[Misleading study in The Lancet on the outcome of the Swedish AAA screening program]. / Stor enighet om att screening för bukaortaaneurysm räddar liv.

In a recent publication in The Lancet Johansson and colleagues claim no effect on aneurysm mortality among men participating in the Swedish AAA screening program, and question its justification. The study is, however, limited by a corrupt study design and incorrect data, making the publication misleading. On the contrary, several RCTs and contemporary nationwide data with sufficient follow-up clearly show that AAA screening saves lives and is highly cost-effective. The program has so far identified about 6000 men with an AAA, of whom 1500 have been operated on to prevent rupture. Thus, more than 750 men have experienced a longer life (by a mean of 8 years) as a result of the program. Continuous evaluation of the program is important but requires a scientifically sound methodology.

Early inflammatory response in patients with ruptured abdominal aortic aneurysm.

Multiorgan failure is the main cause of death in patients operated for ruptured abdominal aortic aneurysm (rAAA). The systemic inflammatory response plays a central role in the generation and maintenance of multiorgan dysfunction. The aim of the current study was to investigate the inflammatory response preoperatively in patients with ruptured and nonruptured AAA in relation to the clinical outcome. A total of 95 patients about to undergo repair of AAA (43 ruptured with shock, 12 ruptured without shock, and 40 elective) and 41 controls without aneurysm matched by age, gender, and smoking habits were investigated by inflammatory markers. There were significantly higher levels of interleukin 6 (IL-6; proinflammatory cytokine) and IL-10 (anti-inflammatory cytokine) in patients operated for ruptured compared to nonruptured AAA. In conclusion, the current data indicate that rupture of an AAA activates the inflammatory system with a compensatory anti-inflammatory response.

Abdominal aortic aneurysm and cytomegalovirus infection.

Cytomegalovirus (CMV) has been implicated in the pathogenesis of atherosclerosis. Abdominal aortic aneurysm is regarded traditionally as a consequence of atherosclerosis. Several microorganisms have been suggested as possible contributing factors for the development of abdominal aortic aneurysm. The relevance of CMV in the processes underlying the development, expansion, and rupture of abdominal aortic aneurysm is unknown. The aim of the present study was to investigate whether CMV infection is related to abdominal aortic aneurysm rupture. One hundred nineteen patients with abdominal aortic aneurysm and 36 matched controls without abdominal aortic aneurysm were investigated prospectively by CMV serology. Patients with ruptured abdominal aortic aneurysm have similar levels of IgG antibodies against CMV as patients with nonruptured abdominal aortic aneurysm, small abdominal aortic aneurysm, and controls without abdominal aortic aneurysm. In conclusion, this study fails to demonstrate a connection between CMV infection and abdominal aortic aneurysm rupture.

Abdominal aortic aneurysm and infection with CagA positive strains of Helicobacter pylori.

The aim of the present study was to investigate whether virulent CagA positive Helicobacter pylori strains are those preferentially related to abdominal aortic aneurysm (AAA) rupture. Several microorganisms have been linked to aneurysm development. Chronic Chlamydophila pneumoniae infection has been suggested as a possible contributing factor for the development and expansion of AAA. Previous studies have shown increased risk of carotid atherosclerosis and coronary heart disease in subjects harbouring CagA positive strains of H. pylori. The relevance of CagA positive H. pylori involved in the processes underlying aneurysmal development, expansion, and rupture is unknown. In a case-control study, 119 patients with AAA and 36 matched controls were prospectively investigated with H. pylori serology. Patients with ruptured AAA have similar levels of IgG antibodies against H. pylori to patients with electively operated AAA, small AAA, and controls. In conclusion, this study fails to demonstrate a connection between H. pylori CagA seropositivity and abdominal aortic aneurysm rupture.

Lack of association between Chlamydophila pneumoniae seropositivity and abdominal aortic aneurysm.

Chronic Chlamydophila pneumoniae infection has been suggested as a possible contributing factor for the development and expansion of abdominal aortic aneurysm (AAA). The relevance of C pneumoniae involved in the processes underlying aneurysmal rupture is unknown. The aim of this study was to examine the relationship between C pneumoniae seropositivity and AAA rupture. In a case-control study, 119 patients with AAA and 36 matched controls were prospectively investigated with C pneumoniae serology. Patients with ruptured AAA have similar levels of IgG antibodies against C pneumoniae as patients with an electively operated AAA, a small AAA, and controls. In conclusion, this study fails to demonstrate a connection between C pneumoniae seropositivity and AAA rupture.