Researchers have disclosed the effects of transthyretin protein levels on heart disease risk.
A team of physician-scientists from the University of Alabama at Birmingham’s Marnix E. Heersink School of Medicine has made important discoveries about how transthyretin, commonly referred to as TTR, protein levels influence the risk of heart disease. Their study, published in Nature Communications, examines the relationship between variations in TTR levels and negative clinical outcomes, shedding light on new strategies for preventing and treating amyloid heart disease. Transthyretin is a liver-produced transport protein, and its misfolding can contribute to cardiac amyloidosis, a serious condition that can lead to heart failure and increased mortality rates.
The research, directed by Pankaj Arora, M.D., and Naman Shetty, M.D., analyzed data from 35,206 individuals in the UK Biobank. The team looked into the clinical relationships of TTR levels, variations in TTR caused by genetic factors, and the impact of TTR levels on health outcomes.
Arora and colleagues discovered that lower TTR levels were notably linked to a heightened risk of heart failure and increased overall mortality. Specifically, those with low TTR levels had a 17 percent greater risk of heart failure and an 18 percent higher risk of death from any cause compared to individuals with elevated TTR levels. This risk was more pronounced among those who possessed the V142I TTR gene variant, known to compromise the stability of the TTR protein.
The research indicated that TTR levels tend to be lower in women than in men and are affected by various health factors. Increased systolic and diastolic blood pressure, total cholesterol, albumin, triglycerides, and creatinine levels were related to higher TTR levels. Conversely, higher levels of C-reactive protein were associated with lower TTR levels. Notably, individuals with the V142I TTR gene variant had significantly reduced TTR levels in comparison to non-carriers, highlighting the gene’s role in influencing this protein.
“Our study emphasizes the vital importance of TTR levels in assessing heart disease risk,” said Arora. “By gaining insights into the factors affecting TTR levels, we can more effectively identify at-risk individuals and develop precise interventions to avert negative health outcomes.”
“These results stress the potential advantages of including TTR level measurements in screening initiatives, particularly for those with a genetic likelihood,” added Shetty.
Arora, who is also a cardiologist at the UAB Cardiovascular Institute, believes the implications of this study are extensive. It suggests that monitoring TTR levels could serve as a crucial strategy in managing heart disease risk, especially for individuals with known genetic variations like the V142I TTR variant. Low TTR levels can elevate the likelihood of a positive genetic test for the V142I variant, which may require significant processing time.
“This information can aid in counseling family members while they wait for genetic testing results,” remarked Arora. “This research represents a major advance in our efforts to understand and reduce the risks associated with cardiac amyloidosis and other heart-related conditions.”
