Milei J, Pesce R, Valero E, Muratore C, Beigelman R, Ferrans V J
Cardiopsis, Hospital Juan A. Fernández, Buenos Aires, Argentina.
Int J Cardiol. 1991 Jul;32(1):65-73. doi: 10.1016/0167-5273(91)90045-q.
We studied the structure and ultrastructure of three chagasic aneurysms, the excision of which abolished malignant arrhythmias. Chronic recurrent ventricular tachycardia often occurs in patients with chagasic aneurysms, and ventricular mapping indicates that these arrhythmias originate in regions adjacent to those aneurysms. In our patients, ventricular tachycardia had been refractory to medical treatment. During surgery, epicardial and endocardial mapping showed abnormal potentials. Sutures were placed in the areas of resection, their sizes approximating those of earliest activation so that these sites could be identified. The myocardium showed chronic inflammatory reaction, myocytolysis and fibrosis. The presence of "islets" was common (normal, "early" damaged or "established" necrotic myocytes surrounded by fibrous tissue). The "early" lesions were predominant at the previously identified areas of arrhythmogenic activity. The ultrastructural studies showed hypertrophy of myocytes and partial or complete loss of myofibrils, swelling of mitochondria and disruption of mitochondrial cristae, accumulation of lipofuscin granules, and intracellular oedema. A most striking alteration was the thickening of the basement membranes of myocytes and vascular endothelial and smooth muscle cells. The interlaced fronts of respectively healthy (fast conducting) and "early" damaged (slow conducting) myocytes seen in serial sectioning produced an ideal configuration for reentry circuits. The final proof that the arrhythmias originated in these endocardial regions was their abolition by resection of the aneurysm.
我们研究了三个恰加斯病性动脉瘤的结构和超微结构,切除这些动脉瘤后恶性心律失常消失。慢性复发性室性心动过速常发生于恰加斯病性动脉瘤患者,心室标测表明这些心律失常起源于与动脉瘤相邻的区域。在我们的患者中,室性心动过速对药物治疗无效。手术过程中,心外膜和心内膜标测显示电位异常。在切除区域放置缝线,其大小与最早激活区域相近,以便识别这些部位。心肌呈现慢性炎症反应、肌细胞溶解和纤维化。“小岛”的存在很常见(正常、“早期”受损或“已形成”坏死的心肌细胞被纤维组织包围)。“早期”病变在先前确定的致心律失常活动区域占主导。超微结构研究显示心肌细胞肥大、肌原纤维部分或完全丧失、线粒体肿胀和线粒体嵴破坏、脂褐素颗粒积聚以及细胞内水肿。最显著的改变是心肌细胞、血管内皮细胞和平滑肌细胞基底膜增厚。在连续切片中看到的分别健康(传导速度快)和“早期”受损(传导速度慢)的心肌细胞交错前沿为折返环路提供了理想的结构。通过切除动脉瘤使心律失常消失,这最终证明了心律失常起源于这些心内膜区域。