Why do arteries sclerose when veins rarely do?

By Naveed Saleh, MD, MS, for MDLinx
Published August 22, 2018

Key Takeaways

Arterial blood flow can cause sclerosis of venous blood vessels—possibly due to differential counts in lymphocytes and neutrophils, according to a new study in Medicine.

“Recently, a number of studies showed that vein grafts used in coronary artery bypass surgery also underwent hardening, similar to original coronary arteries,” wrote the authors, led by Li-Ping Peng, MD, Department of Cardiology, Third Xiangya Hospital of Central South University, Changsha, China.

Angiosclerosis affects arteries but rarely veins, likely due to differences in the anatomy between the two. Various studies have indicated that differences in physiology and the hemodynamic milieu between veins and arteries play a role in vascular sclerosis. Moreover, it is widely understood that serum lipid composition contributes to atherosclerosis.

Vascular sclerosis rarely affects the pulmonary artery, which carries venous blood. This observation has directed experts to hypothesize that vascular sclerosis was linked to features of arterial blood.

“We explored whether arterial blood components were associated with hardening of the venous wall in addition to hemodynamics, and differences in the composition of arterial and venous blood,” the authors wrote.

In this two-part observational study, the investigators first employed ultrasound and immunohistochemistry to assess the distal venous structure of arteriovenous fistulas in 12 patients with uremia. Their goal was to assess whether arterial blood hardened the venous wall.

The team divided the uremic patients into two groups. The control group received surgery to establish arteriovenous fistula within the past month, and the trial group received this surgery 2-plus years before the current study.

During the second phase of the study, the team obtained and tested aortic, arterial, and venous blood from 51 patients who had received coronary angiography.

The researchers found that patients in the trial group experienced vascular sclerosis ≥ 5 cm away from the fistula, and the vein under the fistula had thickened and hardened. Furthermore, the arterial blood consisted of more lymphocytes and fewer neutral granulocytes than did the venous blood.

“On the basis of our findings, we speculate that high lymphocyte levels may promote filtration into venous walls and subsequently contribute to hardening and thickening of the venous wall,” the authors wrote.

The exact mechanisms underlying this have yet to be elucidated. However, the team suggested that the recycling of lymphocytes could result in differences in the percentages of lymphocytes and neutrophils observed in the peripheral arteries and veins.

The researchers noted that they did not observe any differences between venous and arterial blood in terms of lipids and uric acid, despite previous studies implicating these components in the development of atherosclerosis. Dr. Peng and colleagues suggested that this discrepancy in findings could be due to the small sample size and characteristics of patients chosen in the current study.

“We have demonstrated that arterial blood has a substantially higher percentage of lymphocytes, but a lower percentage of neutrophils, compared with venous blood,” the researchers concluded. “This is potentially responsible for the more frequent occurrence of vascular sclerosis in arteries than veins. This hypothesis needs to be further examined in more mechanistic studies, both in vitro and in vivo." 

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