What is the clinical evidence from this study?

Study design: Case-Control. Population: Peripheral artery disease (n=172). Intervention: Peripheral artery disease vs. Healthy control subjects. Primary outcome: Endothelial cell apoptosis (164% higher, p=<0.001).

January 1, 2014Open Access

Greater Endothelial Apoptosis and Oxidative Stress in Patients with Peripheral Artery Disease

Q: What are the key findings of this study?

Sera from patients with peripheral artery disease induced 164% higher endothelial cell apoptosis (P<0.001) and 62% higher reactive oxygen species production (P<0.001) than healthy control sera.

AGAndrew W. GardnerVascular / Pulmonary Vascular DPDonald E. ParkerUniversity of Oklahoma Health Sciences Center PMPolly S. MontgomeryOklahoma City University

Key Result

Sera from patients with peripheral artery disease induced 164% higher endothelial cell apoptosis (P<0.001) and 62% higher reactive oxygen species production (P<0.001) than healthy control sera.

Study Design

Type

Case-Control (n=172)

Structured PICO

Does sera from patients with peripheral artery disease induce greater endothelial apoptosis and oxidative stress compared to healthy controls?

Population

172 subjects, including 156 with peripheral artery disease and 16 healthy controls.

Exposure

Sera from subjects with peripheral artery disease applied to cultured endothelial cells.

Comparator

Sera from healthy control subjects applied to cultured endothelial cells.

Outcome

Endothelial cell apoptosis and cellular reactive oxygen species production.surrogate

Patients with peripheral artery disease exhibit greater systemic oxidative stress and inflammation, which induces higher endothelial apoptosis compared to healthy controls.

Main Result

Effect estimate: 164% higher

p-value: p=<0.001

Abstract

We compared apoptosis, cellular oxidative stress, and inflammation of cultured endothelial cells treated with sera from 156 subjects with peripheral artery disease (PAD) and 16 healthy control subjects. Furthermore, we compared circulating inflammatory, antioxidant capacity, and vascular biomarkers between the two groups. The PAD group had a 164% higher value for endothelial cell apoptosis (P < 0.001) and a 62% higher value for endothelial cellular reactive oxygen species production (P < 0.001) than the control group. Furthermore, the PAD group had lower systemic antioxidant capacity measured by hydroxyl radical antioxidant capacity activity (P < 0.001), higher inflammatory and vascular measures of high-sensitivity C-reactive protein (P < 0.001), interleukin-8 (P < 0.001), serum amyloid A (P < 0.001), vascular cell adhesion molecule-1 (P < 0.001), adiponectin (P < 0.001), apolipoprotein B (P = 0.013), apolipoprotein CIII (P = 0.035), lower vascular endothelial growth factor-A (P < 0.001), and hepatocyte growth factor (P < 0.001) than the control group. Subjects with PAD have greater endothelial apoptosis and oxidative stress than control subjects with low burden of comorbid conditions and cardiovascular risk factors. Furthermore, subjects with PAD have lower systemic antioxidant capacity and angiogenic measures and higher circulating inflammatory parameters.

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