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Transthyretin (TTR) Cardiac Amyloidosis
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Several types of amyloid can infiltrate the heart resulting in progressive diastolic and systolic dysfunction, congestive heart failure, and death. Treatment of cardiac amyloidosis is dictated by the amyloid type and degree of involvement. Consequently, early recognition and accurate classification are essential. The diagnosis of amyloidosis requires histologic identification of amyloid deposits.
Congo Red staining renders amyloid deposits salmon pink by light microscopy, and a characteristic apple green birefringence under polarized light conditions Figure 1. Additional immunohistochemical staining for precursor proteins identifies the type of amyloidosis Figure 2. Congo Red staining of myocardial tissue from a patient with amyloid cardiomyopathy. A Light microscopy, and B polarized light microscopy, X magnification. Endomyocardial biopsies were stained with antibodies to a kappa light-chain, b lambda lightchain, c Serum amyloid A, and d TTR amyloid.
Bright light micrographs at X magnification. Two types of amyloid commonly infiltrate the heart: a immunoglobulin light-chain AL or primary systemic amyloid, and b transthyretin TTR amyloid. Transthyretin-related amyloidoses, in turn, encompass two forms of disease — familial disease arising from misfolding of a mutated or variant transthyretin familial amyloid cardiomyopathy FAC or familial amyloidotic polyneuropathy FAP , and a sporadic, non-genetic disease due to misaggregation of wild-type transthyretin senile systemic amyloidosis SSA.
Cardiac amyloidosis can also be caused by other precursor proteins such as Apoliporotein A1, but the prevalence of disease is low and beyond the scope of this review.