Article

Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men

Massachusetts General Hospital and Harvard Medical School, USA.
AIDS (London, England) (Impact Factor: 6.56). 12/2009; 24(2):243-53. DOI: 10.1097/QAD.0b013e328333ea9e
Source: PubMed

ABSTRACT The degree of subclinical coronary atherosclerosis in HIV-infected patients is unknown. We investigated the degree of subclinical atherosclerosis and the relationship of traditional and nontraditional risk factors to early atherosclerotic disease using coronary computed tomography angiography.
Seventy-eight HIV-infected men (age 46.5 +/- 6.5 years and duration of HIV 13.5 +/- 6.1 years, CD4 T lymphocytes 523 +/- 282; 81% undetectable viral load), and 32 HIV-negative men (age 45.4 +/- 7.2 years) with similar demographic and coronary artery disease (CAD) risk factors, without history or symptoms of CAD, were prospectively recruited. 64-slice multidetector row computed tomography coronary angiography was performed to determine prevalence of coronary atherosclerosis, coronary stenosis, and quantitative plaque burden. RESULTS HIV-infected men demonstrated higher prevalence of coronary atherosclerosis than non-HIV-infected men (59 vs. 34%; P = 0.02), higher coronary plaque volume [55.9 (0-207.7); median (IQR) vs. 0 (0-80.5) microl; P = 0.02], greater number of coronary segments with plaque [1 (0-3) vs. 0 (0-1) segments; P = 0.03], and higher prevalence of Agatston calcium score more than 0 (46 vs. 25%, P = 0.04), despite similar Framingham 10-year risk for myocardial infarction, family history of CAD, and smoking status. Among HIV-infected patients, Framingham score, total cholesterol, low-density lipoprotein, CD4/CD8 ratio, and monocyte chemoattractant protein 1 were significantly associated with plaque burden. Duration of HIV infection was significantly associated with plaque volume (P = 0.002) and segments with plaque (P = 0.0009) and these relationships remained significant after adjustment for age, traditional risk factors, or duration of antiretroviral therapy. A total of 6.5% (95% confidence interval 2-15%) of our study population demonstrated angiographic evidence of obstructive CAD (>70% luminal narrowing) as compared with 0% in controls.
Young, asymptomatic, HIV-infected men with long-standing HIV disease demonstrate an increased prevalence and degree of coronary atherosclerosis compared with non-HIV-infected patients. Both traditional and nontraditional risk factors contribute to atherosclerotic disease in HIV-infected patients.

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    • "It is characterized by a low CD4:CD8 T-cell ratio (<1.2) resulting from the depletion of CD4+ T-cells and the concomitant expansion of the CD8+ population of T-cells in the peripheral blood. Studies have shown that in HIV seropositive individuals receiving long-term combination antiretroviral therapy (cART), CD4:CD8 T-cell ratio dysregulation is correlated with higher risk of developing coronary artery disease [4]. In non-HIV settings, low CD4:CD8 T-cell ratios are also associated with poor clinical outcomes in patients with common variable immune deficiency (CVID) and in healthy individuals over the age of 60 [5], [6]. "
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    ABSTRACT: Successful combination antiretroviral therapy (cART) increases levels of CD4+ T-cells, however this increase may not accurately reflect long-term immune recovery since T-cell dysregulation and loss of T-cell homeostasis often persist. We therefore assessed the impact of a decade of effective cART on immune regulation, T-cell homeostasis, and overall T-cell phenotype. We conducted a retrospective study of 288 HIV+ cART-naïve patients initiating therapy. We identified 86 individuals who received cART for at least a decade, of which 44 consistently maintained undetectable plasma HIV-RNA levels throughout therapy. At baseline, participants were classified into three groups according to pre-treatment CD4+ T-cell counts: Group I (CD4<200 cells/mm3); Group II (CD4: 200-350 cells/mm3); Group III (CD4>350 cells/mm3). Outcomes of interest were: (1) CD4+ T-cell count restoration (CD4>532 cells/mm3); (2) normalization of CD4:CD8 T-cell ratio (1.2-3.3); (3) maintenance of CD3+ T-cell homeostasis (CD3: 65%-85% of peripheral lymphocytes); (4) normalization of the complete T-cell phenotype (TCP). Despite a decade of sustained successful cART, complete T-cell phenotype normalization only occurred in 16% of patients, most of whom had initiated therapy at high CD4+ T-cell counts (>350 cells/mm3). The TCP parameter that was the least restored among patients was the CD4:CD8 T-cell ratio. Failure to normalize the complete T-cell phenotype was most apparent in patients who initiated cART with a CD4+ T-cell count <200 cells/mm3. The impact of this impaired T-cell phenotype on life-long immune function and potential comorbidities remains to be elucidated.
    PLoS ONE 04/2014; 9(4):e94018. DOI:10.1371/journal.pone.0094018 · 3.23 Impact Factor
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    • "Secondly, our data collection preceded the publication of the Serrano-Villar et al. (2012) article to which Ms. Kelso referred. Our study was conducted early in 2011 and its methods were consistent with many previous studies that used the Framingham Risk Score to estimate risk; we refer Ms. Kelso to Bergersen, Sandvik, Bruun, & Tonstad (2004); Falcone et al. (2011); Glass et al. (2006); Hadigan et al. (2003); and Lo et al. (2010). "
    The Journal of the Association of Nurses in AIDS Care: JANAC 01/2014; 25(2). DOI:10.1016/j.jana.2013.11.004 · 1.23 Impact Factor
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    • "HIV infected adults have higher risk of cardiovascular disease than the general population due to an accelerated atherosclerosis process [23]. Several risk factors play an important role in the pathogenesis and progression of atherosclerosis in HIV patients: both HAART toxicity (mitochondrial dysfunction and oxidative stress induced by thymidine analogues or even the accumulation of abnormal laminin A associated with HIV protease inhibitor) and the virus itself induce metabolic disorders, immune activation, and chronic inflammation [24] [25]. "
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    12/2013; 2013:737083. DOI:10.1155/2013/737083
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