TRANSTHYRETIN cardiac amyloidosis (ATTR-CA) is a significant but under-recognised cause of heart failure in older Black individuals, affecting as many as 17% of Black men over the age of 75 according to new research. The condition is much less common in Hispanic patients, and about half of cases in older Black individuals arise in those with a normal TTR gene, highlighting the need for improved diagnostic strategies.
ATTR-CA is a progressive heart disease caused by abnormal deposits of the transthyretin protein in heart tissue, leading to heart failure and symptoms such as breathlessness and fatigue. The protein can become abnormal due to inherited changes in the TTR gene (the most common variant being V142I) or can arise spontaneously in older age. The SCAN-MP study enrolled 646 adults aged over 60 with heart failure, focusing on those with increased heart wall thickness who identified as Black or Caribbean Hispanic. Diagnostic scanning with nuclear imaging and genetic blood tests confirmed ATTR-CA in 6.7% of the total cohort, with overall rates higher in Black people (7.8%) than Hispanic participants (2.2 %). Prevalence rose sharply with age, reaching 17.2% in Black men older than 75. Of those with the V142I genetic variant, 52.8% developed hereditary ATTR-CA. However, most cases in this age group occurred in those without the variant, showing that genotype alone is not enough for effective screening.
These findings show that ATTR-CA is an important, treatable cause of heart failure among older Black men, and highlights the need to broaden screening approaches beyond genetic testing alone. With new disease-specific therapies now available, clinicians should have a low threshold to consider ATTR-CA in any older Black patient with heart failure and increased cardiac wall thickness. Early identification can improve outcomes, provide targeted treatment, and address long-standing disparities in care.
Reference
Ruberg FL et al. Transthyretin cardiac amyloidosis in older black and Hispanic individuals with heart failure. JAMA Cardiol. 2025;DOI:10.1001/jamacardio.2025.2948.
