Serum osteoprotegerin is inversely associated with carotid plaque echogenicity in humans.

Osteoprotegerin (OPG) is a member of the tumour necrosis factor superfamily involved in the regulation of bone metabolism and vascular calcification. High serum values of OPG are associated with cardiovascular disease in humans. The purpose was to investigate serum OPG levels in subclinical carotid atherosclerosis and the relation between OPG levels and plaque morphology. OPG levels were compared in 29 persons with echogenic carotid plaques, 30 persons with echolucent plaques and 41 persons without carotid plaques, all recruited from a population health study. Computerized assessment of plaque echogenicity was done by use of the gray scale median (GSM). Participants with echogenic carotid plaques had lower serum OPG level (1.23 ng/ml; 1.02-1.48) (geometric mean; 95% CI) than persons with echolucent plaques (1.76 ng/ml; 1.46-2.14) and those without plaques (1.89 ng/ml; 1.60-2.21). OPG and PTH were independently related to GSM. A significant trend for decrease in GSM across quartiles of OPG was found (p=0.003) which remained significant even after adjustment for PTH and smoking. The present study demonstrates lower serum OPG levels in persons with subclinical echogenic carotid plaques and identified an inverse relation between serum OPG and plaque echogenicity. The findings support the concept that OPG may play an important role in arterial calcification.

No detectable Chlamydia pneumoniae and cytomegalovirus DNA in leukocytes in subjects with echolucent and echogenic carotid artery plaques.

BACKGROUND: Controversy exists whether persistent Chlamydia pneumoniae or cytomegalovirus infections cause initiation or progression of atherosclerosis. C. pneumoniae DNA in peripheral blood mononuclear cells (PBMC) has been proposed to be a more reliable marker of cardiovascular risk than are C. pneumoniae antibodies. Reported prevalences of C. pneumoniae DNA among cardiovascular patients vary greatly, indicating methodological limitations. There is an increasing concern that published results may have been biased by extensive use of less specific polymerase chain reaction (PCR) technology. METHODS: C. pneumoniae DNA and cytomegalovirus DNA were determined by probe-based real-time PCR technology in PBMCs among subjects with echolucent (n=29) or echogenic (n=28) carotid artery plaques, and in controls without carotid plaques (n=38), all recruited from a population-based study. Samples were examined in multiple repeats with PCR assays targeting two different sequences of the genome for both microorganisms. RESULTS AND CONCLUSION: IgG seropositivity was frequent in all three groups, confirming previous exposure, but C. pneumoniae DNA or cytomegalovirus DNA was not detected in a single PBMC sample by means of probe-based, highly sensitive, and specific real-time PCR assays. Our results indicate that persistent C. pneumoniae or CMV infection is not a common phenomenon in subjects with carotid atherosclerosis.