Imaging-based Indentification of Premature Ventricular Contraction-mediated

室性早搏(PVC)介导的心肌病的原因尚不清楚。 据估计，在普通人群中，PVCS的患病率很高，据报道，有40%-75%的人 动态监测。PVC通常被认为是良性的，但可能与 猝死或与胸痛、晕厥或心力衰竭相关的风险增加 尤其是当出现结构性心脏病时。慢性阻塞性肺疾病患者的长期研究 低聚氯乙烯负荷对小鼠存活率无明显影响。然而，高聚氯乙烯负担与 有或无结构性疾病患者的左心功能降低。不幸的是， 通过消融或抗心律失常药物抑制室性早搏并不总是能改善室性 在病人身上起作用。动物模型已经表明，双胞胎在心尖附近走动可以 诱发心肌病，这种病是可逆的，不会引起心肌结构的改变。然而， 这些模型并不能解释某些受试者缺乏心肌病的原因。 有频繁的静脉曲张，如二重婚。我们认为，频繁的病理性门静脉癌变导致门静脉高压症-- 正常心脏诱发的心肌病和聚氯乙烯加重的心肌病 异常的组织特征。病理性PVCs与良性PVCs可以通过LV来判断 使用先进的实时心动图定量评估心内直视手术期间的功能 磁共振成像(MRI)技术。室性心动过速时的左心室功能可能是由于 包括聚氯乙烯起始点、耦合间隔和传导时间在内的综合因素 通过心肌。与心肌的组织特征一起，通过 心脏MRI和电解剖电压标测，这项建议试图确定血流动力学 和结构特征在PVC诱导或加重心肌病中的作用 接受治疗的病人。

The cause of premature ventricular contraction (PVC)-mediated cardiomyopathy is unknown. The estimated prevalence of PVCs is high in the general population with reported 40-75% on ambulatory monitoring. PVCs are often considered benign, but may be associated with increased risk of sudden death or associated with chest pain, syncope, or heart failure, especially when structural heart disease is present. A long-term study on patients with relatively low PVC burden showed no difference in survival. However, high PVC burden is associated with lower left ventricular function in patients with and without structural disease. Unfortunately, suppressing PVCs by ablation or antiarrhythmic medications do not always improve ventricular function in patients. Animal models have showed that bigeminy pacing near the apex could induce a cardiomyopathy that is reversible without myocardial structural changes. However, these models do not explain the lack of cardiomyopathy development in some human subjects with frequent PVCs such as bigeminy. We propose that frequent pathologic PVCs lead to PVC- induced cardiomyopathy in normal hearts and PVC-worsened cardiomyopathy in hearts with abnormal tissue characteristics. The pathologic versus benign PVCs can be determined by LV function during PVC, which is quantitatively assessed using advanced real-time cardiac magnetic resonance imaging (MRI) techniques. LV function during PVC is likely a result of a combination of factors including PVC site of origin, coupling interval, and conduction time through the myocardium. Together with tissue characterization of the ventricular myocardium by cardiac MRI and electroanatomic voltage mapping, this proposal seeks to identify hemodynamic and structural features in PVC-induced or worsened cardiomyopathy in order to better select patients for treatment.