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Trimethylamine‐N‐oxide is elevated in the acute phase after ischaemic stroke and decreases within the first days
Author(s) -
Schneider C.,
Okun J. G.,
Schwarz K. V.,
Hauke J.,
Zorn M.,
Nürnberg C.,
Ungerer M.,
Ringleb P. A.,
Mundiyanapurath S.
Publication year - 2020
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.14253
Subject(s) - medicine , trimethylamine n oxide , stroke (engine) , biomarker , ischaemic stroke , gastroenterology , prospective cohort study , clinical endpoint , renal function , trimethylamine , ischemia , randomized controlled trial , biochemistry , engineering , mechanical engineering , chemistry
Background and purpose Trimethylamine‐N‐oxide (TMAO) is a biomarker of the gut microbiome and correlates with the risk of cardiovascular diseases. However, conflicting data exist on the specific role of TMAO in ischaemic stroke patients. We aimed to analyze the time course of TMAO levels in stroke patients compared with controls. Methods In this prospective, case‐control study, patients suffering from ischaemic stroke (onset <24 h) and control patients with less than two cardiovascular risk factors were enrolled. Plasma TMAO levels were analyzed on admission, after 48 h and after 3 months. The primary endpoint was the difference in TMAO levels on admission between stroke patients and controls. Results A total of 196 patients with ischaemic stroke and 100 controls were included between February 2018 and April 2019. Plasma TMAO levels on admission were significantly higher in stroke patients than in controls [median value 4.09 (2.87–6.49) vs. 3.16 (2.08–5.16) µmol/L, P = 0.001]. There was a significant decrease in TMAO levels in stroke patients after 48 h [median at 48 h, 3.49 (2.30–5.39) µmol/L, P = 0.027]. TMAO levels increased again 3 months after stroke [median 4.23 (2.92–8.13) µmol/L, P = 0.047]. In controls, TMAO levels did not change between admission and after 48 h [median at 48 h, 3.14 (1.63–4.61) µmol/L, P = 0.11]. An inverse correlation between TMAO values and kidney function was found (Spearman rho −0.334, P < 0.001). Conclusions Our study emphasizes the importance of the time course of TMAO levels after ischaemic stroke. Future studies should define the time point of TMAO analysis, preferably in the acute phase (<24 h).