J Am Heart Assoc. 2026 Sep 9:e052245. doi: 10.1161/JAHA.126.052245. Online ahead of print.
ABSTRACT
Functional tricuspid regurgitation has traditionally been attributed to right ventricular remodeling secondary to pulmonary hypertension or left-sided heart disease. However, contemporary imaging studies increasingly identify patients with significant tricuspid regurgitation despite preserved right ventricular geometry, characterized instead by marked right atrial (RA) enlargement and tricuspid annular dilation, most commonly in the setting of atrial fibrillation. This phenotype, termed atrial functional tricuspid regurgitation (AF-TR), is typically described as regurgitation caused by isolated annular dilation. However, this description focuses on the structural end point of disease rather than the underlying pathophysiological substrate. Emerging evidence suggests that AF-TR represents a valvular manifestation of RA failure, a right-sided extension of the broader atrial failure syndrome described for the left atrium. In this framework, atrial cardiomyopathy, characterized by atrial fibrosis, electrical instability, and impaired atrial mechanics, first produces dysfunction of RA reservoir, conduit, and contractile function. Progressive loss of atrial-annular coupling and chamber dilation subsequently destabilize tricuspid annular geometry, culminating in functional regurgitation despite preserved ventricular structure. In this review, we synthesize current evidence on the mechanistic relationship between RA cardiomyopathy, RA failure, and AF-TR. We examine the epidemiology and clinical phenotypes of AF-TR, discuss diagnostic approaches emphasizing RA structure and mechanics, use pacing-induced tricuspid dysfunction as an iatrogenic model to illustrate the mechanisms linking atrial failure to AF-TR, and review therapeutic strategies targeting both the atrial substrate and its valvular consequences.
PMID:42714426 | DOI:10.1161/JAHA.126.052245