Post-mortem changes after lead extraction from the ovine coronary sinus and great cardiac vein.

We investigated in sheep, non-thoracotomy extraction of leads which had been chronically implanted in the right atrium (RA), coronary sinus/great cardiac vein (CS/GCV) and right ventricle (RV) for atrial implantable defibrillation. Clinical success of extraction as well as gross and histologic findings in the heart are reported. Six of nine sheep had successful extractions. The major complication was laceration of the wall of the great coronary vein with hemorrhage into the pericardial space and cardiac tamponade. Tissue damage included several reversible changes: intra-tissue hemorrhage, thrombosis in the veins, and some necrosis of fat, vascular wall and myocardium. Myocyte necrosis was estimated as 0.03 to 0.3 grams of tissue. Osseous and cartilaginous metaplasia was more common around the RA lead than the CS/GCV lead. In cases where the lead must be removed, removal from the venous insertion site using lead extraction equipment should only be attempted with surgical back-up for emergency thoracotomy to control hemorrhage in the event of vessel laceration. Safer explantation of these leads from the vein entry site will require the development of new extraction procedures.

Cardiac damage in dogs with chronically implanted automatic defibrillator electrode catheters and given four episodes of multiple shocks.

In 14 dogs, a newly designed automatic defibrillator electrode catheter with paired ventricular and superior vena caval electrodes was implanted transvenously into the right ventricular (RV) apex for 26 weeks. Twelve dogs were given multiple (mean total = 21.3) near-threshold (mean delivered energy = 17.6 joules) shocks via the lead at 0, 5, 12, and 26 weeks after implantation. Two days after the last shocks, the dogs were killed and the cardiac alterations were evaluated at necropsy and by histopathology. The lead induced mild to moderate cardiac alterations of (1) endocardial fibrosis, either as flat or papillary lesions, and of (2) segments of smooth thin fibrous sheath formation over the lead with adhesions to the adjacent endocardium. Mild cardiac alterations were induced by the shocks including myocardial necrosis and calcification, concentrated in the ventricular septum and RV free wall adjacent to the ventricular electrodes, and foci of postnecrotic fibrosis. The chronically implanted lead was determined to be safe and effective in dogs.

Therapeutic indices for transchest defibrillator shocks: effective, damaging, and lethal electrical doses.

Although prospective studies of defibrillator shock overdose cannot be performed in man, the therapeutic indices of various defibrillating current waveforms can be measured in animals. We determined the ratios TD50/ED50 and LD50/ED50 (where TD50 = median "toxic" or damage-inducing dose, ED50 = median effective or defibrillating dose, and LD50 = median lethal dose) as measures of the therapeutic index for damped sine wave defibrillator shocks in dogs. Death of an animal and/or any degree of cardiac damage found by gross or microscopic examination were defined as harmful effects of shock, analogous to drug toxicity. In terms of peak current, the ED50, TD50, and LD50 were 1.1, 5.8, and 24 amperes/kg.; the therapeutic indices were TD50/ED50 = 5 for morphologic damage and LD50/ED50 = 22 for death. In terms of delivered energy the ED50, TD50, and LD50 were 1.5, 30, and 470 joules/kg.; the therapeutic indices were TD50/ED50 = 20 for damage and LD50/ED50 = 320 for death. These data indicate a reasonable margin of safety for damped sine wave defibrillator shocks in dogs, and are consistent with reported incidences of suspected shock-induced damage in humans.