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Coronary Aging in HIV-Infected Patients
 
 
  CORRESPONDENCE
 
Clinical Infectious Diseases Oct 15 2010
"these data suggest that accelerated vascular aging is common among HIV-infected persons. To reduce the impact of cardiovascular disease in this population, additional data on the pathogenesis of increasing vascular age-and ultimately therapeutic strategies to slow aging-are needed."
 
"these data suggest that accelerated vascular aging is common among HIV-infected persons. To reduce the impact of cardiovascular disease in this population, additional data on the pathogenesis of increasing vascular age-and ultimately therapeutic strategies to slow aging-are needed......Increased coronary age was observed in 67 patients (89% of patients with CAC and 30% of the total study cohort). The median increase in vascular age was 18 years (IQR, 13-29 years) higher than the chronological age.....our study extends present data by showing that fatty liver disease-and perhaps elevated inflammatory markers (eg, CRP level)-may be related to the development of increased vascular aging."

 
Sheila Medina,1,2 Dylan Wessman,3 David Krause,3 James Stepenosky,4 Gilbert Boswell,4 and Nancy Crum-Cianflone1,2. 1Infectious Disease Clinical Research Program, Uniformed Services University of the Health Sciences, Bethesda, Maryland; and 2HIV Clinic, 3Cardiology Department, and 4Radiology Department, Naval Medical Center San Diego, San Diego, California
 
To the Editor-We read with interest the report by Guaraldi et al [1] on coronary aging among human immunodeficiency virus (HIV)-infected patients. It has been hypothesized that the increased rates of several non-AIDS-defining conditions, including cardiovascular disease, may be attributable in part to accelerated aging in this population.
 
We recently performed a cross-sectional study among HIV-infected adults to evaluate the prevalence of and factors associated with subclinical coronary atherosclerosis as detected by computed tomography (CT) for coronary artery calcium (CAC). Patients also underwent CT for detection of fatty liver disease [2]. Results of this original study were re-evaluated for coronary age on the basis of published sex- and race-specific polynomial equations [3], and differences between the chronologic and coronary age were computed. Logistic regression models were performed for factors associated with increased, compared with expected or decreased, coronary aging. In addition, linear regression models were used to examine factors associated with the degree of coronary aging among those with CAC (Stata software, version 10; Stata).
 
We evaluated 223 HIV-infected adults with a median age of 43 years (interquartile range [IQR], 36-50 years). Of these subjects, 96% were male, 49% were white, 23% were black, and 28% were of other races. Median CD4+ cell count was 586 cells/mm3 (IQR, 393-733 cells/mm3), and 83% were receiving antiretroviral medications. Seventy-five patients had a positive CAC score (defined as >0). Increased coronary age was observed in 67 patients (89% of patients with CAC and 30% of the total study cohort). The median increase in vascular age was 18 years (IQR, 13-29 years) higher than the chronological age. We compared those with and without increased coronary age and found that accelerated coronary aging was univariately associated with chronologic age, hypertension, duration of tobacco use, fatty liver disease, metabolic syndrome, percentage of body fat, hypertriglyceridemia, use of an antilipid medication, low CD4+ cell count nadir, duration of HIV infection, and duration of antiretroviral use (p<.05), with a trend for elevated C-reactive protein (CRP) level (Table 1). In the final multivariate model, fatty liver disease (odds ratio [OR], 4.4; p=.001) and increasing chronological age (OR, 2.6 per 10 years; ) were significantly associated with increased coronary age, with a trend for elevated CRP level (OR, 2.3; p=.05).
 
Table1.Characteristics of Human Immunodeficiency Virus (HIV)-Infected Persons with Increased Coronary Aging, Compared with HIV-Infected Individuals with Expected and/or Decreased Coronary Aging

In our linear regression modeling for predictors of increasing coronary age among those with CAC, we found that both higher current CD4+ cell count (β 0.53 per 50 cells/mm3; 95% confidence interval [CI], 0.05-1.01 cells/mm3; p=.03), and higher nadir CD4+ cell counts (β 1.73 per 50 cells/mm3; 95% CI, 0.86-2.60 cells/mm3; ) were univariately associated with increasing coronary aging; the latter is shown in Figure 1. There was no association between coronary aging with the difference between nadir and current CD4+ cell counts (p=.73). CD4+ cell count nadir and current counts were highly correlated (r=0.46; p<.001). In separate final multivariate models, both nadir (β 1.29; p=.004) and current CD4+ cell counts (β 0.50; p=.03) remained significantly associated with increasing coronary age.
 
Overall, our results confirm many of the findings by Guaraldi et al [1]. In addition, our study extends present data by showing that fatty liver disease-and perhaps elevated inflammatory markers (eg, CRP level)-may be related to the development of increased vascular aging. The precise relationship of these factors is unclear because of the cross-sectional design of the study but may represent markers of an underlying systemic pro-atherogenic state that results in accelerated vascular aging.
 
We found that higher current and nadir CD4+ cell counts were associated with greater increases in coronary aging in our linear regression models. In the final model, nadir CD4+ cell count in our study was particularly associated with coronary aging. Of note, our study was conducted in a cohort of individuals who had received early diagnosis and treatment and, in general, did not experience low nadir CD4+ cell counts. Although higher CD4+ cell counts were not associated with the development of CAC in either study, once atherosclerosis is present, more robust counts may lead to T-cell mediated atherogenesis, faster progression of lesions, and accelerated vascular aging. As noted by Guaraldi et al [1], the exact mechanism is currently unknown.
 
Overall, these data suggest that accelerated vascular aging is common among HIV-infected persons. To reduce the impact of cardiovascular disease in this population, additional data on the pathogenesis of increasing vascular age-and ultimately therapeutic strategies to slow aging-are needed.
 
 
 
 
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