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Page 6 of 14 Porcari et al. Vessel Plus 2022;6:33 https://dx.doi.org/10.20517/2574-1209.2021.134

Figure 2. Atrial amyloidosis. Courtesy of Professor Rossana Bussani, MD, Institute of Pathological Anatomy and Histology, University of
Trieste, Italy. Congo Red staining revealed amyloid infiltration extending to interstitial space (blue arrows) and vessel walls (black
arrows) including the sinoatrial nodal artery. A focus at 40× (bottom left) shows a cardiomyocyte (green arrow) surrounded by amyloid
deposits. Scale bar, 500 μm.

drugs for neurohormonal antagonism should be started at a low dose and slowly up-titrated under close
monitoring of patients, particularly in AL-CA.

Along with anti-neurohormonal drugs, salt restriction (< 6 g/day) and diuretics are the mainstay of
supportive treatment in CA. Fluid overload might result from nephrotic syndrome with hypoalbuminemia
or concomitant therapies such as steroids in AL and diflunisal in ATTR. In the case of scarce response to
[23]
loop diuretics, MRAs are well tolerated . However, over-diuresis may lead to hypotension and acute
kidney injury, especially in patients with orthostatic hypotension and renal dysfunction with nephrotic
[29]
syndrome . Diminishing preload, these drugs may compromise an already fixed stroke volume, leading to
low cardiac output . Therefore, caution is required as the search for the optimal volume balance in CA is
[21]
challenged by a narrow therapeutic window.

Atrial fibrillation: rate control or rhythm control?
AF is the most frequent arrhythmia in CA (45%-70% of patients) [30,31] . It commonly leads to hemodynamic
deterioration in CA mainly because of fast and irregular heart rates compromising ventricular filling and
cardiac output and, to a lesser extent, the loss of atrial contractility. In advanced atrial infiltration, the atrial
contribution to diastolic filling might be irrelevant even in sinus rhythm. The management of AF is