = .02). There was no difference in the density of macrophages in the plaque, media, or adventitia upon comparing splenectomy and control patients. In the control group, there was no correlation between the macrophage densities in the three arterial layers. However, in the splenectomy patients, there was a strong correlation in the macrophage densities across the plaque, media, and adventitia (P = .0002), with resulting slopes that were significantly greater than seen in the control patients (P = .0007-.011). Conclusions: These findings indicate that, in humans, splenectomy is associated with lower coronary artery atherosclerotic plaque severity and altered coronary artery macrophage distribution. These results suggest that the spleen can modulate the recruitment of macrophages into human coronary arteries and the progression of atherosclerosis. (C) 2016 Elsevier Inc. All rights reserved.