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Pathogenesis of aortic sclerosis: association with low BMI, tissue nitric oxide resistance, but not systemic inflammatory activation

机译:主动脉硬化的发病机制:与低BMI,组织一氧化氮抵抗相关,但与全身性炎症激活无关

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Aortic sclerosis (ASc) represents the earliest stage of development of aortic valve thickening, and may eventually progress to aortic valve stenosis (AS). ASc is associated with intra-valvular inflammatory activation, and potentially with attenuation of the anti-inflammatory effect of nitric oxide (NO). We have shown that ASc occurs less frequently in obese individuals, in whom systemic inflammatory activity is generally increased. We explored these relationships further by stratifying a population of 253 ageing individuals according to BMI. Increasing BMI was associated with increased hs-CRP concentrations (r=0.43; p<0.001). However, presence/absence of ASc did not significantly modify this relationship. Furthermore, increasing BMI was independent of tissue responsiveness to NO, as measured via inhibition of platelet aggregation by the NO donor sodium nitroprusside. Therefore the association of low BMI with increased risk of ASc appears to interact neither with systemic inflammatory activation in such individuals, nor with any “paradoxical” occurrence of NO resistance.
机译:主动脉硬化(ASc)代表了主动脉瓣增厚发展的最早阶段,并可能最终发展为主动脉瓣狭窄(AS)。 ASc与瓣膜内炎症激活有关,并可能与一氧化氮(NO)的抗炎作用减弱有关。我们已经表明,ASc在肥胖个体中的发生频率较低,在肥胖个体中,全身炎症活动通常会增加。根据BMI,我们通过对253个衰老个体进行分层来进一步探索这些关系。 BMI升高与hs-CRP浓度升高相关(r = 0.43; p <0.001)。但是,是否存在ASc并不能显着改变这种关系。此外,增加的BMI不依赖于组织对NO的反应性,如通过NO供体硝普钠抑制血小板凝集所测量的。因此,低BMI与ASc风险增加之间的关联似乎既不与此类个体的全身性炎症激活相互作用,也不与NO抵抗的任何“反常”发生相互作用。

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