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Hyaluronan (HA), a primary component of the extracellular matrix, is associated with several cardiovascular diseases. However, its precise cardiac origin and role in atrial fibrillation (AF) remain unclear. We investigated chamber-specific HA levels in patients with paroxysmal AF (PAF) or persistent AF (PSAF). The levels of HA, a diacron-reactive oxygen metabolite (dROM) as a marker for oxidative stress, at different cardiac sites, and peripheral brain natriuretic peptide (BNP) levels were measured in patients with PAF (n = 50) or PSAF (n = 35). HA levels in the coronary sinus (CS-HA) were significantly higher than those other sites, in both PAF and PSAF patients, and CS-HA levels were significantly higher in PSAF patients than in PAF patients [37.1 (interquartile range, 31.2–48.3) vs. 30.6 (23.7–40.2) pg/mL, P

Atrial fibrillation (AF) is associated with oxidative stress and elevated brain natriuretic peptide (BNP) levels. However, the exact cardiac origin of oxidative stress and its association with BNP levels in AF patients remain unclear. Therefore, we investigated the chamber-specific plasma oxidative stress levels in patients with paroxysmal AF (PAF) and persistent AF (PSAF). Diacron-reactive oxygen metabolite (dROM) levels were measured in patients with PAF (n = 50) and PSAF (n = 35) at different cardiac sites before ablation and in peripheral vein 3 months after ablation. For all sites, dROM levels were higher in PSAF patients than in PAF patients; the levels were the highest in the coronary sinus at 429.0 (interquartile range: 392.0-449.0) vs. 374.0 (357.0-397.8) Carratelli units (P < 0.05). dROM levels in the coronary sinus were related to the BNP levels (r = 0.436, P < 0.001). Furthermore, the reduction in the peripheral dROM levels was related to that in the peripheral BNP levels in patients with symptomatic improvement (r = 0.473, P < 0.001). Cardiac oxidative stress may either be a cause or consequence of prolonged AF, and cardiac oxidative stress levels correlated with BNP levels, though a possible source of oxidative stress in AF patients may be systemic circulation.