"Moreover, many additional factors may influence atherogenesis and CVD, such as AIDS-related infections  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 . "
[Show abstract][Hide abstract] 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.
"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. "
[Show abstract][Hide abstract] 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.
"The advantage of having a bacterium as one among other factors involved in atherogenesis is, of course, the possibility to eradicate that factor by antibiotic treatment. However, this notion has been fundamentally shattered by the complete failure of large clinical trials (ACADEMIC, WIZARD and ACES) to show significant amelioration of progredient coronary artery disease and future cardiac events under antibiotic treatment (Muhlestein et al., 2000; O'Connor et al., 2003; Anderson & Muhlestein 2004; Grayston et al., 2005). "
[Show abstract][Hide abstract] ABSTRACT: Since its description in 1986, Chlamydia pneumoniae has remained one of the most enigmatic pathogens. This intracellular bacterium is highly seroprevalent, but rarely recovered from cell culture, it can genetically switch between a proliferative and a nonreplicative state and has been linked to a vast number of chronic diseases, most notably to atherosclerosis, as it can be found in the plaques. It has become quite clear that persistent bacteria in atherosclerotic lesions cannot be eradicated by currently available antibiotic treatments and that attempts to do so without a better understanding of the pathobiology of chlamydial persistence are futile. However, there is growing knowledge on how vascular chlamydial infection may lead to the pathological reprogramming of the host cell signaling pathways. Chlamydia pneumoniae is now well known to induce, at least in vitro, the two pathogenetic main events that define atherosclerosis: angiogenesis and inflammation. In vivo a contribution of chlamydial infection to the progression of atherosclerosis remains unproven. This minireview provides a brief overview on the proproliferative and proinflammatory effects of vascular C. pneumoniae infection and their potential link to atherogenesis.
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