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Author Spotlight: Assessing the Cardiovascular Profile of Patients with Metabolic Syndrome
Published on: September 27, 2024
Associations between pulse pressure amplification and inflammation in young adults according to body composition: The
Yolandi Breet1,2, Christian Delles3, Paul Welsh3
1Hypertension in Africa Research Team (HART), North-West University, Potchefstroom, South Africa. yolandi.breet@nwu.ac.za.
Abstract:
Pulse pressure amplification (PPA) is a measure of arterial function and wave reflection dynamics. The potential contribution of low-grade systemic inflammation to PPA-particularly in the context of overweight and obesity (OW/OB)-remains unclear, especially in young adults. We assessed differences in PPA and inflammatory markers (leptin, interleukin-6, interleukin-8, tumour necrosis factor-α, adiponectin, interleukin-10, and C-reactive protein) in young adults stratified by body composition. We further determined the relationship of PPA and inflammatory markers within these groups. This cross-sectional study included 1202 adults aged between 20-30 years. Participants were stratified into groups with underweight (N = 82) healthy weight (N = 598), overweight (N = 326) and obesity (N = 196). PPA was defined as the ratio of brachial pulse pressure to central pulse pressure. Inflammatory biomarkers were measured in serum. PPA was lower in the OW and OB groups (p < 0.001), while the inflammatory profile (tumour necrosis factor-α, adiponectin, leptin and C-reactive protein) was also more adverse in the OW and OB groups (all p < 0.001). In multivariate adjusted regression analysis, PPA was adversely associated with tumour necrosis factor-α, adiponectin, leptin and C-reactive protein in the OW or OB groups only (all p < 0.025). In young adults, a higher BMI is associated with a lower PPA and higher levels of inflammatory markers. Adverse associations between PPA as a measure of arterial function and several inflammatory markers are also seen in the setting of increased adiposity, highlighting inflammation as a potential mechanistic link between adiposity and changes in arterial function.
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