Central blood pressure (BP) has been suggested to be a better predictor of cardiovascular disease risk than brachial BP. Given that central BP and arterial waveform are both influenced by insulin resistance, major initiators of insulin resistance, such as serum-free fatty acid (FFA), are suspected of potentially being involved in central hemodynamics. To confirm that insulin signaling is an important modulator of central hemodynamics, we investigated this hypothesis in a large-scale general population. Brachial BP and radial arterial waveform were measured simultaneously in 9393 middle-aged to elderly individuals. The augmentation index was calculated from the radial waveform as the ratio of the height of the late systolic peak to that of the first peak. Central systolic BP was defined as the absolute pressure of the late systolic peak of the waveform. Differences in central and brachial pulse pressure (PP) were considered to represent PP amplification. PP amplification differed significantly among serum FFA level quartiles (Q1, 7.8±5.3; Q2, 8.6±5.0; Q3, 9.3±5.7; Q4, 10.3±6.1 mm Hg; P<0.001), and the maximum difference in combination with diabetes mellitus status was 4.9 mm Hg. Multivariate analysis adjusted for major covariates indicated that higher serum FFA was an independent determinant for higher PP amplification ((3=0.145, P<0.001) and lower augmentation index (β=-0.122, P<0.001) and central systolic BP (β=-0.044, P<0.001), whereas the association between FFA and PP amplification significantly decreased ((3=0.022, P<0.001) after further adjustment for augmentation index. Serum FFA is an overlooked factor favorably influencing central hemodynamics. A low-magnitude refection pressure wave might be involved in this paradoxical relationship.
CITATION STYLE
Tabara, Y., Takahashi, Y., Kawaguchi, T., Setoh, K., Terao, C., Yamada, R., … Matsuda, F. (2014). Association of serum-free fatty acid level with reduced reflection pressure wave magnitude and central blood pressure the Nagahama study. Hypertension, 64(6), 1212–1218. https://doi.org/10.1161/HYPERTENSIONAHA.114.04277
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