A population-based case-control study with historical and current data was conducted in a population with a high prevalence of disease to explore the hypothesis that the fibrinolytic system may be involved in the early pathogenesis of abdominal aortic aneurysm (AAA).
Forty-two patients found to have AAA at population-based screening were compared with 100 controls matched for age and sex. Mass concentration of tissue plasminogen activator (tPA mass) and tissue plasminogen activator/plasminogen activator inhibitor-1 complex (tPA/PAI-1 complex mass) were analyzed in blood samples obtained at the screening (current), and in blood samples obtained from a study conducted 12 years previously on the same population (historical).
Current tPA mass levels were significantly higher in AAA patients compared with controls (13.6 vs 11.4 μg/L, P = .016). A similar trend was observed in historical tPA mass levels (9.8 vs 8.2 μg/L, P = .062). Current and historical mass concentrations of tPA/PAI complex in AAA patients were similar to those in controls. Current tPA mass levels retained the associations with AAA in a logistic regression model after adjustment for history of atherosclerosis (odds ratio [OR], 1.1 per μg/L, P = .039) and current smoking (OR 1.1 per μg/L, P = .039). When family history of AAA was added in a logistic regression model, the OR for current tPA mass was 1.1 per μg/L (P = .056) and 1.1 per μg/L (P = .070) when treated hypertension was added.
The finding of elevated tPA mass, in contrast to tPA/PAI-1 complex, in plasma among patients with screening-detected AAA supports the hypothesis that the fibrinolytic system may be important in the early pathogenesis of AAA.
Early detection by screening and repair is the only option to reduce mortality from abdominal aortic aneurysm (AAA) in the population. As a consequence, AAA screening programs have been launched in many countries. Most AAAs detected by screening are small, however, and the current treatment of these is limited to watchful waiting. Other therapeutic or preventive strategies are needed, necessitating a profound knowledge of the pathogenesis of AAA.
2007. Vol. 45, no 6, 1109-1113 p.