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(Stroke. 2005;36:1901.)
© 2005 American Heart Association, Inc.

Original Contributions

Editorial Comment—Is Heme Oxygenase-1 a Causal Player for Plaque Stability?

Christine Espinola-Klein, MD; Stefan Blankenberg, MD Thomas Münzel, MD, FAHA

Department of Medicine II, Johannes Gutenberg University, Mainz, Germany

Key Words: atherosclerosis • carotid arteries • infection • inflammation • stroke

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Inflammatory mechanisms play an important role in all stages of the atherosclerotic process.¹ Various studies implicate that certain infectious agents represent candidates that trigger these inflammatory responses.² An association of viral infection with atherosclerosis was first reported in the 1970s, when experimental infection of germ-free chickens with an avian herpes virus was found to produce arterial disease.³ Although several infectious pathogens have been detected within the atherosclerotic plaque, including Chlamydia pneumoniae, Cytomegalovirus, and Helicobacter pylori, the precise role of these pathogens in causing atherosclerosis or in aggravating the atherosclerotic process remains to be established.⁴ In addition, a pathogen resident in an atherosclerotic vessel wall may be just an "innocent bystander" rather than a causally relevant agent, and atherosclerotic arteries might be simply more susceptible to infections. Although multiple seroepidemiological studies could demonstrate associations between atherosclerosis and antibodies against different pathogens, other studies did not.^2,5 More important, recent secondary prevention studies failed to prevent cardiovascular events by administering antibiotics.^6,7 Because several types of pathogens may contribute to the multifaceted process of atherosclerosis, it seems to be unlikely that a single microbe causes atherosclerosis. Instead, the total pathogen burden of infection at various sites may affect atherosclerosis progression.^5,8

Various mechanisms and hypotheses have been proposed to explain possible interactions between pathogen agents and the atherosclerotic vessel wall.⁵ These include induction of specific antibodies or alteration of circulating cytokines, acute phase proteins, and white blood cells. Results from several studies also point to a significant role of immune responses contributing to . . . [Full Text of this Article]

Related Article:

Heme Oxygenase-1 Is Expressed in Carotid Atherosclerotic Plaques Infected by Helicobacter pylori and Is More Prevalent in Asymptomatic Subjects

Sebastian F. Ameriso, Agustina Ruiz Villamil, Christine Zedda, Juan C. Parodi, Sergio Garrido, María Inés Sarchi, Marcelo Schultz, Jorge Boczkowski, and Gustavo E. Sevlever
Stroke 2005 36: 1896-1900. [Abstract] [Full Text] [PDF]

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