BACKGROUND Left atrium (LA) physiology is influenced by changes in left ventricular (LV) performance and load. OBJECTIVES The purpose of this study was to define the effect of acute changes in LV loading conditions on LA physiology in subacute myocardial infarction (MI). METHODS MI was percutaneously induced in 19 Yorkshire pigs. One to 2 weeks after MI, 14 pigs underwent acute LV unloading using a percutaneous LV assist device, Impella. The remaining 5 pigs underwent acute LV loading by percutaneous induction of aortic regurgitation. A pressure-volume catheter was inserted into the LA using a percutaneous transseptal approach, and LA pressure-volume loops were continuously monitored. Atrial arrhythmia inducibility was examined by burst-pacing of the right atrium. Nicotinamide adenine dinucleotide phosphate oxidase (NOX) levels and ryanodine receptor phosphorylation were examined in LA tissues to study the potential effect of stretch-dependent oxidative stress. RESULTS MI resulted in reduced LV ejection fraction and increased LV end-diastolic pressure with concomitant increase in LA pressure and volumes. Acute LV unloading resulted in a reduction of LV end-diastolic pressure, which led to proportional decreases in mean LA pressure and maximum LA volume. LA pressure-volume loops exhibited a pump flow-dependent, left-downward shift. This was associated with reduced LA passive stiffness, suggesting the alleviation of the LA stretch that was present after MI. Prior to acute unloading of the LV, 71% of the pigs were arrhythmia-inducible; LV unloading reduced this to 29% (p = 0.02). Time to spontaneous termination of atrial arrhythmias was decreased from median 55 s (range 5 to 300 s) to 3 s (range 0 to 59 s). In contrast, acute LV loading with aortic regurgitation increased LA pressure without a significant effect on arrhythmogenicity. Molecular analysis of LA tissue revealed that NOX2 expression was increased after MI, whereas acute LV unloading reduced NOX2 levels and diminished ryanodine receptor phosphorylation. CONCLUSIONS Acute LV unloading relieves LA stretch and reduces atrial arrhythmogenicity in subacute MI.

中文翻译：

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急性左心室卸荷减少心房舒张并抑制房性心律失常

背景 左心房 (LA) 生理机能受左心室 (LV) 性能和负荷变化的影响。目的 本研究的目的是确定 LV 负荷条件的急性变化对亚急性心肌梗死 (MI) 中 LA 生理学的影响。方法 在 19 头约克夏猪中经皮诱导 MI。MI 后 1 至 2 周，14 头猪使用经皮 LV 辅助装置 Impella 进行了急性 LV 卸载。其余 5 头猪通过经皮诱导主动脉瓣反流进行急性 LV 负荷。使用经皮经中隔方法将压力容积导管插入 LA，并持续监测 LA 压力容积环。通过右心房的突发起搏检查房性心律失常的可诱导性。在 LA 组织中检查了烟酰胺腺嘌呤二核苷酸磷酸氧化酶 (NOX) 水平和兰尼碱受体磷酸化，以研究拉伸依赖性氧化应激的潜在影响。结果 MI 导致 LV 射血分数降低和 LV 舒张末期压力增加，同时 LA 压力和容积增加。急性 LV 卸载导致 LV 舒张末期压力降低，导致平均 LA 压力和最大 LA 容积成比例降低。LA 压力-容积循环表现出依赖于泵流量的左下移。这与 LA 被动僵硬度降低有关，表明 MI 后存在的 LA 拉伸减轻。在 LV 急性卸载之前，71% 的猪可诱发心律失常；LV 卸载减少到 29% (p = 0.02)。房性心律失常自发终止的时间从中位数 55 秒（范围 5 至 300 秒）减少到 3 秒（范围 0 至 59 秒）。相反，伴有主动脉瓣关闭不全的急性 LV 负荷增加了 LA 压力，但对致心律失常没有显着影响。LA 组织的分子分析显示，MI 后 NOX2 表达增加，而急性 LV 卸载降低了 NOX2 水平并减少了兰尼碱受体磷酸化。结论 急性 LV 卸载可减轻 LA 牵张并降低亚急性 MI 中的房性心律失常性。LA 组织的分子分析显示，MI 后 NOX2 表达增加，而急性 LV 卸载降低了 NOX2 水平并减少了兰尼碱受体磷酸化。结论 急性 LV 卸载可减轻 LA 牵张并降低亚急性 MI 中的房性心律失常性。LA 组织的分子分析显示，MI 后 NOX2 表达增加，而急性 LV 卸载降低了 NOX2 水平并减少了兰尼碱受体磷酸化。结论 急性 LV 卸载可减轻 LA 牵张并降低亚急性 MI 中的房性心律失常性。