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SEATTLE -- Chronic obstructive pulmonary disease (COPD) was linked with a two-fold increased risk of acute myocardial infarction (MI) in people living with HIV, a researcher said here.

People living with HIV with existing COPD were associated with a higher risk of all types of MI, even after adjusting for demographics, cardiovascular confounders, and smoking (adjusted HR 2.08, 95% CI 1.61-2.70), reported Kristina Crothers, MD, of the University of Washington in Seattle, at a press conference at the Conference on Retroviruses and Opportunistic Infections (CROI).

When examining MIs by type, people living with HIV with COPD were associated with a higher risk of type 2 MI (T2MI), defined as supply-demand mismatch as with sepsis, compared with type 1 MI (T1MI), defined here as atherothrombotic coronary plaque rupture.

"Pulmonary disease and COPD is underdiagnosed in people living with HIV, and we need to make sure we are screening ... for it. The study can't say it's a causal effect, but reminds us that we need to pay attention in optimizing therapy for pulmonary disease," commented press conference moderator Judith Currier, MD, of the University of California, Los Angeles.

Crothers and colleagues said that there is an increased risk of cardiovascular disease, including MI, in people living with HIV, and that COPD is one of the most common chronic diseases in people living with HIV (15%-20%).

"COPD is a known risk factor for myocardial infarction in uninfected patients, but we know less about this relationship in people living with HIV," Crothers said at the press conference.

They examined data from six sites in the Centers for AIDS Research (CFAR) Network of Integrated Systems cohort, with MIs "adjudicated by two reviewers," and COPD defined by electronic health record algorithms validated against spirometry.

Overall, about 22,600 people living with HIV were included, and of those, 423 met the definition of moderate-to-severe COPD. Patients with no COPD tended to be younger, a smaller portion were women, a larger portion had a viral load <400 copies/ml, and a higher CD4 count compared to people living with HIV who had COPD during follow-up or COPD at baseline.

There was a median of 6 years from the index date to the end of follow-up, and a median of about 3 years from COPD diagnosis to MI. Of the 704 MIs during the study period, 55% were T1MI and 45% were T2MI.

People living with HIV who had COPD were associated with a more than two-fold higher risk of T2MI (adjusted HR 2.65, 95% CI 1.82-3.86), and an almost two-fold higher risk of T1MI (adjusted HR 1.73, 95% CI 1.21-2.48).

When looking at T2MI, there was an increased risk linked with T2MI due to sepsis/bacteremia (adjusted HR 2.43, 95% CI 1.25-4.73), researchers said.

To explore this association further, Crothers' group performed an exploratory analysis on COPD control, to find out "what inhalers these patients were being treated with," she said. In those with COPD and no MI, 66% were on any type of inhaler, but 75% of these were short-acting inhalers, Crothers noted.

"It does raise questions -- people had, on average, 3 years between when COPD criteria were met and a MI event, but in that time, they were continued on short-acting therapies," she said, adding that this potentially raises questions about management and risk factors for COPD exacerbations.

Ultimately, Crothers said that the mechanisms involved in these associations are "unclear," and "the data don't help us understand exactly what those are." One potential hypothesis was COPD exacerbation, with inflammation also present in HIV. Other theories presented by the researchers included endothelial dysfunction, smoking/other substance use, and pneumonia/sepsis.

They concluded that further research is needed into the mechanisms behind this association, to "optimize preventive and therapeutic strategies."

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