High Levels of Cytomegalovirus Antibody in Patients Requiring Vascular Surgery for Atherosclerosis

Adam, Ervín; Probtsfield, J.L.; Burek, Joyce; Cn, McCollum; Melnick, Joseph L.; Petrie, Betty L.; Bailey, Kent R.; DeBakey, Michael E.

doi:10.1016/s0140-6736(87)90888-9

Cited by 262 publications

(125 citation statements)

References 17 publications

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“…The result of this study showed that ABPI, LDL-C/HDL-C ratio at baseline and HCV infection independently determine and thus predict the increase in cfPWV in ESRD patients treated with HD. Previous studies suggested a link between infection with microorganisms such as Chlamydia pneumonia, 18 cytomegalovirus, 19 Helicobacter pylori 20 and herpes simplex virus, 21 and increased the risk of cardiovascular diseases; however, the atherogenic effect of viral hepatitis remains controversial. A study of the northeast German population reported no correlation between various serological markers for HBV and HCV infection and the risk of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

What factors accelerate aortic stiffening in hemodialysis patients? An observational study

Matsumae¹,

Abe

Nishimura³

et al. 2010

Hypertens Res

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Increased aortic stiffness is an independent predictor of death from cardiovascular disease in patients with end-stage renal disease (ESRD). Various factors that contribute to carotid-femoral pulse wave velocity (cfPWV) as a surrogate of aortic stiffness have been identified, but determinants of long-term worsening of aortic stiffness remain to be elucidated. To clarify the factors that accelerate aortic stiffness in hemodialysis patients, 148 patients with ESRD on hemodialysis were evaluated. At baseline, cfPWV and ankle-brachial blood pressure index (ABPI) were measured and clinical status including biochemical parameters, with or without hepatitis c virus (HCV) infection, diabetes mellitus (DM), cardiovascular disease, cerebrovascular disease and peripheral arterial disease at baseline, were evaluated. The cfPWV was measured again after a 3-year follow up and the annual change in cfPWV was calculated. The cfPWV decreased in 54 patients, worsened slowly in 47 (annual change in cfPWV ranged from 0 to 0.33 m s À1 per year), and worsened rapidly in 47 patients (annual change in cfPWV was more than 0.33 m s À1 per year). The prevalences of DM, HCV infection and peripheral arterial disease were the highest in the rapid progression group. Univariate analysis showed that age, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), LDL-C/HDL-C ratio, HCV infection, ABPI and number of vasculopathies were significantly associated with annual change in cfPWV. Stepwise regression analysis identified ABPI, LDL-C/HDL-C ratio and HCV infection as independent determinants of worsening of cfPWV. Further studies are needed to investigate the mechanism of HCV-related enhancement of aortic stiffness in ESRD patients.

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Section: Discussionmentioning

confidence: 99%

What factors accelerate aortic stiffening in hemodialysis patients? An observational study

Matsumae¹,

Abe

Nishimura³

et al. 2010

Hypertens Res

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“…11 Both antigens and nucleic acid sequences of CMV were detected in smooth muscle cells from carotid artery plaques, 12 and polymerase chain reactions demonstrated CMV DNA in arterial samples from patients with atherosclerosis who underwent vascular surgery more often than control subjects. 13 It has been demonstrated that patients with atherosclerosis had higher antibody titer against CMV 14 and that one-third of the atherosclerotic lesions obtained by coronary atherectomy contained CMV DNA sequences. 4 Smooth muscle cells that were grown from such lesions expressed IE84 (one of the immediate early proteins of the virus that binds and inhibits p53).…”

Section: The Infectious Theorymentioning

confidence: 99%

Viral load of the human immunodeficiency virus could be an independent risk factor for endothelial dysfunction

et al. 2005

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SummaryBackground: Recent reports of myocardial infarction in young persons infected with human immunodeficiency virus (HIV) who are receiving protease inhibitor therapy have raised concerns about premature coronary artery disease in this population. However, endothelial dysfunction, hypercoagulability, hypertriglyceridemia, and abnormal coronary artery pathology have been observed in association with HIV infection prior to the availability of protease inhibitor therapy.Hypothesis: The study was undertaken to determine the association between endothelial function, viral load, CD4+ count, and other well-established risk factors for atherosclerosis.Methods: This prospective, case-controlled study compared viral (HIV) load and the CD4+ T-lymphocyte count and endothelial function in 24 HIV-positive carriers. Brachial artery diameter, HIV viral load, and CD4 count were measured.Results: We found that viral load correlated inversely with endothelial function; the higher the viral load, the worse the endothelial dysfunction (p < 0.005).Conclusion: High viral load appears to be associated with endothelial dysfunction in patients with HIV. This preliminary observation supports the infectious theory that viruses may play an important role in the pathogenesis of atherosclerosis.

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“…Epidemiological data (9)(10)(11)28) indicate the frequent infection of arteries with microbial pathogens. It is conceivable that successful immune responses against these pathogens are crucial to limit direct cytopathic and indirect immunopathological damage during vascular infections.…”

Section: Mutual Chronic Perpetuation Of Vascular Inflammation and Chomentioning

confidence: 99%

Linking immune-mediated arterial inflammation and cholesterol-induced atherosclerosis in a transgenic mouse model

Ludewig

Freigang

Jäggi

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

126

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Arterial inflammatory responses are thought to be a significant component of atherosclerotic disease. We describe here, using a transgenic approach, the mutual perpetuation of immune-mediated arterial inflammation and cholesterol-induced atherosclerosis. Mice expressing the bacterial transgene ␤-galactosidase exclusively in cardiomyocytes and in smooth muscle cells in lung arteries and the aorta (SM-LacZ), and hypercholesterolemic apolipoprotein E-deficient SM-LacZ mice (SM-LacZ͞apoE ؊/؊ ) developed myocarditis and arteritis after immunization with dendritic cells presenting a ␤-galactosidase-derived immunogenic peptide. Hypercholesterolemia amplified acute arteritis and perpetuated chronic arterial inflammation in SM-LacZ͞apoE ؊/؊ mice, but had no major impact on acute myocarditis or the subsequent development of dilated cardiomyopathy. Conversely, arteritis significantly accelerated cholesterol-induced atherosclerosis. Taken together, these data demonstrate that the linkage of immune-mediated arteritis and hypercholesterolemia favors initiation and maintenance of atherosclerotic lesion formation. Therapeutic strategies to prevent or disrupt such self-perpetuating vicious circles may be crucial for the successful treatment of atherosclerosis.

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High Levels of Cytomegalovirus Antibody in Patients Requiring Vascular Surgery for Atherosclerosis

Cited by 262 publications

References 17 publications

What factors accelerate aortic stiffening in hemodialysis patients? An observational study

What factors accelerate aortic stiffening in hemodialysis patients? An observational study

Viral load of the human immunodeficiency virus could be an independent risk factor for endothelial dysfunction

Linking immune-mediated arterial inflammation and cholesterol-induced atherosclerosis in a transgenic mouse model

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