Department of Surgery, Institute of Clinical Medicine, University of Tartu, 8 Puusepa Street, 51014 Tartu, Estonia
Anders Wanhainen
Department of Surgical Sciences, Section of Vascular Surgery, Uppsala University, SE-751 85 Uppsala, Sweden
Aigar Ottas
Department of Biochemistry, Institute of Biomedicine and Translational Medicine, Centre of Excellence for Genomics and Translational Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
Mare Vähi
Institute of Mathematics and Statistics, University of Tartu, 18 Narva mnt. Street, 51009 Tartu, Estonia
Mihkel Zilmer
Department of Biochemistry, Institute of Biomedicine and Translational Medicine, Centre of Excellence for Genomics and Translational Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
Ursel Soomets
Department of Biochemistry, Institute of Biomedicine and Translational Medicine, Centre of Excellence for Genomics and Translational Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia
Martin Björck
Department of Surgical Sciences, Section of Vascular Surgery, Uppsala University, SE-751 85 Uppsala, Sweden
Jaak Kals
Department of Surgery, Institute of Clinical Medicine, University of Tartu, 8 Puusepa Street, 51014 Tartu, Estonia
Abdominal aortic aneurysm (AAA) is characterized by structural deterioration of the aortic wall, leading to aortic dilation and rupture. The aim was to compare 183 low molecular weight metabolites in AAA patients and aorta-healthy controls and to explore if low molecular weight metabolites are linked to AAA growth. Blood samples were collected from male AAA patients with fast (mean 3.3 mm/year; range 1.3–9.4 mm/year; n = 39) and slow growth (0.2 mm/year; range −2.6–1.1 mm/year; n = 40), and from controls with non-aneurysmal aortas (n = 79). Targeted analysis of 183 metabolites in plasma was performed with AbsoluteIDQ p180 kit. The samples were measured on a QTRAP 4500 coupled to an Agilent 1260 series HPLC. The levels of only four amino acids (histidine, asparagine, leucine, isoleucine) and four phosphatidylcholines (PC.ae.C34.3, PC.aa.C34.2, PC.ae.C38.0, lysoPC.a.C18.2) were found to be significantly lower (p < 0.05) after adjustment for confounders among the AAA patients compared with the controls. There were no differences in the metabolites distinguishing the AAA patients with slow or fast growth from the controls, or distinguishing the patients with slow growth from those with fast growth. The current study describes novel significant alterations in amino acids and phosphatidylcholines metabolism associated with AAA occurrence, but no associations were found with AAA growth rate.
