HIV-positive patients may be at greater risk of atherosclerosis

HIV-infected individuals without any traditional cardiovascular disease risk factors still show signs of vascular thickening, compared with HIV-negative controls, researchers reported in a British study.

A team led by Dr. Kathleen A.M. Rose of the cardiovascular biomedical research unit at London’s Royal Brompton Hospital performed carotid cardiovascular magnetic resonance imaging on 33 HIV-infected patients and 35 HIV-negative controls, with both groups being at low cardiovascular risk. The study showed HIV infection was associated with a significantly greater ratio of carotid wall to outer wall thickness (36.7% vs. 32.5%, P less than .0001) – an indicator of carotid intima-media thickening that has been shown in HIV-negative populations to be predictive of future cardiovascular events.

©pixologicstudio/Thinkstock.com

Women with HIV had an even greater increase in carotid intima-media thickening, compared with men with HIV, according to the study results (JAIDS. 2015 Nov 16. doi: 10.1097/QAI.0000000000000900)

While there were no significant differences between the cases and controls in total carotid lumen volume, carotid artery volume, and carotid wall volume, total wall volume was higher in HIV-infected individuals, and there was a nonsignificant decrease in carotid artery distensibility in the HIV-infected group.

“Although traditional cardiovascular risk factors are highly prevalent and accepted to play a role in HIV-associated cardiovascular disease, the role of long-term cART [combination antiretroviral therapy] and HIV infection itself remains controversial,” wrote Dr. Rose and her coauthors.

The researchers cited earlier studies linking the antiretroviral agents indinavir, abacavir, and lopinavir with increased cardiovascular risk, although they pointed out there was conflicting evidence of a link with type of antiretroviral therapy.

The HIV-infected participants were all stable on combination antiretroviral therapy for a median duration of 7 years (2-21 years), and all had a plasma HIV-1 RNA viral load below 50 copies/mL.

Years of antiretroviral therapy and use of nonnucleoside reverse transcriptase inhibitors or protease inhibitors did not significantly impact carotid intima-media thickness, although patients taking abacavir – which is associated with increased cardiovascular risk – had a lower wall/outer wall ratio than those on zidovudine.

“This result may also reflect a channeling bias whereby clinicians only use abacavir in subjects they consider to have very low cardiovascular risk,” the authors wrote.

Other parameters such as age, ethnicity, CD4 cell count, nadir CD4 cell count, and years since HIV diagnosis did not impact atherosclerosis in HIV-positive subjects.

“Although our study has not followed up patients or controls longitudinally, the diverging lines between the groups with increasing age suggests that HIV infection and/or its treatment may be associated with progression of vascular wall thickening beyond that normally seen with age,” the authors reported.

“As increasing C-IMT [carotid intima-media thickness] has been found to be independently predictive of future stroke and myocardial infarction in HIV-uninfected populations, the findings of this study suggest that the rate of vascular events is likely to remain elevated in HIV-patients despite aggressive treatment of cardiovascular risk factors, highlighting the need for improved patient and health care provider education to detect and manage aggressively early signs of cardiovascular disease.”

The study was supported by the National Institute of Health Research cardiovascular biomedical research unit at Royal Brompton and Harefield NHS Foundation Trust, and Imperial College London. Three authors declared honoraria, grants, sponsorship, and consultancies from the pharmaceutical industry.

HIV-infected individuals without any traditional cardiovascular disease risk factors still show signs of vascular thickening, compared with HIV-negative controls, researchers reported in a British study.

A team led by Dr. Kathleen A.M. Rose of the cardiovascular biomedical research unit at London’s Royal Brompton Hospital performed carotid cardiovascular magnetic resonance imaging on 33 HIV-infected patients and 35 HIV-negative controls, with both groups being at low cardiovascular risk. The study showed HIV infection was associated with a significantly greater ratio of carotid wall to outer wall thickness (36.7% vs. 32.5%, P less than .0001) – an indicator of carotid intima-media thickening that has been shown in HIV-negative populations to be predictive of future cardiovascular events.

©pixologicstudio/Thinkstock.com

Women with HIV had an even greater increase in carotid intima-media thickening, compared with men with HIV, according to the study results (JAIDS. 2015 Nov 16. doi: 10.1097/QAI.0000000000000900)

While there were no significant differences between the cases and controls in total carotid lumen volume, carotid artery volume, and carotid wall volume, total wall volume was higher in HIV-infected individuals, and there was a nonsignificant decrease in carotid artery distensibility in the HIV-infected group.

“Although traditional cardiovascular risk factors are highly prevalent and accepted to play a role in HIV-associated cardiovascular disease, the role of long-term cART [combination antiretroviral therapy] and HIV infection itself remains controversial,” wrote Dr. Rose and her coauthors.

The researchers cited earlier studies linking the antiretroviral agents indinavir, abacavir, and lopinavir with increased cardiovascular risk, although they pointed out there was conflicting evidence of a link with type of antiretroviral therapy.

The HIV-infected participants were all stable on combination antiretroviral therapy for a median duration of 7 years (2-21 years), and all had a plasma HIV-1 RNA viral load below 50 copies/mL.

Years of antiretroviral therapy and use of nonnucleoside reverse transcriptase inhibitors or protease inhibitors did not significantly impact carotid intima-media thickness, although patients taking abacavir – which is associated with increased cardiovascular risk – had a lower wall/outer wall ratio than those on zidovudine.

“This result may also reflect a channeling bias whereby clinicians only use abacavir in subjects they consider to have very low cardiovascular risk,” the authors wrote.

Other parameters such as age, ethnicity, CD4 cell count, nadir CD4 cell count, and years since HIV diagnosis did not impact atherosclerosis in HIV-positive subjects.

“Although our study has not followed up patients or controls longitudinally, the diverging lines between the groups with increasing age suggests that HIV infection and/or its treatment may be associated with progression of vascular wall thickening beyond that normally seen with age,” the authors reported.

“As increasing C-IMT [carotid intima-media thickness] has been found to be independently predictive of future stroke and myocardial infarction in HIV-uninfected populations, the findings of this study suggest that the rate of vascular events is likely to remain elevated in HIV-patients despite aggressive treatment of cardiovascular risk factors, highlighting the need for improved patient and health care provider education to detect and manage aggressively early signs of cardiovascular disease.”

The study was supported by the National Institute of Health Research cardiovascular biomedical research unit at Royal Brompton and Harefield NHS Foundation Trust, and Imperial College London. Three authors declared honoraria, grants, sponsorship, and consultancies from the pharmaceutical industry.

HIV-infected individuals without any traditional cardiovascular disease risk factors still show signs of vascular thickening, compared with HIV-negative controls, researchers reported in a British study.

A team led by Dr. Kathleen A.M. Rose of the cardiovascular biomedical research unit at London’s Royal Brompton Hospital performed carotid cardiovascular magnetic resonance imaging on 33 HIV-infected patients and 35 HIV-negative controls, with both groups being at low cardiovascular risk. The study showed HIV infection was associated with a significantly greater ratio of carotid wall to outer wall thickness (36.7% vs. 32.5%, P less than .0001) – an indicator of carotid intima-media thickening that has been shown in HIV-negative populations to be predictive of future cardiovascular events.

©pixologicstudio/Thinkstock.com

Women with HIV had an even greater increase in carotid intima-media thickening, compared with men with HIV, according to the study results (JAIDS. 2015 Nov 16. doi: 10.1097/QAI.0000000000000900)

While there were no significant differences between the cases and controls in total carotid lumen volume, carotid artery volume, and carotid wall volume, total wall volume was higher in HIV-infected individuals, and there was a nonsignificant decrease in carotid artery distensibility in the HIV-infected group.

“Although traditional cardiovascular risk factors are highly prevalent and accepted to play a role in HIV-associated cardiovascular disease, the role of long-term cART [combination antiretroviral therapy] and HIV infection itself remains controversial,” wrote Dr. Rose and her coauthors.

The researchers cited earlier studies linking the antiretroviral agents indinavir, abacavir, and lopinavir with increased cardiovascular risk, although they pointed out there was conflicting evidence of a link with type of antiretroviral therapy.

The HIV-infected participants were all stable on combination antiretroviral therapy for a median duration of 7 years (2-21 years), and all had a plasma HIV-1 RNA viral load below 50 copies/mL.

Years of antiretroviral therapy and use of nonnucleoside reverse transcriptase inhibitors or protease inhibitors did not significantly impact carotid intima-media thickness, although patients taking abacavir – which is associated with increased cardiovascular risk – had a lower wall/outer wall ratio than those on zidovudine.

“This result may also reflect a channeling bias whereby clinicians only use abacavir in subjects they consider to have very low cardiovascular risk,” the authors wrote.

Other parameters such as age, ethnicity, CD4 cell count, nadir CD4 cell count, and years since HIV diagnosis did not impact atherosclerosis in HIV-positive subjects.

“Although our study has not followed up patients or controls longitudinally, the diverging lines between the groups with increasing age suggests that HIV infection and/or its treatment may be associated with progression of vascular wall thickening beyond that normally seen with age,” the authors reported.

“As increasing C-IMT [carotid intima-media thickness] has been found to be independently predictive of future stroke and myocardial infarction in HIV-uninfected populations, the findings of this study suggest that the rate of vascular events is likely to remain elevated in HIV-patients despite aggressive treatment of cardiovascular risk factors, highlighting the need for improved patient and health care provider education to detect and manage aggressively early signs of cardiovascular disease.”

The study was supported by the National Institute of Health Research cardiovascular biomedical research unit at Royal Brompton and Harefield NHS Foundation Trust, and Imperial College London. Three authors declared honoraria, grants, sponsorship, and consultancies from the pharmaceutical industry.