E. S. Lee1, K. C. Chun2, Z. T. Irwin2, A. T. Nguyen2, K. J. Dolan2, R. E. Noll1, P. A. Ghosh2 1Sacramento Veterans Affairs Medical Center,Surgery,Mather, CA, USA 2Sacramento Veterans Affairs Medical Center,Research,Mather, CA, USA
Introduction: Predicting abdominal aortic aneurysm (AAA) expansion rates upon first clinical presentation is challenging to clinicians. AAA is an inflammatory disease and monocyte/ macrophage infiltration is important for AAA development. However, a link between inflammation and AAA expansion has not been well defined. We hypothesize that expanding AAA will have increased inflammation versus stable AAA. The purpose of this study is to explore the relationship of inflammation and AAA expansion rates.
Methods: Patients screened for AAA with 1-yr minimum follow up were recruited for this study. Subjects received a one-time study abdominal ultrasound and 30mL blood draw after ultrasound. The expansion rate (cm/yr) was calculated from the AAA screening results and the study ultrasound. Patients were then divided into stable (<0.1 cm/yr) or expanding (≥0.1 cm/yr) AAA groups. Inflammation status was determined by monocyte activity via activated RhoA protein levels from collected patient blood using Western-blot assay. RhoA was then compared to current cardiovascular risk factors such as age, race, blood pressure, total cholesterol, body mass index, hypertension, diabetes, current smoking status, statin use, coronary artery disease, peripheral vascular disease, chronic obstructive pulmonary disease, stroke, and estimated glomerular filtration rate for analysis between stable and expanding groups. A univariate analysis of risk factors and backwards selection logistic regression of significant univariate variables were then used to determine statistical significance.
Results: A total of 83 patients (mean±stdev: 73.4 ± 7.2 years old) were recruited for the study. There were 33 patients with stable AAAs and 50 patients with expanding AAAs. Average maximum aortic diameter was smaller in the stable AAA group versus the expanding AAA group (3.3 ± 0.8 cm vs 4.9 ± 0.9 cm, p<.01). Only increased RhoA (p=.01; OR=2.75, 1.26-5.98) and eGFR<60 ml/min (p=.01; OR=.27, 0.10-0.77) were significantly associated with AAA expansion.
Conclusion: Patients with stable AAA have smaller aortic diameters, less monocyte RhoA activity, and greater renal function when compared to patients with expanding AAA. Patients with larger AAA may have higher inflammation levels and expansion rates versus patients with smaller AAA. There is insufficient data to suggest that RhoA would serve as a viable biomarker for AAA expansion.