Department of Cardiology, Royal Melbourne Hospital, Melbourne 3050, Australia.
Department of Medicine and Physiology, The University of Melbourne, Melbourne, Australia.
Europace. 2021 May 21;23(5):691-700. doi: 10.1093/europace/euaa275.
Obstructive sleep apnoea (OSA) associates with atrial fibrillation (AF), but the relationship of OSA severity and AF phenotype with the atrial substrate remains poorly defined. We sought to define the atrial substrate across the spectrum of OSA severity utilizing high-density mapping.
Sixty-six consecutive patients (male 71%, age 61 ± 9) having AF ablation (paroxysmal AF 36, persistent AF 30) were recruited. All patents underwent formal overnight polysomnography and high-density left atrial (LA) mapping (mean 2351 ± 1244 points) in paced rhythm. Apnoea-hypopnoea index (AHI) (mean 21 ± 18) associated with lower voltage (-0.34, P = 0.005), increased complex points (r = 0.43, P < 0.001), more low-voltage areas (r = 0.42, P < 0.001), and greater voltage heterogeneity (r = 0.39, P = 0.001), and persisted after multivariable adjustment. Atrial conduction heterogeneity (r = 0.24, P = 0.025) but not conduction velocity (r = -0.09, P = 0.50) associated with AHI. Patchy regions of low voltage that co-localized with slowed conduction defined the atrial substrate in paroxysmal AF, while a diffuse atrial substrate predominated in persistent AF. The association of AHI with remodelling was most apparent among paroxysmal AF [LA voltage: paroxysmal AF -0.015 (-0.025, -0.005), P = 0.004 vs. persistent AF -0.006 (-0.017, 0.005), P = 0.30]. Furthermore, in paroxysmal AF an AHI ≥ 30 defined a threshold at which atrial remodelling became most evident (nil-mild vs. moderate vs. severe: 1.92 ± 0.42 mV vs. 1.84 ± 0.28 mV vs. 1.34 ± 0.41 mV, P = 0.006). In contrast, significant remodelling was observed across all OSA categories in persistent AF (1.67 ± 0.55 mV vs. 1.50 ± 0.66 mV vs. 1.55 ± 0.67 mV, P = 0.82).
High-density mapping observed that OSA associates with marked atrial remodelling, predominantly among paroxysmal AF cohorts with severe OSA. This may facilitate the identification of AF patients that stand to derive the greatest benefit from OSA management.
阻塞性睡眠呼吸暂停（OSA）与心房颤动（AF）相关，但 OSA 严重程度和 AF 表型与心房基质的关系仍未得到明确界定。我们试图利用高密度标测来定义整个 OSA 严重程度范围内的心房基质。
连续招募了 66 例接受 AF 消融的患者（男性占 71%，年龄 61±9 岁）（阵发性 AF36 例，持续性 AF30 例）。所有患者均接受了正式的过夜多导睡眠图和左心房（LA）高密度标测（平均 2351±1244 个点）。呼吸暂停-低通气指数（AHI）（平均 21±18）与较低的电压（-0.34，P=0.005）、更多的复杂点（r=0.43，P<0.001）、更多的低电压区域（r=0.42，P<0.001）和更大的电压异质性（r=0.39，P=0.001）相关，并在多变量调整后仍然存在。心房传导异质性（r=0.24，P=0.025）而非传导速度（r=-0.09，P=0.50）与 AHI 相关。与传导速度减慢共存的局灶性低电压区域定义了阵发性 AF 的心房基质，而弥漫性心房基质在持续性 AF 中占主导地位。AHI 与重塑的相关性在阵发性 AF 中最为明显[LA 电压：阵发性 AF-0.015（-0.025，-0.005），P=0.004 与持续性 AF-0.006（-0.017，0.005），P=0.30]。此外，在阵发性 AF 中，AHI≥30 定义了心房重塑变得最明显的阈值（无轻度 vs. 中度 vs. 重度：1.92±0.42 mV vs. 1.84±0.28 mV vs. 1.34±0.41 mV，P=0.006）。相比之下，在持续性 AF 中，所有 OSA 类别均观察到显著的重塑（1.67±0.55 mV vs. 1.50±0.66 mV vs. 1.55±0.67 mV，P=0.82）。
高密度标测观察到 OSA 与明显的心房重塑相关，主要发生在严重 OSA 的阵发性 AF 患者中。这可能有助于识别从 OSA 管理中获益最大的 AF 患者。
