Key result
BNP was elevated in 76% of patients with familial amyloidotic polyneuropathy and correlated significantly with interventricular septal thickness, whereas troponin T and I were rarely abnormal.
Why the study?
Do troponin T, troponin I, and BNP detect cardiomyopathy in patients with familial amyloidotic polyneuropathy?
Population
29 patients evaluated for familial amyloidotic polyneuropathy (FAP) at a tertiary referral centre
Design
Cohort
Authors
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May inform BNP-based screening for cardiomyopathy in FAP; leaves open prognostic utility versus imaging in prospective studies.
Observational (n=29)
No
Do troponin T, troponin I, and BNP detect cardiomyopathy in patients with familial amyloidotic polyneuropathy?
BNP is a sensitive marker for detecting cardiomyopathy in familial amyloidotic polyneuropathy, whereas troponins are less frequently elevated, suggesting transthyretin amyloid is less directly toxic to myocytes than AL amyloid.
Suhr et al. (2007) conducted an observational in Familial amyloidotic polyneuropathy (FAP) (n=29). Measurement of Troponin T, Troponin I, and BNP was evaluated on Markers for myocardial damage and failure (Troponin T, Troponin I, and BNP). BNP was elevated in 76% of patients with familial amyloidotic polyneuropathy and correlated significantly with interventricular septal thickness, whereas troponin T and I were rarely abnormal.
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