Prevalence of risk factors, coronary and systemic atherosclerosis in abdominal aortic aneurysm: Comparison with high cardiovascular risk population

Abstract

Background: Abdominal aortic aneurysm (AAA) is considered a manifestation of atherosclerosis, however there are epidemiologic, biochemical, and structural differences between occlusive atherosclerosis and AAA. The pathogenesis of AAA involves several factors, fi rst of all destruction of collagen and elastin in the aortic wall. Classical risk factors may infl uence the evolution and development of AAA, though no consistent association has been found. Aims of the study were to evaluate associations between risk factors and to establish the prevalence of carotid, peripheral vascular and coronary atherosclerosis in patients with AAA. Methods: We studied 98 patients with AAA (Group 1) awaiting surgery compared with high cardiovascular risk population having two or more risk factors (n = 82 Group 2). We evaluated traditional risk factors and we studied by eco-doppler and echocardiography the presence of carotid peripheral and coronaric atherosclerosis in two groups. Results: We found a higher incidence of AAA in males (p Ͻ 0.01). The prevalence of infrarenal AAA was signifi cantly higher than suprarenal AAA (81 vs 17 p Ͻ 0.001). No differences in total cholesterol (199 ± 20 vs. 197 ± 25 mg/dl), low-density lipoprotein (142 ± 16 vs. 140 ± 18 mg/dl), triglycerides (138 ± 45 vs. 144 ± 56 mg/dl), glycemia (119 ± 15 vs. 122 ± 20 mg/dl), and fi brinogen (388 ± 154 vs. 362 ± 92 mg/dl) were found between groups. We demonstrated signifi cant differences for cigarette smoking (p Ͻ 0.002), systolic and diastolic blood pressure (150 ± 15 vs. 143 ± 14 mmHg and 88 ± 6 vs. 85 ± 7 mmHg, p Ͻ 0.0001 and p Ͻ 0.05, respectively) and high sensititivity C reactive protein (2.8 ± 1.3 vs. 1.3 ± 0.7 mg/dl, p Ͻ 0.001). High-density lipoprotein (HDL) cholesterol levels were signifi cant greater in Group 1 than Group 2 (p Ͻ 0.003). Subgroups of patients with AAA and luminal thrombus showed higher fi brinogen levels (564 ± 235 vs. 341 ± 83 mg/dl, p Ͻ 0.001) and lower HDL than in controls (46.6 ± 6.5 vs. 52.1 ± 7.8 mg/dl, p Ͻ 0.01). We did not fi nd any difference in body mass index, or prevalence of coronary and peripheral atherosclerosis between groups. Conversely, we found higher prevalence of carotid atherosclerosis in Group 2 (9% vs. 25%, p Ͻ 0.004). Conclusion: Our AAA patients had fewer and different risk factors respect to patients with atherosclerosis. Only elevated blood pressure, C reactive protein, and smoking showed a signifi cant association with AAA. Atherosclerosis in other arterial districts did not differ respect to subjects with high cardiovascular risk. Our results confi rm the hypothesis that AAA and atherosclerosis are two different pathological entities with different risk profi les.

Risk factors in abdominal aortic aneurysm and aortoiliac occlusive disease and differences between them in the Polish population

“…data consistent with reports of other researchers11. When compared with random population, AAA patients also comprised higher percentage of individuals suffering from diabetes type II (Table 2).…”

Abdominal Aortic Aneurysm in Patients with Coronary Artery Disease: A Review Article

“…Despite such heterogeneity between these observational cross -sectional studies, one can fairly say that AAA prevalence among CAD patients exceeds that observed in population -based studies. It is also of interest that the prevalence of AAA in CAD patients was comparable to that reported in AAA screening studies of patients with peripheral vascular disease (7% -17%) and cerebrovascular disease (8.4% -20.2%) (Bentgsson et al, 1996;Kurvers et al, 2003;Palazzuoli et al, 2008;Simons et al, 1999).…”

“…Whereas proliferation of vascular smooth muscle cells (VSMCs) is a typical feature of atherosclerosis affecting vascular media and intima, the density of these cells is low in media and adventitia of aneurismal wall due to apoptosis. Atherosclerosis is also characterized by migrating VSMCs and macrophages, foam cell formation, lipid deposition, leading to endothelial dysfunction and increased intima -media thickness (Palazzuoli et al, 2008). On the other hand, AAA involves dilation of all layers of the aortic wall, destructive remodeling of medial elastin and collagen fibers by matrix metalloproteinases released by activated aortic wall macrophages (Wassef et al, 2007).…”

Periadventitial Adipose-Derived Stem Cell Treatment Halts Elastase-Induced Abdominal Aortic Aneurysm Progression

“…Systemic delivery or direct wall injection of a stem cell-based AAA therapy would encounter practical resistance at the clinic. Essentially, all AAA patients present with an intraluminal thrombus (ILT) [14,15], a collection of clotting material and cells adherent to the luminal side of the aneurysm wall. The ILT presents a physical barrier to systemically delivered treatment cells as few cells are found deeper than 10% into the ILT [16].…”