TTR protein clumps may help drive blood vessel damage in ATTR-CM

In people with transthyretin amyloid cardiomyopathy (ATTR-CM), the buildup of faulty transthyretin (TTR) protein in the heart may contribute to blood clots that block capillaries, the smallest blood vessels, and trigger molecular events that ultimately lead to heart damage, according to a new study.

The researchers’ proposed mechanism, based on detailed analyses of diseased heart tissue collected from two people with late-stage ATTR-CM who underwent a heart transplant, suggests that the disease may also be a microangiopathy — a condition affecting the body’s smallest blood vessels.