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Am Heart J. 2004 Nov;148(5):818-25.

Oxidized low-density lipoprotein levels circulating in plasma and deposited in the tissues: comparison between Helicobacter pylori-associated gastritis and acute myocardial infarction.

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Department of Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.



Oxidized low-density lipoprotein (ox-LDL) is a key factor in the progression of atherosclerosis. We developed a sensitive method for measuring plasma ox-LDL levels using a novel anti-ox-LDL antibody. Recently, several studies have shown positive associations between Helicobacter pylori (H pylori) infection and coronary heart disease. Thus the question arises whether an increase in the plasma levels of ox-LDL occurs in patients with H pylori gastritis.


We measured plasma ox-LDL levels in patients with H pylori gastritis (n = 27) and compared them with those in patients with acute myocardial infarction (AMI) (n = 62) and stable angina pectoris (SAP; n = 63) and those in control subjects (n = 64). In addition, ox-LDL localization and the presence of macrophages and neutrophils were studied immunohistochemically in gastritis specimens and in coronary culprit lesions obtained from patients with AMI.


Plasma ox-LDL levels in patients with AMI were significantly higher than those in patients with SAP (P <.0001), patients with H pylori gastritis (P <.0001), or in control subjects (P <.0001; AMI, 1.34 +/- 0.95; SAP, 0.61 +/- 0.29; Gastritis, 0.53 +/- 0.17; control, 0.57 +/- 0.23 ng/5 microg LDL protein). Immunohistochemically, H pylori gastritis specimens showed distinct infiltration of macrophages and myeloperoxidase-positive neutrophils; however, ox-LDL localization was not detected. In contrast, coronary culprit plaques revealed strong positivity for ox-LDL in ruptured lipid cores with abundant macrophage-derived foam cells, and these plaques also contained myeloperoxidase-positive neutrophils.


Our results suggest that plasma ox-LDL levels do not seem to be associated with H pylori infection, but do relate to coronary plaque instability in AMI.

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