EATG » CROI 2018: Link between HIV and elevated CV risk further confirmed

CROI 2018: Link between HIV and elevated CV risk further confirmed

Two studies presented at the annual Conference on Retroviruses and Opportunistic Infections, or CROI, showed elevated CV risk among men with HIV and suggested avenues for future study.

The two studies focused on narrowing the knowledge gap that exists in prevalence and CV risk factors among this patient set.

“HIV-infected individuals are surviving longer due to effective antiretroviral therapy, and CVD has emerged as a leading cause of morbidity and mortality. However, the mechanisms for increased risk are incompletely understood,” Wendy Post, MD, professor of medicine at Johns Hopkins University, said in her presentation.

PAD prevalence in HIV

According to a presentation from Andreas D. Knudsen, MD, PhD, from Rigshospitalet in Copenhagen, Denmark, those living with HIV had an increased rate of peripheral artery disease compared with healthy controls.

“It is well-known that persons living with HIV have increased risk of CVD, but less is known about PAD,” Knudsen said. “The aims of this study were to characterize the prevalence and risk factors of PAD among persons living with HIV.”

Knudsen and colleagues conducted a study consisting of 908 adults living with HIV (median age, 52 years) and 11,106 controls (median age, 53 years).

Using questionnaires, researchers obtained data on smoking history and medication. Ankle-brachial index was used to diagnose PAD.

Logistic regression models were adjusted for age, sex, smoking status, dyslipidemia, diabetes, high-sensitivity C-reactive protein and hypertension to assess PAD predictors.

The researchers found that among adults living with HIV, there was a lower prevalence of hypertension (P < .0001), but there were higher rates of current smoking and intermittent claudication in those living with HIV compared with the control group (P < .0001 for both).

Knudsen and colleagues found that PAD was prevalent in 12% of adults living with HIV and 6% of control patients (adjusted OR = 2.4; 95% CI, 1.9-2.9).

Irrespective of HIV status, age, female sex, smoking status, hypertension, intermittent claudication and kidney function were independently associated with PAD, according to the researchers.

“PAD is more prevalent among persons living with HIV, and HIV is independently associated with disease,” Knudsen said. “More studies are needed to investigate the mechanisms of the atherosclerotic process in HIV.”

Coronary plaque risk

According to the presentation from Post, HIV was linked to an increased incidence and progression of high-risk coronary plaque.

A baseline and follow-up coronary CT angiography of 409 men (253 with HIV; mean age, 54 years; 32% black) showed that plaque was prevalent in 30%. Of the 36 men, 24 developed both noncalcified plaque and calcified plaque (mixed plaque) and 12 developed noncalcified plaque only. Low-attenuation plaque developed in 27 participants, according to the abstract.

There was a greater adjusted incidence of noncalcified plaque (incidence rate ratio [IRR] = 2.13; P = .03), low-attenuation plaque (IRR = 2.84; P = .05) and mixed plaque (IRR = 3.09; P = .01) found among men with HIV.

The researchers found that, compared with men without HIV, the incidence of low-attenuation plaque was greatest among men with HIV and viremia (IRR = 5.4; P = .009).

Two hundred ninety-one men had baseline plaque. Among men with the greatest noncalcified plaque volume change, the adjusted increases were greater among men with HIV compared with men without HIV (P = .03), and trends for total plaque and low-attenuation plaque were similar, according to the researchers.

According to Post, the results suggest the need for additional studies to determine the importance of controlling viremia to limit the excess CVD burden in those with HIV.

“To our knowledge, this is the first study to document and quantify progressions of coronary plaque and people living with HIV in a large longitudinal study,” Post said. “It will be important now to focus on possible mechanisms of why coronary plaque progresses faster in HIV-infected men than in similar uninfected men, such as coinfections or greater immune activation and inflammation and on mechanisms for racial differences in HIV-related plaque progression.”

By Dave Quaile


Knudsen AD, et al. Abstract 76.

Post W, et al. Abstract 77. Presented at: Conference on Retroviruses and Opportunistic Infections; March 4-7, 2018; Boston.

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News categories: Comorbidities, CROI 2018