AHA Scientific Sessions 2026 Abstract

Gene variant linked to heart changes without heart failure

Compared with noncarriers, people with one copy had 2.09 times the odds of reduced heart-pumping function; those with two copies had 11.03 times the odds.

A heart cutaway holds a large pool of blood beside smaller, more contracted chambers holding less, with blood cells scattered around them.

Our read

Biomarkers
Studied:
Genetic association study of 14,508 African-ancestry participants without heart failure (Dose-response)
What changed:
People with two copies had 11.03 times the odds of reduced heart-pumping function compared with noncarriers
The catch:
Other genetic differences between carriers and noncarriers could contribute to the heart-function association
In the record:
The 9th paper on CD36 with results in people; 131 on record in all.
Why it’s aging research:
It bears on staying healthy in midlife and later life.

Editor of record: Boris Djordjevic · AgingResearch.News

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Of 459,245 participants without heart failure in three population cohorts, 14,508 were of African ancestry. An observational analysis examined the CD36 Y325* gene variant in the African-ancestry participants. CD36 encodes a protein involved in the heart’s uptake of fatty acids for energy.

Carriers had higher odds of an ejection fraction below 50%: the heart’s main pumping chamber expelled less than half its blood per beat. The association was stronger with two copies than with one. Carriers also had higher blood levels of ketone bodies, an alternative fuel, and lower levels of CD36 protein. Blood markers of heart muscle stretch and injury were not elevated. Carriers of another genetic cause of heart muscle disease also showed a link to reduced pumping function, but had a different blood-marker pattern.

Why it matters

Heart failure is an age-related disease. The authors suggest that the distinct profile may help identify risk earlier and implicates disrupted energy use in heart muscle.

Caveats

Other genetic or health differences between carriers and noncarriers could have contributed to the observed associations with heart function and blood markers. The CD36 analysis covered participants of African ancestry without heart failure, and the findings were reported in a conference abstract.

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