Animal models of pulmonary hypertension and hypoxia provide evidence of right atrial remodeling in atrial fibrillationNew Research Methods Help Identify Heart Issues Linked to Lung Pressure

Chronic hypoxia increases pulmonary vascular resistance and pulmonary arterial pressure through pulmonary vasoconstriction and structural remodeling, subsequently elevating right ventricular afterload, tricuspid regurgitation, and right atrial pressure-volume load, thereby promoting right atrial dilation, fibrosis, and electrophysiological heterogeneity. Current clinical and experimental studies support associations between pulmonary hypertension (PH) and right heart loading with right atrial (RA) remodeling and increased susceptibility to atrial arrhythmias. However, the claims that “the RA is abnormal,” “the RA has greater pro-arrhythmic advantage than the left atrium (LA),” and “the RA contributes to arrhythmia maintenance” belong to different levels of evidence and cannot substitute for one another. This article employs a structured narrative review approach, focusing on comparative analysis of hypoxia-related models including chronic sustained hypoxia (CSH), chronic intermittent hypoxia (CIH), SU5416 combined with hypoxia (SuHx), and Tsk+/− under hypoxia, while using monocrotaline (MCT) and pulmonary artery banding (PAB) as reference models representing non-hypoxia-specific mechanisms of PH and right heart loading. We propose an unvalidated three-tier methodological framework that categorizes evidence into RA involvement, RA-dominant arrhythmogenic substrate for AF, and RA-dominant contribution to arrhythmia maintenance, applying the “principle of minimal sufficient evidence” to limit extrapolation of conclusions. Supplementary evidence evaluation reveals that direct evidence regarding RA in MCT-induced right heart disease models is more extensive than previously summarized; SuHx has existing studies directly assessing RA remodeling and AF susceptibility, but evidence remains insufficient regarding biatrial regional dominance and maintenance-phase drivers; CIH has multiple studies supporting atrial structural and electrical remodeling and increased AF susceptibility, though most do not provide RA-specific maintenance evidence; PAB primarily supports mechanical right heart loading-induced RA involvement. The article further distinguishes direct RA evidence from supportive evidence based on right heart loading and mechanistic extrapolation, and recommends future research enhance spatial mapping of both atria, precise localization during maintenance phase, co-localization of structural-electrical-molecular features, and systematic reporting of sex, age, and comorbid backgrounds to improve reproducibility and translational value of findings.