Frequent Premature Atrial Contractions Lead to Adverse Atrial Remodeling and Atrial Fibrillation in a Swine Model.
Frequent Premature Atrial Contractions Lead to Adverse Atrial Remodeling and Atrial Fibrillation in a Swine Model.
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在猪模型中，频繁的心房过早收缩会导致不良的心房重塑和心房颤动。
DOI：
10.1161/circulationaha.123.065874
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发表时间：
2024
期刊：
影响因子：
37.8
通讯作者：
Gerstenfeld,EdwardP
中科院分区：
文献类型：
--
作者：
Higuchi,Satoshi;Voskoboinik,Aleksandr;Im,SungIl;Lee,Adam;Olgin,Jeffrey;Arbil,Ayla;Afzal,Junaid;Marcus,GregoryM;Stillson,Carol;Bibby,Dwight;Abraham,Theodore;Wilson,Emily;Gerstenfeld,EdwardP
研究背景频发的房性早搏(PAC)与未来发生的房颤(房颤)有关，但PAC是否通过不良的心房重构参与房颤的发生尚未有研究。本研究旨在探讨不同部位频繁PAC对猪心房重构的影响。方法对40只猪进行基础电生理和超声心动图检查，然后植入起搏器，并以250ms的耦合间隔(50%负荷)起搏16周：(1)左心房外侧冠状静脉窦旁PAC(Lat-PAC；n=10)；(2)房间隔间PAC(Sep-PAC；n=10)；(3)常规LA起搏130次/min(REG-130；n=10)；(4)对照组(n=10)。结果与SEP-PAC组和对照组相比，SLAT-PAC组P波持续时间(93.00±9.0vs74.2±8.2ms；P<；0.001)和超声心动图机械不同步程度(57.5士11.6vs.35.7±13.0和24.4±11.1ms；P<；0.001)明显延长。16周后，LAT-PAC组房室传导速度减慢(1·1±0·2比1·3±0·2[SEP-PAC]比1·3±0·1[REG-130]比1·5±0·2[对照组]m/S；P<；0.001)，但无明显变化。Lat-PAC组肝纤维化百分率显著增加，细胞外基质蛋白(赖氨酸氧化酶和1、8胶原蛋白)、转化生长因子-β1(转化生长因子-β1)信号蛋白(潜伏期和单体转化生长因子-Smad1和磷酸化/总Smad2/3比值上调；P<；0.05)。LAT-PAC组有最长的可诱发房颤持续时间(终末至基线：131秒[四分位范围30,192]秒对16[6，26]秒[SEP-PAC]对22[11，]秒[REG-130]对−1[−16，7]秒[对照]；P<；0.001)。与间隔起源的PAC相比，起源于LA外侧的PAC可产生更大的心房重构和更长的房颤持续时间。这些数据提供的证据表明，频繁的PAC可导致不良的心房重构和房颤，并且异位PAC的位置可能具有临床意义。
BACKGROUNDFrequent premature atrial complexes (PACs) are associated with future incident atrial fibrillation (AF), but whether PACs contribute to development of AF through adverse atrial remodeling has not been studied. This study aimed to explore the effect of frequent PACs from different sites on atrial remodeling in a swine model.METHODSForty swine underwent baseline electrophysiologic studies and echocardiography followed by pacemaker implantations and paced PACs (50% burden) at 250-ms coupling intervals for 16 weeks in 4 groups: (1) lateral left atrium (LA) PACs by the coronary sinus (Lat-PAC; n=10), (2) interatrial septal PACs (Sep-PAC; n=10), (3) regular LA pacing at 130 beats/min (Reg-130; n=10), and (4) controls without PACs (n=10). At the final study, repeat studies were performed, followed by tissue histology and molecular analyses focusing on fibrotic pathways.RESULTSLat-PACs were associated with a longer P-wave duration (93.0±9.0 versus 74.2±8.2 and 58.8±7.6 ms;P<0.001) and greater echocardiographic mechanical dyssynchrony (57.5±11.6 versus 35.7±13.0 and 24.4±11.1 ms;P<0.001) compared with Sep-PACs and controls, respectively. After 16 weeks, Lat-PACs led to slower LA conduction velocity (1.1±0.2 versus 1.3±0.2 [Sep-PAC] versus 1.3±0.1 [Reg-130] versus 1.5±0.2 [controls] m/s;P<0.001) without significant change in atrial ERP. The Lat-PAC group had a significantly increased percentage of LA fibrosis and upregulated levels of extracellular matrix proteins (lysyl oxidase and collagen 1 and 8), as well as TGF-β1 (transforming growth factor–β1) signaling proteins (latent and monomer TGF-β1 and phosphorylation/total ratio of SMAD2/3;P<0.05). The Lat-PAC group had the longest inducible AF duration (terminal to baseline: 131 [interquartile range 30, 192] seconds versus 16 [6, 26] seconds [Sep-PAC] versus 22 [11, 64] seconds [Reg-130] versus −1 [−16, 7] seconds [controls];P<0.001).CONCLUSIONSIn this swine model, frequent PACs resulted in adverse atrial structural remodeling with a heightened propensity to AF. PACs originating from the lateral LA produced greater atrial remodeling and longer induced AF duration than the septal-origin PACs. These data provide evidence that frequent PACs can cause adverse atrial remodeling as well as AF, and that the location of ectopic PACs may be clinically meaningful.
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1985
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