Patients with cardiac amyloidosis have a greater neurohormonal activation than those with non-amyloidotic heart failure
Giuseppe Vergaro, Alberto Aimo, Alessandro Campora, Vincenzo Castiglione, Concetta Prontera, Silvia Masotti, Veronica Musetti, Michela Chianca, Alessandro Valleggi, Valentina Spini, Michele Emdin, Claudio Passino
Abstract
Background Neurohormonal activation has never been investigated in patients with cardiac amyloidosis (CA).Methods Forty-seven patients with amyloid light-chain (AL)-CA and 61 with transthyretin (ATTR)-CA were matched to non-amyloidotic heart failure (HF) patients based on age, sex, left ventricular ejection fraction ranges, renal function and HF therapies. N-terminal pro-B-type natriuretic peptide (NT-proBNP), norepinephrine and renin were dosed. The primary and secondary endpoints were 1-year cardiovascular death or HF hospitalisation, and 5-year cardiovascular death, respectively.Results Patients with AL-CA had a 10-fold higher NT-proBNP than HF patients (6548 ng/L [2059–15,097] vs. 692 [243–2241], p < 0.001), and slightly higher norepinephrine (595 ng/L [383–869] vs. 416 [250–693], p = 0.047). Patients with ATTR-CA had higher NT-proBNP (3984 ng/L [2275–9505] vs. 1751 [470–4768], p = 0.006), norepinephrine (552 ng/L [344–855] vs. 441 [323–601], p = 0.020), and renin (14 mU/L [8–80] vs. 10 [4–34], p = 0.017). Patients with AL- or ATTR-CA had more often 2 or 3 neurohormones above the corresponding upper reference limits than matched HF patients. NT-proBNP and aldosterone were univariate predictors of the primary endpoint in patients with ATTR-CA, but not in matched controls. NT-proBNP and renin predicted the secondary endpoint in patients with AL-CA, but not in matched controls.Conclusions Patients with CA display a neurohormonal activation, with some prognostic significance.