Objective: Cardiac amyloidosis (CA) is an infiltrative disorder caused by deposition of amyloid fibrils in the myocardial extracellular matrix. Although there is a wide scientific literature regarding amyloid heart disease, no data about aortic viscoelastic properties in these patients are available. This studio has the aims to start filling this gap.Design and method: 113 outpatients attending the Pavia Amyloid Center either with suspected or already diagnosed amyloidosis were enrolled; 58 of them were affected by cardiac amyloidosis. Arterial applanation tonometry (PulsePen, DiaTecne, Milan, Italy) was performed in carotid and femoral arteries to calculate carotid-to-femoral pulse wave velocity (PWV) as index of aortic stiffness. Carotid pressure wave was calibrated with oscillometric brachial blood pressure (BP) to obtain central BP, pulse pressure amplification (PPA) and augmentation index (AIx). Tonometric data were related to biochemical parameters, clinical data and treatment. Populations with and without cardiac involvement (NCA) were compared. Results: Carotid-femoral PWV was not significantly higher in CA subjects compared to NCA (p = 0.462). PPA was significantly reduced in subjects with CA (26.9 ± 10.6% in NCA, 19.8 ± 12.4% in CA, p = 0.0014). Multivariate Regression Analysis highlighted that the presence of cardiac involvement is the main element in determining a reduction in PPA. CA subjects had lower both peripheral pressure values and central ones. There were no significant differences in central pulse pressure (42.6 ± 12.3 in NCA vs 39.5 ± 12.6 mmHg in CA, p = 0.187), and AIx. The morphological analysis of the central pulse wave in its components (direct and reflected wave) did not show significant differences in the parameters studied, with the exception of Ti, detecting an early wave overlap in CA. Conclusions: Although there were no significant differences in aortic stiffness evaluated by PWV in subjects with CA, a reduced PPA was found. An altered electromechanical cardio-aortic connection, with preserved aortic properties, may be an explanation for this finding. In other words, amyloid cardiopathy strongly impairs cardiac function without significantly alteration in aortic function. Significantly reduced central and peripheral pressure values could be caused by the inability of the diseased heart to develop a post load compared to that of subjects without cardiac involvement.