Related Experiment Video
Updated: Mar 15, 2026
Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
Published on: May 17, 2015
The impact of splenectomy on human coronary artery atherosclerosis and vascular macrophage distribution
1Harvard T.H. Chan School of Public Health, Boston, MA, 02115, USA; Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, 02114, USA.
Insights
Splenectomy, the removal of the spleen, was linked to reduced coronary artery atherosclerosis in patients. This suggests the spleen plays a role in regulating plaque development and macrophage distribution in arteries.
Area of Science:
- Cardiovascular Research
- Immunology
- Surgical Outcomes
Background:
- Splenectomy may influence atherosclerosis via lipid homeostasis, coagulation, and macrophage recruitment.
- Previous studies show conflicting results in humans and mice regarding splenectomy's effect on atherosclerosis and monocyte supply.
Purpose of the Study:
- To investigate the direct impact of splenectomy on human coronary artery atherosclerotic plaque severity.
- To evaluate the effect of splenectomy on macrophage content within coronary artery plaques.
Main Methods:
- Autopsy assessment of coronary artery atherosclerosis severity in 18 splenectomy patients (≥10 years post-surgery) and 90 controls.
- Evaluation of coronary artery macrophage content in mild plaques of 11 splenectomy patients (≥1 year post-surgery) and 11 matched controls.
Main Results:
- Splenectomy was associated with significantly reduced coronary artery atherosclerosis (P=.03), particularly in those splenectomized ≥20 years prior (P=.02).
- No difference in macrophage density was observed between splenectomy and control groups in plaque, media, or adventitia.
- Splenectomy patients showed a strong correlation in macrophage densities across arterial layers, unlike controls.
Conclusions:
- Human splenectomy is linked to decreased coronary artery atherosclerotic plaque severity and altered macrophage distribution.
- Findings suggest the spleen modulates macrophage recruitment into coronary arteries and influences atherosclerosis progression.
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.
