Could Asthma Have Protective Effect in MI?

NEW ORLEANS — Asthma patients hospitalized for myocardial infarction (MI) had lower mortality risk than patients without asthma a year after the event, analysis of a nationwide hospital inpatient database indicated.

Inpatient mortality was lower in patients with asthma vs controls in the examination of data on approximately 13,000 patients with and without asthma from the 2016 National Inpatient Sample (odds ratio 0.74, 95% CI 0.62-0.89; P=0.001), reported Nour Tashtish, MD, of Case Western Reserve University in Cleveland.

In his presentation of the preliminary findings at CHEST 2019, the annual meeting of the American College of Chest Physicians, Tashtish noted that the association remained after the team adjusted for sex, ST-elevation myocardial infarction (STEMI), percutaneous coronary intervention (PCI), cancer, and other variables.

Tashtish told MedPage Today that animal studies suggest that T helper 2 (Th2) cytokine response — including interleukins 4 and 5 — may help protect against atherosclerosis and MI and that interleukin 17 has been shown to protect against adverse cardiac remodeling in mice after induced MI. Asthma is driven by T cell activation, and Th2 cells and their cytokines play a critical role in the pathophysiology of allergic and non-allergic asthma, he explained.

He noted that the team had hypothesized that the Th2 cytokine response may convey protection after a heart attack, and therefore performed propensity score matching (1:1) that included 34 patient variables to match asthma patients with controls without asthma using nearest neighbor matching.

A total of 12,926 MI patients were included in the analysis, including 6,463 with asthma and 6,463 without. Compared with the control group, asthma patients were slightly more likely to be male (44.6% vs 42.1%, P=0.005), have STEMI (20% vs 18.5%; P=0.038), have PCI (41.6% vs 39.6%; P=0.019), and have a lower prevalence of cancer (3% vs 3.8%; P=0.015), the researchers found.

They did not have access to data on asthma medications taken by the patients, which Tashtish acknowledged was a significant study limitation, adding that studying patients on drugs that target Th2 expression could offer insights into the role of Th2 expression, if any, in MI.

In his presentation at the meeting, Tashtish said these and other studies are needed to identify the mechanisms underlying the findings.

Gilbert Seda, MD, PhD, of Naval Medical Center San Diego, who moderated the session at which the study was presented, told MedPage Today that the observational findings seem counterintuitive, given what is known about widely used asthma treatments: “You would think patients with asthma would have a higher MI risk because many rescue inhalers make the heart beat faster,” he said. “There is also evidence in African Americans that the use of beta agonists is associated with a greater risk for MI.”

But the data are intriguing and worthy of further study, Seda added.

Tashtish reported having no relevant relationships with industry related to the research.