Key result
Single shocks via implanted defibrillator leads induce amplitude-dependent myocardial necrosis and ultrastructural damage in dogs.
Why the study?
The ultrastructural cardiac tissue alterations induced by shocks from chronically implanted automatic defibrillator leads were not well characterized.
Does delivering single shocks of 10-30 A through chronically implanted defibrillator leads cause ultrastructural alterations in the fibrous sheath, endocardium, and myocardium in dogs?
Does delivering single shocks of 10-30 A through chronically implanted defibrillator leads cause ultrastructural alterations in the fibrous sheath, endocardium, and myocardium in dogs?
High-energy shocks delivered through chronically implanted defibrillator leads cause dose-dependent myocardial necrosis and ultrastructural alterations in surrounding tissues in a canine model.
May warrant minimizing shock energy in ICDs; leaves open human myocardial injury risk and optimal programming.
SUMMARY Catheter-mounted automatic implantable defibrillator leads were implanted in 10 dogs for 11 to 21 months (mean 15.0 months). Single shocks of 10 A, 20 A, or 30 A (peak current) were then delivered through the chronically implanted leads. Two days after the shock, the dogs were euthanatized and necropsied. The intracardiac segment of the lead was covered by a fibrous sheath, the endocardium in contact with the lead was thickened by fibrous tissue, and shock-induced myocardial necrosis was present surrounding the distal pair of electrodes, with the largest amount of damage found in the dogs given the large shocks. Ultrastructurally, the fibrous sheath was covered by endothelium and contained numerous spindle cells and identified as smooth muscle cells by their prominent cytoplasmic filaments and external laminae or myofibroblasts with prominent endoplasmic reticulum. The spindle cells were surrounded by abundant collagen fibrils but not by elastic fibers. The thickened endocardium contained numerous fibroblasts, abundant collagen fibrils, and a few small elastic fibers. The shock-induced myocardial alterations included necrosis of cardiac muscle cells with prominent mitochondrial mineralization, interstitial edema, and infiltration of macrophages.
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Vleet et al. (1982) studied this question. Single shocks via chronically implanted automatic defibrillator leads was evaluated on Ultrastructural alterations and myocardial necrosis. Single shocks delivered through chronically implanted defibrillator leads in dogs induced myocardial necrosis and ultrastructural alterations, with greater damage observed at higher shock amplitudes.
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