Abstract
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.
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.
| Original language | English |
|---|---|
| Pages (from-to) | 276-282 |
| Number of pages | 7 |
| Journal | International Angiology |
| Volume | 31 |
| Issue number | 3 |
| Publication status | Published - 2012 |
Subject classification (UKÄ)
- Cardiac and Cardiovascular Systems
Free keywords
- Aortic aneurysm, abdominal
- CD40 ligand
- Endothelin-1
- Growth
- Interleukin-6
- Tumour necrosis factor-alpha