Heart Amyloid Drug Tafamidis Linked to Healthier Blood Vessel Cells

The study combines two kinds of evidence. Most of it is laboratory work on human umbilical vein endothelial cells, which are lab-grown cells of the kind that line blood vessels. A smaller part is a longitudinal check of arterial stiffness in patients. It is not a randomised trial.

The disease is transthyretin cardiac amyloidosis, or ATTR-CM. In it, the protein transthyretin (TTR) misfolds and damages the heart. The study looked at two forms: the wild-type form (ATTRwt-CM) and the hereditary form (ATTRv-CM). Until now, the authors write, the effects of these forms on blood vessels, and the effect of tafamidis on them, have been unclear.

The team applied serum, the liquid part of blood, from patients to the cells. Samples were taken before treatment and six months after starting tafamidis. Serum from elderly and young people without the disease served as controls. The researchers then measured cell survival, movement and stress responses. They also profiled inflammatory signals and proteins in the serum.

According to the paper, serum from patients with either form reduced the survival and movement of the cells. It also caused proteotoxic stress, meaning strain on the cell's systems for handling and clearing proteins, and oxidative stress, a form of chemical damage. The serum showed inflammation-related signatures. All of these effects were attenuated when cells were exposed to serum taken after tafamidis treatment.

Purified, recombinant TTR also caused proteotoxic stress in the cells. Tafamidis added alongside it reduced that stress, within a concentration the authors call a safety range of up to 16 micromolar. This suggests the protein itself can be toxic to these cells.

The study also looked at people. Pulse wave velocity, a measure of arterial stiffness, was followed over time in patients with the wild-type form before and after tafamidis, and in elderly controls. It was lower in treated patients than in controls. The change tracked with higher serum transthyretin and lower proteasome activity in white blood cells. The proteasome is the cell's protein-disposal machinery.

The authors conclude that tafamidis may have protective vascular effects beyond stabilising transthyretin in the heart muscle. That is an interpretation, not a proven result. Umbilical vein cells are not aged human arteries. Serum exposure in a dish is not the same as what happens in the body.

The findings also differ in kind from The Arising's October 15 report on brown fat scans, which described an association in about 100,000 patients.

What to watch next

What to watch next is whether larger studies in patients confirm the drop in arterial stiffness and show whether it changes outcomes such as strokes or heart events.

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