Key result
In patients with persistent atrial fibrillation, serum kynurenic acid levels were independently and positively correlated with the aortic stiffness index (β = 0.389, P = 0.029).
Why the study?
Pathogenesis of arterial stiffness remains elusive, little is known about aortic elasticity in supraventricular arrhythmias, and disturbed kynurenine metabolism has been suggested in cardiovascular disease.
Cross-Sectional (n=100)
No
Effect estimate: β = 0.389
p-value: p=0.029
In patients with persistent atrial fibrillation, serum kynurenic acid levels independently correlate with aortic stiffness, suggesting a potential role of kynurenine metabolism in arterial stiffening.
KYNA-aortic stiffness association in persistent AF should not change practice; hypothesis-generating and requires prospective studies to assess causality.
OBJECTIVE: Although a number of modifiable and non-modifiable causes were implicated in arterial stiffness, its pathogenesis remains elusive, and very little is known about aortic elasticity in supraventricular arrhythmias. The potential role of disturbed kynurenine metabolism in the pathogenesis of cardiovascular disease has been recently suggested. Thus, we studied the correlations of aortic stiffness and echocardiographic parameters with biochemical markers and serum level of kynurenic acid (KYNA), an endothelial derivative of tryptophan, formed along the kynurenine pathway, among patients with atrial fibrillation (AF). METHODS: Study cohort comprised 100 patients with persistent AF (43 females/57 males). Arterial stiffness index (ASI), structural and functional indices of left atrium (LA) and left ventricle (LV) were evaluated electrocardiographically. Biochemical analyses included the measurements of serum KYNA (HPLC) and of the selected markers of lipids and glucose metabolism, thyroid status, kidney function, inflammation and coagulation. RESULTS: KYNA (β = 0.389, P = 0.029), homocysteine (β = 0.256, P = 0.40), total cholesterol (β = 0.814; P = 0.044), LDL (β = 0.663; P = 0.44), TSH (β = 0.262, P = 0.02), fT3 (β = -0.333, P = 0.009), fT4 (β = -0.275, P = 0.043) and creatinine (β = 0.374, P = 0.043) were independently correlated with ASI. ASI was also independently associated with LV end-systolic diameter (LVEDd; β = 1.751, P = 0.045), midwall fractional shortening (mFS; β = -1.266, P = 0.007), ratio mFS/end-systolic stress (mFS/ESS; β = -0.235, P = 0.026), LV shortening fraction (FS; β = -0.254, P = 0.017), and LA volume index (LAVI; β = 0.944, P = 0.022). CONCLUSIONS: In patients with AF, aortic stiffness correlated positively with KYNA, biochemical risk factors of atherosclerosis and with the indices of diastolic dysfunction of LV and LA. Revealed relationship between ASI and KYNA is an original observation, suggesting a potential role of disturbed kynurenine metabolism in the pathogenesis of arterial stiffening. KYNA, synthesis of which is influenced by homocysteine, emerges as a novel, non-classical factor associated with ASI in patients with AF.
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Zapolski et al. (2020) conducted a cross-sectional in Persistent atrial fibrillation (n=100). Serum kynurenic acid (KYNA) levels was evaluated on Correlation between Aortic Stiffness Index (ASI) and serum KYNA levels (β = 0.389, p=0.029). In patients with persistent atrial fibrillation, serum kynurenic acid levels were independently and positively correlated with the aortic stiffness index (β = 0.389, P = 0.029).
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