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Background: There is a clinical need for treatments that can slow or prevent the growth of an abdominal aortic aneurysm, not only to reduce the need for surgery, but to provide a means to treat those who cannot undergo surgery. Methods: Analysis of the UK Aneurysm Growth Study (UKAGS) prospective cohort was conducted to test for an association between cardiometabolic medications and the growth of an abdominal aortic aneurysm above 30 mm in diameter, using linear mixed-effect models. Results: A total of 3670 male participants with data available on abdominal aortic aneurysm growth, smoking status, co-morbidities, and medication history were included. The mean age at recruitment was 69.5 years, the median number of surveillance scans was 6, and the mean(s.e.) unadjusted abdominal aortic aneurysm growth rate was 1.75(0.03) mm/year. In a multivariate linear mixed-effect model, smoking (mean(s.e.) +0.305(0.07) mm/year, P = 0.00003) and antiplatelet use (mean(s.e.) +0.235(0.06) mm/year, P = 0.00018) were found to be associated with more rapid abdominal aortic aneurysm growth, whilst metformin was strongly associated with slower abdominal aortic aneurysm growth (mean(s.e.) −0.38(0.1) mm/year, P = 0.00019), as were angiotensin-converting enzyme inhibitors (mean(s.e.) −0.243(0.07) mm/year, P = 0.0004), angiotensin II receptor antagonists (mean(s.e.) −0.253(0.08) mm/year, P = 0.00255), and thiazides/related diuretics (mean(s.e.) −0.307(0.09) mm/year, P = 0.00078). Conclusion: The strong association of metformin with slower abdominal aortic aneurysm growth highlights the importance of the ongoing clinical trials assessing the effectiveness of metformin with regard to the prevention of abdominal aortic aneurysm growth and/or rupture. The association of angiotensin-converting enzyme inhibitors, angiotensin II receptor antagonists, and diuretics with slower abdominal aortic aneurysm growth points to the possibility that optimization of cardiovascular risk management as part of abdominal aortic aneurysm surveillance may have the secondary benefit of also reducing abdominal aortic aneurysm growth rates. Abdominal aortic aneurysm growth rates were compared with smoking status, co-morbidities, and medication history in the UK Aneurysm Growth Study (UKAGS) prospective cohort. It was found that: smoking and antiplatelet use were associated with a more rapid abdominal aortic aneurysm growth rate; the drug metformin was strongly associated with a slower abdominal aortic aneurysm growth rate; and drugs in the angiotensin-converting enzyme inhibitor, angiotensin II receptor antagonist, and thiazide/related diuretic classes were also associated with a slower abdominal aortic aneurysm growth rate. These results suggest that common cardiometabolic medications may be useful therapeutic options to slow abdominal aortic aneurysm growth rates. [ABSTRACT FROM AUTHOR]

Atherosclerosis is an inflammatory process resulting in local plaque deposition in the vessel wall of arteries with symptoms to various areas of vascular tree. Identification of patients with progressive advanced atherosclerotic disease is mainly based on the known characteristics of the vulnerable or recently ruptured plaque. Molecular and cellular features associated with the vulnerable plaque are considered potential diagnostic markers for plaque rupture and thrombosis. Here, protein expression levels of the metalloproteases MMP-1, MMP-9, osteopontin (OPN), and cytokines TNFα and IL-6 in tissue extracts of carotid plaques in patients after endarterectomy were estimated by Western immunoblotting, after SDS-PAGE analysis and evaluated based on the ultrasonographic plaque morphology. The gender and age effect was also examined. MMP-1, MMP-9, and IL-6 were expressed in higher levels compared to OPN and TNFa as well as in symptomatic (with type II and III carotid plaque classification) than asymptomatic (type IV) patients with differences considered statistically significant (P values <0.05). A significant positive correlation between MMP-1 and IL-6 (with Pearson correlation coefficient 0.748) is also notable. The data give further insight into the possible role of specific biomarker and enhance the need for further studies in order to clarify the proper one(s) for detection of the vulnerable plaque and help identify patients at risk for cardiovascular events. [ABSTRACT FROM AUTHOR]