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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Flondell-Sité D., Lindblad B., Gottsäter A.
University of Lund, Vascular Centre, Skåne University Hospital, Malmö, Sweden
AIM: The etiology of abdominal aortic aneurysm (AAA) includes inflammation, coagulation, and endothelial dysfunction. We have prospectively evaluated relations between these mechanisms and AAA growth. Tumour necrosis factor (TNF)-α, interleukin (IL)-6, endothelin (ET)-1, CD40 ligand and the complex formed between activated protein C (APC) and protein C inhibitor (PCI) were measured annually and related to AAA growth during up to 5 years in 206 patients with conservatively followed AAA.
METHODS: We evaluated 163 patients up to 1 year, 126 patients up to 2 years, 83 patients up to 3 years, 53 patients up to 4 years, and 33 patients up to 5 years. The total number of patient follow-up years was 458.
RESULTS: ET-1 remained unchanged except for a tendency to increase in the third and fourth years of follow-up. TNF-α decreased significantly during the first year and thereafter increased back to baseline values. There were no changes in IL-6, CD40 ligand, and APC-PCI complex. When patients in the highest and lowest quartiles of AAA growth up to 5 years follow-up were compared, APC-PCI complex levels tended to be higher (P=0.06) in the highest quartile of growth at three years (0.45 µg/l [i.q.r. 0.40-0.77] versus 0.28 µg/L [i.q.r. 0.14-0.36]). Δ-values of ET-1 and TNF-α did not show any correlation to growth. The 14 AAA patients that ruptured during follow-up did not differ from patients with non-ruptured AAA regarding biomarkers.
CONCLUSION: In conclusion, none of the investigated mediators could be used to predict growth or rupture, or help to prolong intervals between ultrasound examinations in follow-up of AAA patients.