Vyndamax

Patient has documented cardiac disease due to wild-type or hereditary TTR-mediated amyloidosis cardiomyopathy (ATTR-CM)
i) Documented wild-type ATTR-CM consists of all of the following:
• absence of a variant TTR genotype;
• evidence of cardiac involvement by echocardiography with end-diastolic interventricular septal wall thickness >12 mm;
• positive findings on technetium-99m pyrophosphate (Tc-99m-PYP) scintigraphy with single-photon emission computed tomography (SPECT) scanning
OR
• presence of amyloid deposits in biopsy tissue¹ (fat aspirate, salivary gland, median nerve connection tissue sheath, or cardiac) and TTR precursor protein identification by immunohistochemistry, scintigraphy, or mass spectrometry.

ii) Documented hereditary ATTR-CM consists of all of the following:
• presence of a variant TTR genotype associated with cardiomyopathy and presenting with a cardiomyopathy phenotype;
• evidence of cardiac involvement by echocardiography with end-diastolic interventricular septal wall thickness greater than12 mm;
• positive findings on Tc-99m-PYP scintigraphy with SPECT scanning OR presence of amyloid deposits in biopsy tissue¹ (fat aspirate, salivary gland, median nerve connective tissue sheath, or cardiac) 

Patient with New York heart Association (NYHA) class I to III 

History of heart failure, defined as at least one prior hospitalization for heart failure or clinical evidence of heart failure that required treatment with a diuretic. 

Request is from a prescriber with experience in the diagnosis and management of ATTR-CM.