Researchers at UT Southwestern Medical Center have identified 18 proteins in blood samples that are associated with both heart failure and frailty, two conditions often seen in older adults.
This discovery, published in JAMA Cardiology, could pave the way for new methods to predict, prevent, or treat these interconnected health issues.
The study, led by Dr. Amil Shah, a professor of internal medicine and public health, highlights the shared biological pathways between heart failure and frailty. This suggests that treatments targeting one condition might also alleviate the other.
“Our findings support shared biological pathways underlying both heart failure and frailty, suggesting interventions to prevent or treat one outcome may help decrease the burden of the other,” Dr. Shah explained.
As the global population ages, heart failure and frailty are becoming more common, particularly among people in their seventies and older. Heart failure occurs when the heart can’t pump enough blood to meet the body’s needs, leading to symptoms like shortness of breath and fatigue.
Frailty, on the other hand, involves a general decline in physical function, often marked by unintentional weight loss, exhaustion, and reduced activity levels. These conditions frequently coexist, with frailty affecting up to half of those with heart failure, and vice versa.
The link between inflammation and these conditions has been suggested before, but the exact molecular pathways were unclear. To investigate, Dr. Shah and his colleagues used data from the Atherosclerosis Risk in Communities (ARIC) study, a long-term study that started in the late 1980s.
This study includes participants from North Carolina, Mississippi, Minnesota, and Maryland and has expanded over the years to cover various health assessments, including frailty.
The researchers analyzed medical records and blood samples from 10,630 ARIC participants to identify those hospitalized for heart failure. By comparing nearly 5,000 proteins in the blood samples of those with and without heart failure, they identified 83 proteins associated with heart failure.
They then focused on those who developed frailty in later life, narrowing down the list to 18 proteins linked to both conditions. These findings were validated with data from another study, the Cardiovascular Health Study, involving 3,189 participants.
Several of the 18 proteins are known to play roles in inflammation, which is a common factor in both heart failure and frailty. Other proteins are involved in fibrosis (the thickening and scarring of tissue), lipid metabolism, and cell death. Further genetic analysis suggested that five of these proteins might directly cause both conditions.
Dr. Shah noted that future research will explore how these proteins contribute to or result from heart failure and frailty. Understanding these mechanisms could lead to the development of drugs that prevent or treat both conditions simultaneously.
The study involved multiple contributors from UT Southwestern, including first author Dr. Diego Ramonfaur and data scientist Dr. Victoria Lamberson. Their work represents a significant step towards better understanding and managing the dual burdens of heart failure and frailty in aging populations.
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The research findings can be found in JAMA Cardiology.
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