Aortic stiffness-Is kynurenic acid a novel marker? Cross-sectional study in patients with persistent atrial fibrillation.

摘要: Objective Although a number of modifiable and non-modifiable causes were implicated in arterial stiffness, its pathogenesis remains elusive, very little is known about aortic elasticity supraventricular arrhythmias. The potential role disturbed kynurenine metabolism the cardiovascular disease has been recently suggested. Thus, we studied correlations stiffness echocardiographic parameters with biochemical markers serum level kynurenic acid (KYNA), an endothelial derivative tryptophan, formed along pathway, among patients atrial fibrillation (AF). Methods Study cohort comprised 100 persistent AF (43 females/57 males). Arterial index (ASI), structural functional indices left atrium (LA) ventricle (LV) evaluated electrocardiographically. Biochemical analyses included measurements KYNA (HPLC) selected lipids glucose metabolism, thyroid status, kidney function, inflammation coagulation. Results (β = 0.389, P 0.029), homocysteine 0.256, 0.40), total cholesterol 0.814; 0.044), LDL 0.663; 0.44), TSH 0.262, 0.02), fT3 -0.333, 0.009), fT4 -0.275, 0.043) creatinine 0.374, independently correlated ASI. ASI was also associated LV end-systolic diameter (LVEDd; β 1.751, 0.045), midwall fractional shortening (mFS; -1.266, 0.007), ratio mFS/end-systolic stress (mFS/ESS; -0.235, 0.026), fraction (FS; -0.254, 0.017), LA volume (LAVI; 0.944, 0.022). Conclusions In AF, positively KYNA, risk factors atherosclerosis diastolic dysfunction LA. Revealed relationship between original observation, suggesting stiffening. synthesis which influenced by homocysteine, emerges as novel, non-classical factor AF.