Issue: June 2019
May 07, 2019
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Subclinical findings may explain heart failure risk in women with HIV

Issue: June 2019
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Asymptomatic aging women with HIV who are being treated with ART exhibited increased myocardial fibrosis and reduced diastolic function compared with women who are not infected with HIV, according to a study results.

Researchers said the findings “may partially explain epidemiologic observations of increased heart failure risk and worse heart failure outcomes among women with vs. without HIV.”

“Our research team is dedicated to producing work geared toward helping women with HIV maximize longevity, health and wellness,” Markella V. Zanni, MD, associate professor of medicine at Harvard Medical School and director of women’s health research in the Program in Nutritional Metabolism at Massachusetts General Hospital, told Infectious Disease News.

“Previous work from our group highlighted that women with HIV face an increased risk for heart failure and worse heart failure outcomes compared with non-HIV-infected women. Additionally, women with HIV and heart failure tended to have a heart failure subtype called heart failure with preserved ejection fraction, which does not respond satisfactorily to conventional medical therapies.”

Knowing this, Zanni and colleagues “set out to study upstream mechanisms underlying the development of heart muscle dysfunction among women with HIV and no known heart failure” in hopes that it might lead to strategies that could preserve their heart muscle health and prevent the development of heart failure, Zanni explained.

The researchers prospectively recruited ART-treated women with HIV between ages 40 and 75 years who did not knowingly have cardiovascular disease or diabetes and an additional group of non-HIV-infected women who were matched based on age and body mass index. In total, 20 women with HIV and 14 controls were enrolled and completed procedures providing evaluable cardiac MRI data.

According to the results, women with HIV showed increased myocardial fibrosis, reduced diastolic function and heightened systemic monocyte activation. Zanni said that, compared with non-HIV-infected women, women with HIV demonstrated higher levels of a monocyte activation marker, soluble CD163, and increased expression of the cell-surface chemokine receptor C-C chemokine receptor type 2 (CCR2) on circulating inflammatory monocytes. Additionally, she explained that among women with HIV, levels of soluble CD163 correlated with the degree of myocardial fibrosis, whereas circulating inflammatory monocyte CCR2 expression related directly to myocardial fibrosis and inversely to diastolic function.

“If the hyperactive immune pathways identified here are subsequently confirmed to predispose women with HIV to the development of myocardial pathology — en route to heart failure — then strategies to dampen immune activation along these pathways might be tested for the potential to help prevent progression toward heart failure,” Zanni said.

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“Physicians with expertise in primary care, infectious diseases and cardiology should be aware that women with HIV face an increased risk of heart failure compared with non-HIV-infected women,” she said. “Thus, when women with HIV seek routine clinical care, known, modifiable risk factors for heart failure — such as cigarette smoking, [being] overweight and hypertension — should be identified, discussed, and addressed. In the future, there may be opportunities to assess for heightened immune activation as an additional risk factor for heart failure among women with HIV and to pursue safe, targeted preventive-care approaches to mitigate inflammatory cardiometabolic risk.” – by Caitlyn Stulpin

Disclosures: Zanni reports receiving investigator-initiated research grant funding from Gilead Sciences to her institution. Please see the study for all other authors’ relevant financial disclosures.