VALVE DISEASES IN CARDIAC AMYLOIDOSIS: WHAT WE HAVE TO KNOW

Cardiac amyloidosis (CA) is an infiltrative cardiomyopathy caused by extracellular deposition of amyloid fibrils, most commonly derived from immunoglobulin light chains (AL) or transthyretin (ATTR). While myocardial involvement has been extensively characterized, valvular disease in CA has received comparatively less attention, despite its frequent occurrence and significant clinical impact. Aortic stenosis (AS) represents the most prevalent valvular manifestation, particularly in wild-type ATTR amyloidosis, where shared demographic and pathophysiological factors contribute to a frequent overlap. Concomitant CA and AS create a synergistic interaction, leading to disproportionate ventricular dysfunction, a high prevalence of the low-flow low-gradient phenotype and increased perioperative risk. Echocardiographic strain analysis, dedicated scoring systems and advanced imaging such as cardiac magnetic resonance and computed tomography allow earlier recognition of this association and aid in patient stratification. Mitral and tricuspid regurgitation, usually functional and related to atrial enlargement, annular dilatation and restrictive physiology, are also common in CA and carry important prognostic implications. Severe regurgitation is associated with heart failure progression, systemic congestion and increased mortality. Although surgical approaches are rarely feasible, transcatheter interventions (TAVR, TEER and emerging tricuspid devices) offer promising therapeutic alternatives in selected patients. Management of valvular disease in CA must therefore integrate interventional options with disease-modifying therapies targeting amyloid deposition, such as TTR stabilizers and silencers, to optimize outcomes. Thus, considering the valves involvement in patients with CA, the aim of this review was to illustrate the main valvular alterations in CA, their prognostic role and their treatment.