Biomedical subjects

M P Schollmeyer

Publications and source records attributed to M P Schollmeyer.

5 recordsLinked to original sources

PubMed1985

Catheter electrode defibrillation in dogs: threshold dependence on implant time and catheter stability.

A catheter-mounted electrode system designed for intracavitary ventricular defibrillation was implanted in the right ventricular apex of 12 dogs. Defibrillation thresholds were obtained in all dogs at the time of implant using an external defibrillator. Roentgenograms obtained 3 weeks after catheter implantation revealed that six dogs had catheters intact at the site of implant (group A) and six dogs had catheters that had dislodged from the original implant site (group B). There were no statistically significant differences (p less than 0.05) in mean body weight or mean defibrillation threshold between group A and group B dogs, respectively, at implant. Defibrillation thresholds were obtained for both groups of animals at 5, 12, and 26 weeks after catheter implantation. At all post implant monitors mean threshold for group B was significantly higher (p less than 0.05) than mean threshold for group A. Moreover, mean defibrillation threshold for both groups had increased by week 5 and remained stable through week 26. Catheter dislodgement increases defibrillation threshold, but does not prevent successful defibrillation. Also, defibrillation threshold increases to a stable value by 5 weeks post implant.

Animals↗

PubMed1983

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.

Animals↗

PubMed1983

Alterations induced by a single defibrillating shock applied through a chronically implanted catheter electrode.

In ten beagles ranging in weight from 7.4 to 13.0 kg, a defibrillating shock of 10 A (three dogs), 20 A (four dogs), or 30 A (three dogs) intensity was applied through a chronically implanted right ventricular catheter electrode. Ten-lead ECG, right ventricular electrogram, and right ventricular impedance were recorded prior to, immediately following, and 48 hours post-shock. A single shock of 10 A, 20 A, and 30 A intensity succeeded in defibrillating nine of ten dogs. One dog required two 20 A shocks to defibrillate. No shock was fatal. Post-shock arrhythmias increased in duration and severity as the shock strength increased. ECG vector analysis suggested damage to the right ventricle in eight of ten dogs. The impedance signal amplitude increased directly after the shock, but dropped below control level by 200 seconds post-shock and remained below control by 48 hours post-shock. Pale areas of shock-induced myocardial necrosis were concentrated in the right ventricular walls adjacent to the distal electrode. The mean weight of necrotic myocardium was 0.043 + 0.006 grams at 10 A, 1.203 + 0.268 grams at 20 A, and 1.397 + 1.218 grams at 30 A (mean + sd). Defibrillation was effective after long-term implantation. The alterations sustained from defibrillation were minimized by using a low intensity shock.

Animals↗

PubMed1982

Ultrastructural alterations in the fibrous sheath, endocardium, and myocardium of dogs shocked with chronically implanted automatic defibrillator leads.

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.

Animals↗

PubMed1981

Cardiovascular alterations induced by chronic transvenous implantation of an automatic defibrillator electrode catheter in dogs.

Six dogs (three large, three small) had defibrillator electrode catheters implanted transvenously via the right jugular vein for 17 weeks. The dogs remained healthy throughout the study. At necropsy, the lead-induced cardiovascular alterations were characterized by (1) formation of a thin white fibrous sheath over portions of the lead along its course in the veins, right atrium and right ventricle; (2) adhesion of parts of the sheathed segments of the lead to the adjacent venous intima or endocardium of the right atrium, tricuspid valve and right ventricle; (3) endocardial fibrosis with foci of cartilaginous metaplasia in areas traumatized by the lead; (4) thrombus formation at ends of sheathed segments of the lead but lack of pulmonary embolism; and (5) partial penetration of the myocardium at the apex of the right ventricle by the end of the lead in two of the small dogs. The lead-induced lesions were similar in type and severity to those produced by chronically-implanted pacemaker leads.

Animals↗