Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis
Activation delay after premature stimulation in chronically diseased human myocardium relates to the architecture of interstitial fibrosis
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DOI：
10.1161/hc5001.100833
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发表时间：
2001-12-18
期刊：
影响因子：
37.8
通讯作者：
de Bakker, JMT
中科院分区：
文献类型：
--
作者：
Kawara, T;Derksen, R;de Bakker, JMT
背景-在长耦合间隔的过早刺激中开始的进行性激活延迟已被证明与肥厚性心肌病患者的心源性猝死相关。本研究的目的是阐明慢性病变心肌激活延迟增加的机制。方法和结果：在I I移植的人类心脏进行过早刺激时，对心外膜电活动进行高分辨率单极测绘（105、208或247个记录点，电极间距分别为0.8、0.5或0.3 mm）。这些心脏来自接受心脏移植并处于心力衰竭终末期的患者（冠状动脉疾病4例；肥厚性心肌病1例；扩张性心肌病6例）。8颗心脏进行了朗根多夫熔接。从剩余的心脏中取出心外膜，在组织浴中进行研究。构建激活图和传导曲线，并与组织学相关联。显示激活延迟显著增加的传导曲线与具有长纤维链的致密斑片状纤维化区相关。致密、弥漫性纤维化伴短纤维链仅轻微影响传导曲线。斑块性纤维化区传导曲线的过程在很大程度上取决于相对于纤维方向的传播方向。结论-该研究表明，在慢性患病的人心肌中，由长纤维化链施加的非均匀各向异性特征导致激活延迟的逐渐增加，从过早刺激的长耦合间隔开始。这种增加很大程度上取决于相对于纤维方向和纤维化结构的波前方向。
Background - Progressive activation delay starting at long coupling intervals of premature stimuli has been shown to correlate with sudden cardiac death in patients with hypertrophic cardiomyopathy. The purpose of this study was to elucidate the mechanism of increased activation delay in chronically diseased myocardium.Methods and Results - High-resolution unipolar mapping (105, 208, or 247 recording sites with interelectrode distances of 0.8, 0.5, or 0.3 mm, respectively) of epicardial electrical activity was carried out during premature stimulation in I I explanted human hearts. The hearts came from patients who underwent heart transplantation and were in the end stage of heart failure (coronary artery disease, 4; hypertrophic cardiomyopathy, 1; and dilated cardiomyopathy, 6). Eight hearts were Langendorff-per-fused. Epicardial sheets were taken from the remaining hearts and studied in a tissue bath. Activation maps and conduction curves were constructed and correlated with histology. Conduction curves revealing prominent increase of activation delay were associated with zones of dense, patchy fibrosis with long fibrotic strands. Dense, diffuse fibrosis with short fibrotic strands only marginally affected conduction curves. The course of conduction curves in patchy fibrotic areas greatly depended on the direction of propagation relative to fiber direction.Conclusions - The study demonstrates that in chronically diseased human myocardium, nonuniform anisotropic characteristics imposed by long fibrotic strands cause a progressive increase of activation delay, starting at long coupling intervals of premature stimuli. The increase strongly depends on the direction of the wave front with respect to fiber direction and the architecture of fibrosis.