Sir,—Two recent letters to the editor1 2 have argued against an association betweenHelicobacter pylori infection and coronary artery disease via the development of hyperhomocysteinaemia, which was hypothesised by Sung and Sanderson.3 However, both groups of authors relied on indirect seroepidemiological evidence for H pylori infection.

 Recently, Blasi et al evaluated the presence ofH pylori in atherosclerotic plaques of abdominal aortic aneurysms from patients who had had abdominal aortic aneurysm surgery.4 They found no evidence for the presence ofH pylori in plaque specimens, even though 21 of their 23 patients were seropositive for H pylori. Thus, their elegant study ruled out the possibility of a direct involvement ofH pylori infection in atherosclerosis, no matter how intriguing the hypothesis by Sung and Sanderson might initially seem.5