Carotid Intima-Media Thickness in Heavily Pretreated HIV-Infected Patients

Chironi, Gilles; Escaut, L.; Gariepy, Jérôme; Cogny, Anne; Teicher, Elina; Monsuez, Jean‐Jacques; Levenson, Jaime; Simon, Alain; Vittecoq, D.

doi:10.1097/00126334-200304150-00004

Cited by 61 publications

(43 citation statements)

References 17 publications

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“…In line with results of the present study, previous studies revealed that HIV patients had significantly increased common carotid artery IMT if compared to the IMT of healthy controls [8,9,10,11,12,13]. The mean IMT value of HIV patients revealed in our study (0.74 mm) fell within the range of mean IMT values of HIV patients reported by others (0.53–0.91 mm) [8,9,10,11,12].…”

Section: Discussionsupporting

confidence: 93%

“…A well-accepted surrogate marker for atherosclerosis is the measurement of the common carotid artery intima-media thickness (IMT) with high-resolution B mode ultrasound [7]. Previous studies have consistently shown that the common carotid artery IMT is significantly increased in HIV patients compared to healthy controls [8,9,10,11,12,13]. In non-HIV-infected patients it has been demonstrated that asymptomatic atherosclerosis of carotid arteries is independently associated with cognitive impairment and decline [14].…”

Section: Introductionmentioning

confidence: 99%

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Carotid Intima-Media Thickness in HIV-Infected Individuals: Relationship of Premature Atherosclerosis to Neuropsychological Deficits?

Yaldizli

Kastrup²,

Obermann³

et al. 2006

Eur Neurol

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Background: Intima-media thickness (IMT) measured by extracranial duplex sonography is a surrogate marker for atherosclerosis. It is well known that IMT is greater in HIV patients than in age-matched healthy controls due to HIV- induced endothelial damage and metabolic side-effects of antiretroviral therapy. However, it remains unclear whether atherosclerosis has an additional impact on cognitive function in HIV patients. Therefore, the objective of this study was to investigate the correlation between IMT and neuropsychological deficits in HIV patients. Methods: 47 HIV patients and 40 age-matched healthy controls were examined by extracranial ultrasound 2 and 3 cm before the flow divider to evaluate differences in IMT. Possible neuropsychological deficits in HIV patients were assessed using a battery of 10 neuropsychological tests. Results of neuropsychological tests and markers of disease severity were correlated with IMT in HIV patients. Results: IMT was significantly greater in patients than in healthy controls (p < 0.001). However, none of the neuropsychological tests correlated significantly with IMT measurements in HIV patients. There was only a weak correlation between deficits in attention and IMT in HIV patients (r = 0.44; p = 0.005), which was non-significant after correction for multiple comparisons. Markers of disease severity (CD4 cell count, HIV load in plasma, duration of HIV disease) did not correlate with IMT either. Conclusion: IMT was greater in HIV patients compared to age-matched controls but it appears that premature atherosclerosis has no additional impact on the evolution of neuropsychological deficits in HIV patients. IMT did not correlate with the severity of immunodeficiency.

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Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Carotid Intima-Media Thickness in HIV-Infected Individuals: Relationship of Premature Atherosclerosis to Neuropsychological Deficits?

Yaldizli

Kastrup²,

Obermann³

et al. 2006

Eur Neurol

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“…15 Because carotid IMT measurements correlate satisfactorily with pathological measurements 16 and are potent predictors of myocardial infarction and stroke, even after adjustment for other risk factors, [17][18][19][20] carotid B-mode high-resolution ultrasound imaging has been used in several studies to evaluate cardiovascular risk in HIVinfected patients. 7,8,[21][22][23][24][25][26][27] Most but not all of these studies have in fact shown an increased prevalence of subclinical atherosclerosis in patients receiving CART. The main result of the present study was that CART exposure was the most powerful predictor of carotid atherosclerosis in HIV-infected patients after controlling for Framingham risk score.…”

Section: Discussionmentioning

confidence: 99%

Subclinical Carotid Atherosclerosis in HIV-Infected Patients

Jericó

Knobel

Calvo

et al. 2006

Stroke

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Background and Purpose-Whether or not combination antiretroviral therapy (CART) alone directly contributes to accelerating atherosclerosis in HIV-infected patients has not been studied in depth. This study aimed to ascertain the relationship between this therapy and subclinical carotid atherosclerosis according to cardiovascular risk. Methods-Sixty-eight HIV-infected patients with Յ1 cardiovascular risk factors and 64 with Ն2 risk factors completed the study protocol consisting of clinical, laboratory, and vascular evaluation by carotid high-resolution B-mode ultrasonography. Univariate and multivariate logistic regression analyses were performed with the presence of subclinical carotid atherosclerosis, defined by carotid intima-media thickness Ͼ0.8 mm or the presence of plaque being the dependent variable. Results-Among the 132 enrolled patients, 93 (70.5%) were on CART and 39 (29.5%) had never been on antiretroviral therapy. In accordance with cardiovascular risk stratification, subclinical carotid atherosclerosis was found in 26.6% (17 of 64 patients) of the very low-risk group (10-year coronary risk Ͻ5%), 35.3% (12 of 34 patients) of the low-risk group (10-year coronary risk between 5% and 9%) and 76.5% (26 of 34 patients) of the moderate/high-risk group (10-year coronary risk Ն10%). Thus, 55 (41.7%) of the 132 HIV-infected patients had subclinical carotid atherosclerosis, and independent variables associated with carotid atherosclerosis (odds ratio; 95% CI) were: CART exposure (10.5; 2.8 to 39) and 10-year coronary risk Ն10% (4.2; 1.5 to 12). In very low coronary risk patients (Ͻ5%), age (per 10-year increment: 4.01; 1.12 to 14.38), systolic blood pressure (per unit mm Hg 1.07; 1.01 to 1.14), and CART exposure (8.65; 1.54 to 48.54) were independently associated with subclinical carotid atherosclerosis. Conclusions-CART should be considered a strong, independent predictor for the development of subclinical atherosclerosis in HIV-infected patients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy. (Stroke. 2006;37:812-817.)

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“…Seminari et al 43 found that carotid IMT was increased in 28 HIV patients receiving protease inhibitors compared with measurements in 15 protease inhibitornaive patients and 16 HIV-negative subjects. Chironi et al 44 reported that 36 HIV patients receiving protease inhibitors had carotid IMT equal to that of non-HIV subjects with similar lipid and glucose disturbances; both groups had increased carotid IMT compared with control subjects without lipid and glucose abnormalities. In another study of 423 HIV-infected patients, conventional risk factors but not lipodystrophy or HAART were independent predictors of increased carotid IMT.…”

Section: Previous Studiesmentioning

confidence: 99%

Progression of Atherosclerosis as Assessed by Carotid Intima-Media Thickness in Patients With HIV Infection

et al. 2004

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Background-HIV-infected patients may be at increased risk for coronary events. The purpose of this study was to identify predictors of carotid intima-media thickness (IMT) in HIV patients at baseline and to measure IMT progression over 1 year. Methods and Results-We measured blood lipids, inflammatory markers, and IMT in 148 HIV-infected adults (mean age, 45Ϯ8 years) and in 63 age-and sex-matched HIV-uninfected control subjects. The mean duration of HIV infection was 11 years, and the median duration of protease inhibitor treatment was 3.3 years. Mean baseline IMT was 0.91Ϯ0.33 mm in HIV patients and 0.74Ϯ0.17 mm in control subjects (Pϭ0.0001). Multivariable predictors of baseline IMT in HIV patients were age (PϽ0.001), LDL cholesterol (PϽ0.001), cigarette pack-years (Pϭ0.005), Latino race (Pϭ0.062), and hypertension (Pϭ0.074). When the control group was added to the analysis, HIV infection was an independent predictor of IMT (Pϭ0.001). The rate of progression among the 121 HIV patients with a repeated IMT measurement at 1 year was 0.074Ϯ0.13 mm, compared with Ϫ0.006Ϯ0.05 mm in 27 control subjects (Pϭ0.002). Age (PϽ0.001), Latino race (Pϭ0.02), and nadir CD4 count Յ200 (Pϭ0.082) were multivariable predictors of IMT progression. Conclusions-Carotid IMT is higher in HIV patients than in age-matched control subjects and progresses much more rapidly than previously reported rates in non-HIV cohorts. In HIV patients, carotid IMT is associated with classic coronary risk factors and with nadir CD4 count Յ200, suggesting that immunodeficiency and traditional coronary risk factors may contribute to atherosclerosis.

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Carotid Intima-Media Thickness in Heavily Pretreated HIV-Infected Patients

Cited by 61 publications

References 17 publications

Carotid Intima-Media Thickness in HIV-Infected Individuals: Relationship of Premature Atherosclerosis to Neuropsychological Deficits?

Carotid Intima-Media Thickness in HIV-Infected Individuals: Relationship of Premature Atherosclerosis to Neuropsychological Deficits?

Subclinical Carotid Atherosclerosis in HIV-Infected Patients

Progression of Atherosclerosis as Assessed by Carotid Intima-Media Thickness in Patients With HIV Infection

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