Inflammation may increase risk of heart damage among people with asthma
East Carolina University researchers have found a link between asthma-related inflammation and heart and blood vessel illness.
The illnesses, such as congestive heart failure, angina and vasculitis, or inflammation of blood vessels, previously had been attributed to medications used to treat asthma.
From left, Dr. Robert Lust, Surovi Hazarika and Dr. Michael Van Scott. Contributed photo
Researchers with the Department of Physiology at the Brody School of Medicine at East Carolina University discovered that inflammation associated with asthma affects the heart’s recovery from a heart attack, confirming the growing body of evidence that indicates asthma may affect the cardiovascular system.
“The findings are clinically important because they provide the first evidence of a direct contribution of asthmatic conditions to cardiovascular complications, independent of any asthma drug therapy,” said Surovi Hazarika, a physiology graduate student and lead author of the study. “If the findings are confirmed in human trials, asthma could be identified as a potential risk factor for post-operative complications and recurrent events following such cardiology interventions as angioplasty.”
Hazarika presented the research at the 35th congress of the International Union of Physiological Sciences in San Diego March 31-April 5. Hazarika completed medical school in India and is working on her doctorate in physiology. She plans to defend her research, a final step in completing her doctorate, in July.
In addition to Hazarika, Dr. Michael Van Scott, professor of physiology; and Dr. Robert Lust, professor and chairman of the Department of Physiology, participated in the research. The research is part of a collaborative project between Lust, who studies acute coronary syndromes, a term for various symptoms, such as chest pain, associated with a prolonged deficit in blood flow to the heart; and Van Scott, who studies lung diseases, including asthma, chronic obstructive pulmonary disease and cystic fibrosis.
“The goal of the current study was to investigate the inflammatory mechanisms underlying the asthma-associated increase in cardiac injury following a heart attack,” Hazarika said.
These findings could lead to better treatments for people with asthma and heart or blood vessel disease, Hazarika said. “And in the longer term, identification of the precise cause of cardiac changes induced by asthma and the appropriate therapeutic targets should provide better, specific alternatives for patients symptomatic for both asthma and cardiovascular disease.”
Previous studies have shown blood levels of certain markers of inflammation are related to increased risk of heart and vessel problems. Inflammation associated with asthma has been shown to increase the ability of the heart to attract inflammatory cells when injured, and the inflammatory cells that are attracted are more prone to be damaging, Hazarika said. Those cells are white blood cells called neutrophils, which release a substance known as MPO, or myeloperoxidase, in the presence of inflammation.
“The increased MPO release suggests that the neutrophils have been ‘primed’ to produce a proportionally larger inflammatory response if stimulated,” Hazarika said.
Inflammation also underlies asthma, which is characterized by higher numbers of inflammatory cells in airways and other parts of the respiratory system. As in cardiovascular disease, neutrophils play a significant role in the pathology of asthma. Earlier studies from the Van Scott-Lust laboratory showed the amount of damaged heart tissue increases after an acute heart attack in laboratory animals with asthma symptoms.