Persistent asthma linked to increased plaque buildup in arteries leading to the brain – Zoo House News

Persistent asthma linked to increased plaque buildup in arteries leading to the brain – Zoo House News

  • Science
  • November 23, 2022
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Adults with persistent asthma may be at increased risk of heart attack or stroke because of excessive plaque buildup in the carotid arteries, according to a new study published today in the Journal of the American Heart Association, an open-access, peer-reviewed journal of the American Heart Association . The participants in the study had more deposits in the carotid arteries, large arteries on the left and right side of the neck that carry blood to the brain, compared to people without asthma.

Asthma is a respiratory disease that causes a person’s airways to become inflamed – often due to allergic reactions – and makes it difficult to breathe. Chronic inflammation is known to contribute to the build-up of arterial plaque over time, known as atherosclerosis, and is associated with a higher risk of plaque rupturing and triggering a heart attack or stroke.

“Many doctors and patients are unaware that asthmatic airway inflammation can affect the arteries, so addressing risk factors for cardiovascular disease can be very helpful for people with ongoing asthma,” said study lead author Matthew C Tattersall, DO, MS, Assistant Professor at the University of Wisconsin School of Medicine at Madison. “The presence and burden of carotid plaque is a strong predictor of future cardiovascular events.”

For this analysis, the researchers used data from participants in the Multi-Ethnic Study of Atherosclerosis (MESA) study to examine the possible association between asthma and carotid plaques. MESA is a research study of nearly 7,000 adults that began in 2000 and is still following participants in six locations across the United States: Baltimore; Chicago; New York; Los Angeles County, California; Forsyth County, North Carolina; and St. Paul, Minnesota. At the time of enrollment, all MESA participants were cardiovascular disease free.

The researchers examined the health records of 5,029 adults with a median age of 61 years who had baseline risk factors for cardiovascular disease and had carotid ultrasound data. The participant population was diverse: 26% of adults self-identified as African American, 23% self-identified as Hispanic, and 12% self-identified as Chinese. In addition, more than half of the group (53%) was female.

Participants in the cohort of this analysis were categorized as having persistent asthma, intermittent asthma, or no asthma. The persistent asthma subgroup, defined as daily use of control medication to control asthma symptoms, consisted of 109 participants; the subgroup with intermittent asthma, defined as a history of asthma but without daily medication to control asthma symptoms, consisted of 388 participants; and the remaining participants had no asthma.

At baseline in the MESA study, all participants underwent left and right carotid artery ultrasound to identify any carotid artery plaque. The total plaque score defines the number of plaques in the walls of both carotid arteries. Blood levels of the inflammatory biomarkers interleukin-6 (IL-6) and C-reactive protein (CRP) were also measured at the start of the MESA study.

The analysis revealed:

Carotid plaque was present in 67% of participants with persistent asthma and 49.5% of participants with intermittent asthma. Patients with persistent asthma had an average of two carotid plaques and patients with intermittent asthma about one carotid plaque. Carotid plaques were present in 50.5% of participants without asthma, with an average of about one carotid plaque. After accounting for age, gender, race, weight, other health conditions, prescription drug use, and smoking, participants with persistent asthma were almost twice as likely to have plaque in their carotid arteries as those without asthma.

Compared to participants without asthma, those with persistent asthma had higher levels of inflammatory biomarkers. (Individuals with ongoing asthma had a mean IL-6 level of 1.89 pg/mL, while those without asthma had a mean IL-6 level of 1.52 pg/mL.) The researchers found that IL- 6 and CRP in the fully fitted analysis did not reduce the association between persistent asthma and carotid plaque.

“This analysis tells us that the increased risk of carotid plaques in people with persistent asthma is likely influenced by multiple factors,” Tattersall said. “Participants with persistent asthma had elevated blood levels of inflammation despite their asthma being treated with medication, underscoring the inflammatory characteristics of asthma. We know that higher levels of inflammation result in adverse cardiovascular effects.”

In 2019, the American Heart Association released guidelines for primary prevention of cardiovascular disease, which included inflammatory diseases such as arthritis and lupus as risk-increasing factors for cardiovascular disease. This study contributes to the understanding of the impact of inflammatory diseases on cardiovascular health.

“The main takeaway from our results is that more severe forms of asthma are associated with more cardiovascular disease and cardiovascular events,” said Tattersall. “Treating cardiovascular risk factors through lifestyle and behavioral modifications can be a powerful preventive tool for patients with more severe forms of asthma.”

Everyone can improve their cardiovascular health by following the American Heart Association’s Life’s Essential 8: healthy eating, physical activity, not smoking, getting enough sleep, maintaining a healthy weight, and controlling cholesterol, blood sugar, and blood pressure. According to the American Heart Association, cardiovascular disease kills more people in the United States each year than all forms of cancer and chronic lower respiratory tract disease combined.

The main limitation of the study is that it is an observational study as it is a data analysis. Therefore, the results suggest an association between asthma and an increased risk of cardiovascular disease, not cause and effect.

Co-authors are Alison S. Dasiewicz, MS; Robyn L. McClelland, Ph.D.; Nizar N Jarjour, MD; Claudia E. Korcarz, DVM; Carol C. Mitchell, Ph.D.; Stephane Esnault, Ph.D.; Moyses Szklo, MD, MPH; and James H. Stein, MD, FAHA.

The study was supported by a Peer Development Award from the American Heart Association.

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