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Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study

Cardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Cross-sectional study of HIV-infected participants and c... Full description

Journal Title: AIDS (London) 2009, Vol.23 (14), p.1841-1849
Main Author: GRUNFELD, Carl
Other Authors: DELANEY, Joseph A. C , O'LEARY, Daniel , BACCHETTI, Peter , KRONMAL, Richard A , WANKE, Christine , CURRIER, Judith S , SCHERZER, Rebecca , BIGGS, Mary L , TIEN, Phyllis C , SHLIPAK, Michael G , SIDNEY, Stephen , POLAK, Joseph F
Format: Electronic Article Electronic Article
Language: English
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Publisher: Hagerstown, MD: Lippincott Williams & Wilkins
ID: ISSN: 0269-9370
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title: Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study
format: Article
creator:
  • GRUNFELD, Carl
  • DELANEY, Joseph A. C
  • O'LEARY, Daniel
  • BACCHETTI, Peter
  • KRONMAL, Richard A
  • WANKE, Christine
  • CURRIER, Judith S
  • SCHERZER, Rebecca
  • BIGGS, Mary L
  • TIEN, Phyllis C
  • SHLIPAK, Michael G
  • SIDNEY, Stephen
  • POLAK, Joseph F
subjects:
  • Adult
  • Aged
  • AIDS/HIV
  • Arteriosclerosis
  • Atherosclerosis (general aspects, experimental research)
  • Atherosclerosis - pathology
  • Atherosclerosis - virology
  • Biological and medical sciences
  • Blood and lymphatic vessels
  • Bulbs
  • Cardiology. Vascular system
  • Cardiovascular diseases
  • Carotid Artery Diseases - pathology
  • Carotid Artery Diseases - virology
  • Carotid Artery, Common - pathology
  • Carotid Artery, Internal - pathology
  • Cross-Sectional Studies
  • Demography
  • Diabetes. Impaired glucose tolerance
  • Endocrine pancreas. Apud cells (diseases)
  • Endocrinopathies
  • Etiopathogenesis. Screening. Investigations. Target tissue resistance
  • Female
  • HIV Infections - complications
  • Human immunodeficiency virus
  • Human viral diseases
  • Humans
  • Infection
  • Infectious diseases
  • Male
  • Medical sciences
  • Middle Aged
  • Morbidity
  • Mortality
  • Risk Factors
  • Sex Factors
  • Smoking
  • Smoking - adverse effects
  • Tunica Intima - pathology
  • Tunica Media - pathology
  • Viral diseases
  • Viral diseases of the lymphoid tissue and the blood. Aids
ispartof: AIDS (London), 2009, Vol.23 (14), p.1841-1849
description: Cardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Cross-sectional study of HIV-infected participants and controls without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Preclinical atherosclerosis was assessed by carotid intima-medial thickness (cIMT) measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional CVD risk factors. For internal carotid, mean IMT was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < 0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P < 0.0001]. Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater IMT (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with IMT was similar to that of smoking, which was also associated with greater IMT (internal 0.173 mm, common 0.020 mm). Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.
language: eng
source:
identifier: ISSN: 0269-9370
fulltext: no_fulltext
issn:
  • 0269-9370
  • 1473-5571
url: Link


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titlePreclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study
creatorGRUNFELD, Carl ; DELANEY, Joseph A. C ; O'LEARY, Daniel ; BACCHETTI, Peter ; KRONMAL, Richard A ; WANKE, Christine ; CURRIER, Judith S ; SCHERZER, Rebecca ; BIGGS, Mary L ; TIEN, Phyllis C ; SHLIPAK, Michael G ; SIDNEY, Stephen ; POLAK, Joseph F
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descriptionCardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Cross-sectional study of HIV-infected participants and controls without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Preclinical atherosclerosis was assessed by carotid intima-medial thickness (cIMT) measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional CVD risk factors. For internal carotid, mean IMT was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < 0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P < 0.0001]. Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater IMT (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with IMT was similar to that of smoking, which was also associated with greater IMT (internal 0.173 mm, common 0.020 mm). Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.
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subjectAdult ; Aged ; AIDS/HIV ; Arteriosclerosis ; Atherosclerosis (general aspects, experimental research) ; Atherosclerosis - pathology ; Atherosclerosis - virology ; Biological and medical sciences ; Blood and lymphatic vessels ; Bulbs ; Cardiology. Vascular system ; Cardiovascular diseases ; Carotid Artery Diseases - pathology ; Carotid Artery Diseases - virology ; Carotid Artery, Common - pathology ; Carotid Artery, Internal - pathology ; Cross-Sectional Studies ; Demography ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; HIV Infections - complications ; Human immunodeficiency virus ; Human viral diseases ; Humans ; Infection ; Infectious diseases ; Male ; Medical sciences ; Middle Aged ; Morbidity ; Mortality ; Risk Factors ; Sex Factors ; Smoking ; Smoking - adverse effects ; Tunica Intima - pathology ; Tunica Media - pathology ; Viral diseases ; Viral diseases of the lymphoid tissue and the blood. Aids
ispartofAIDS (London), 2009, Vol.23 (14), p.1841-1849
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1DELANEY, Joseph A. C
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7SCHERZER, Rebecca
8BIGGS, Mary L
9TIEN, Phyllis C
10SHLIPAK, Michael G
11SIDNEY, Stephen
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0Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study
1AIDS (London)
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descriptionCardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Cross-sectional study of HIV-infected participants and controls without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Preclinical atherosclerosis was assessed by carotid intima-medial thickness (cIMT) measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional CVD risk factors. For internal carotid, mean IMT was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < 0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P < 0.0001]. Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater IMT (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with IMT was similar to that of smoking, which was also associated with greater IMT (internal 0.173 mm, common 0.020 mm). Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.
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2AIDS/HIV
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6Atherosclerosis - virology
7Biological and medical sciences
8Blood and lymphatic vessels
9Bulbs
10Cardiology. Vascular system
11Cardiovascular diseases
12Carotid Artery Diseases - pathology
13Carotid Artery Diseases - virology
14Carotid Artery, Common - pathology
15Carotid Artery, Internal - pathology
16Cross-Sectional Studies
17Demography
18Diabetes. Impaired glucose tolerance
19Endocrine pancreas. Apud cells (diseases)
20Endocrinopathies
21Etiopathogenesis. Screening. Investigations. Target tissue resistance
22Female
23HIV Infections - complications
24Human immunodeficiency virus
25Human viral diseases
26Humans
27Infection
28Infectious diseases
29Male
30Medical sciences
31Middle Aged
32Morbidity
33Mortality
34Risk Factors
35Sex Factors
36Smoking
37Smoking - adverse effects
38Tunica Intima - pathology
39Tunica Media - pathology
40Viral diseases
41Viral diseases of the lymphoid tissue and the blood. Aids
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titlePreclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study
authorGRUNFELD, Carl ; DELANEY, Joseph A. C ; O'LEARY, Daniel ; BACCHETTI, Peter ; KRONMAL, Richard A ; WANKE, Christine ; CURRIER, Judith S ; SCHERZER, Rebecca ; BIGGS, Mary L ; TIEN, Phyllis C ; SHLIPAK, Michael G ; SIDNEY, Stephen ; POLAK, Joseph F
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39Tunica Media - pathology
40Viral diseases
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atitlePreclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study
jtitleAIDS (London)
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issue14
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pages1841-1849
issn0269-9370
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abstractCardiovascular disease (CVD) is an increasing cause of morbidity and mortality in HIV-infected patients. However, it is controversial whether HIV infection contributes to accelerated atherosclerosis independent of traditional CVD risk factors. Cross-sectional study of HIV-infected participants and controls without pre-existing CVD from the study of Fat Redistribution and Metabolic Change in HIV Infection (FRAM) and the Multi-Ethnic Study of Atherosclerosis (MESA). Preclinical atherosclerosis was assessed by carotid intima-medial thickness (cIMT) measurements in the internal/bulb and common regions in HIV-infected participants and controls after adjusting for traditional CVD risk factors. For internal carotid, mean IMT was 1.17 +/- 0.50 mm for HIV-infected participants and 1.06 +/- 0.58 mm for controls (P < 0.0001). After multivariable adjustment for demographic characteristics, the mean difference of HIV-infected participants vs. controls was 0.188 mm [95% confidence interval (CI) 0.113-0.263, P < 0.0001]. Further adjustment for traditional CVD risk factors modestly attenuated the HIV association (0.148 mm, 95% CI 0.072-0.224, P = 0.0001). For the common carotid, HIV infection was independently associated with greater IMT (0.033 mm, 95% CI 0.010-0.056, P = 0.005). The association of HIV infection with IMT was similar to that of smoking, which was also associated with greater IMT (internal 0.173 mm, common 0.020 mm). Even after adjustment for traditional CVD risk factors, HIV infection was accompanied by more extensive atherosclerosis measured by IMT. The stronger association of HIV infection with IMT in the internal/bulb region compared with the common carotid may explain previous discrepancies in the literature. The association of HIV infection with IMT was similar to that of traditional CVD risk factors, such as smoking.
copHagerstown, MD
pubLippincott Williams & Wilkins
pmid19455012
doi10.1097/QAD.0b013e32832d3b85
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