Article

Infection, Antibiotics, and Atherothrombosis — End of the Road or New Beginnings?

New England Journal of Medicine (Impact Factor: 55.87). 05/2005; 352(16):1706-9. DOI: 10.1056/NEJMe058019
Source: PubMed
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    • "Moreover, many additional factors may influence atherogenesis and CVD, such as AIDS-related infections [13] or the fact that certain “classical” vascular risk factors are overrepresented in the HIV-infected population (i.e., cigarette smoking). On the other hand, recent studies have shown that, similarly to the observation made in the general population, HCV coinfection seems to be associated with lower blood levels of cholesterol in HIV patients receiving ART [14]. "
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    ABSTRACT: Many infections favor or are directly implicated with lipid metabolism perturbations and/or increased risk of coronary heart disease (CHD). HIV itself has been shown to increase lipogenesis in the liver and to alter the lipid profile, while the presence of unsafe habits, addiction, comorbidities, and AIDS-related diseases increases substantially the risk of cardiovascular disease (CVD) in the HIV-infected population. Antiretroviral therapy reduces such stimuli but many drugs have intrinsic toxicity profiles impacting on metabolism or potential direct cardiotoxicity. In a moment when the main guidelines of HIV therapy are predating the point when to start treating, we mean to highlight the contribution of HIV-1 to lipid alteration and inflammation, the impact of antiretroviral therapy, the decisions on what drugs to use to reduce the probability of having a cardiovascular event, the increasing use of statins and fibrates in HIV-1 infected subjects, and finally the switch strategies, that balance effectiveness and toxicity to move the decision to change HIV drugs. Early treatment might reduce the negative effect of HIV on overall cardiovascular risk but may also evidence the impact of drugs, and the final balance (reduction or increase in CHD and lipid abnormalities) is not known up to date.
    Full-text · Article · Oct 2010 · Cholesterol
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    • "The hypothesis prompted a series of trials that tested secondary prevention of cardiovascular events by treatment with macrolides assumed to be active against C. pneumoniae in the vascular wall (Anderson et al., 1999; Gupta et al., 1997; Gurfinkel et al., 1997). The results were promising, and a number of large prevention trials were launched (overviews: Anderson, 2005; Gluud et al., 2008; Hoymans et al., 2007), one of which was the CLARICOR trial (Hansen et al., 2001; Jespersen et al., 2006). Here we randomized 4372 patients with stable CHD with the primary objective of obtaining sufficient data to reliably assess whether brief intervention with a macrolide antibiotic, clarithromycin, reduces the frequency of future coronary events and deaths. "
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    ABSTRACT: The association observed between coronary heart disease (CHD) and Chlamydia (Chlamydophila) pneumoniae antibodies prompted, during the 1990s, several primary and secondary prevention trials with various antibiotics. In our CLARICOR trial, a randomized placebo-controlled trial in 4372 patients with stable CHD, a brief clarithromycin regimen was followed, unexpectedly, by increased long-term mortality. We now compare C. pneumoniae antibody levels at entry with population levels, with the patients' individual histories, and with their subsequent outcomes. IgG antibody levels were somewhat raised, but elevated IgA and IgG titers were unrelated to entry data (including prior acute myocardial infarction), except for an association with smoking and with not using statins. Hazards of mortality and of other outcomes tended to slightly increase with IgA and decrease with IgG titers, but the unfavorable clarithromycin effect was unrelated to antibody levels and remains unexplained. Smoking-related lung disease probably underlies the link between heart disease and increased IgG titers.
    Full-text · Article · Apr 2010 · Diagnostic microbiology and infectious disease
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    • "In the present study we used CAC as a marker of sub-clinical atherosclerosis in HIV-infected patients and found it to be strongly associated with LD. The evaluation of cardiovascular risk in HIVinfected patients requires consideration of a complex interplay of diverse factors, including direct and indirect vascular effects of chronic exposure to HIV[3,4], metabolic effects of prolonged ART use[6], aging[32], and exposure to known cardiovascular risk fac- tors[3]. CAC has been previously utilized in eight studies of HIV-infected individuals. "
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    ABSTRACT: Although anti-retroviral therapy (ART) prolonged survival in HIV-infected persons, an increase in cardiovascular disease has also been observed. A frequent complication of ART is the development of lipodystrophy (LD) with its multiple phenotypes that may be associated with cardiovascular disease. We assessed the contribution of chronic HIV infection, ART use and LD to the presence of sub-clinical atherosclerosis as evaluated by coronary artery calcium (CAC) imaging. Observational cross-sectional study of 372 HIV-infected patients receiving ART who attended a cardiometabolic clinic (48.2+/-8-year old; 74% men). All patients underwent CAC surveillance with computed tomography and the Agatston score was used to quantitate CAC. Presence of CAC was defined as a score >10. Multivariable logistic regression was used to evaluate associations between HIV clinical factors, ART and LD with the presence of CAC. CAC was found in 134 patients (36%) with a median CAC score of 50 (range 10; 1243). Lipoatrophy alone (OR 3.82, 95% CI: 1.11; 13.1), fat accumulation alone (OR 7.65, 95% CI: 1.71; 37.17) and mixed lipodystrophy phenotypes (OR 4.36, 95% CI: 1.26; 15.01) were strongly associated with presence of CAC after adjusting for age, sex, hypertension and cumulative exposure to ART. CAC is common among long-term ART users. The association between CAC and LD underscores the potential atherosclerosis risk inherent with ART and the need to undertake routine cardiovascular surveillance in patients treated with these drugs.
    Full-text · Article · Jun 2009 · Atherosclerosis
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