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Vascular Inflammation, Calf Muscle Oxygen Saturation, and Blood Glucose are Associated With Exercise Pressor Response in Symptomatic Peripheral Artery Disease.

Andrew W GardnerPolly S MontgomeryMing WangChixiang ChenMarcos KurokiDanielle Jin-Kwang Kim
Published in: Angiology (2019)
We determined whether calf muscle oxygen saturation (StO2) and vascular biomarkers of inflammation and oxidative stress were associated with an exercise pressor response during treadmill walking in 179 patients with symptomatic peripheral artery disease (PAD). The exercise pressor response was measured as the change in blood pressure from rest to the end of the first 2-minute treadmill stage (2 mph, 0% grade). There was a wide range in the change in systolic blood pressure (-46 to 50 mm Hg) and in diastolic blood pressure (-23 to 38 mm Hg), with mean increases of 4.3 and 1.4 mm Hg, respectively. In multiple regression analyses, significant predictors of systolic pressure included glucose (P < .001) and insulin (P = .039). Significant predictors of diastolic pressure included cultured endothelial cell apoptosis (P = .019), the percentage drop in exercise calf muscle (StO2; P = .023), high-sensitivity C-reactive protein (P = .032), and glucose (P = .033). Higher levels in pro-inflammatory vascular biomarkers, impaired calf muscle StO2 during exercise, and elevated blood glucose were independently associated with greater exercise pressor response in patients with symptomatic PAD. The clinical implication is that exercise and nutritional interventions designed to improve inflammation, microcirculation, and glucose metabolism may also lower blood pressure during exercise in patients with symptomatic PAD.
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