Furthermore, Hein et al. demonstrated that the plasma of healthy individuals or patients with hereditary transthyretin amyloidosis with polyneuropathy promotes hypertrophy of neonatal rat cardiomyocytes induced by phenylephrine, while the plasma of patients with hereditary transthyretin cardiac amyloidosis or wild-type ATTR cardiac amyloidosis attenuated the hypertrophic response in vitro. Here, TTR is linked to cardiac amyloidosis.