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Electrophysiologic-structural correlations in chagasic aneurysms causing malignant arrhythmias
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Surgical removal of chagasic aneurysms eliminated malignant arrhythmias in patients. This study reveals how aneurysm-adjacent myocardial damage creates reentry circuits, proving their arrhythmogenic role.
Area of Science:
- Cardiology
- Pathology
- Cardiac Electrophysiology
Background:
- Chagasic aneurysms are associated with chronic, recurrent ventricular tachycardia.
- Arrhythmias in these patients often originate near aneurysms and are refractory to medical treatment.
Purpose of the Study:
- To investigate the structural and ultrastructural basis of arrhythmias in chagasic aneurysms.
- To demonstrate the arrhythmogenic role of myocardial changes adjacent to aneurysms.
Main Methods:
- Histological and ultrastructural examination of three resected chagasic aneurysms.
- Intraoperative epicardial and endocardial mapping to identify arrhythmogenic sites.
- Surgical resection of aneurysm-associated myocardial tissue.
Main Results:
- Myocardial tissue showed chronic inflammation, myocytolysis, fibrosis, and "islets" of damaged myocytes.
- Ultrastructural findings included myocyte hypertrophy, myofibril loss, mitochondrial damage, and thickened basement membranes.
- Interlaced healthy and damaged myocytes formed potential reentry circuits.
Conclusions:
- Aneurysm resection abolished malignant arrhythmias, confirming their origin in adjacent myocardial regions.
- Structural and ultrastructural alterations, particularly "early" myocyte damage, create substrates for reentry arrhythmias.
- This study elucidates the mechanism linking chagasic aneurysms to life-threatening ventricular tachycardia.
Abstract:
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.