The electrode-tissue interface: the revolutionary role of steroid elution.
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Biomedical subjects
Publications and source records attributed to H G Mond.
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Catheter-induced His bundle ablation for refractory supraventricular arrhythmias is most commonly performed with direct-current shock energy of 200-300 joules. The high energy pulse delivered by direct-current shock produces a lesion in the atrioventricular node by fulguration, with the residual energy being dissipated as a pressure wave. The effect of direct-current shock His bundle ablation on global and regional ventricular function was assessed in 14 consecutive patients by radionuclide ventriculography performed before and after ablation and again three months later. All studies were performed with ventricular pacing at 110 bpm. Global left ventricular ejection fraction was found to be significantly reduced at the three month study (0.43 +/- 0.03 vs 0.50 +/- 0.03, pre ablation, p = 0.02). A significant reduction in wall-motion score was also seen in six of the seven patients who had normal wall motion in pacing rhythm prior to ablation. Deterioration was mainly seen at the left and right ventricular apices. The observed reduction in ventricular function that follows direct-current shock His bundle ablation may result from myocardial damage from electro-coagulation or from barotrauma and supports continued investigation into alternative, less traumatic energy sources for the procedure.
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Twenty-two patients with refractory supraventricular arrhythmias were treated by catheter-delivered high-energy shocks to the atrioventricular conduction system. All patients had a minimum follow-up period of six months (mean +/- SD, 15 +/- 9 months), at which time 21 of the 22 patients were free of symptoms and required no antiarrhythmic therapy. Permanent pacemakers were implanted in all patients. These results show that transvenous ablation or modification of atrioventricular conduction is a safe and effective technique to treat a wide range of supraventricular arrhythmias, and obviates the need for open-heart surgery for the interruption of atrioventricular nodal conduction.
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A 37 year old man who presented with a cardiomyopathy, conduction defects and atrial and ventricular arrhythmias was found to have the neuromuscular manifestations of myotonic dystrophy. Despite implantation of a permanent cardiac pacemaker, antiarrhythmic drug therapy and antiarrhythmic surgery, sudden death occurred. The results of electrophysiologic studies, coronary arteriography and pathologic findings are described. This case confirms previous observations that ventricular arrhythmias, in addition to atrial arrhythmias and conduction disturbances, are cardiac manifestations of myotonic dystrophy and can lead to sudden death.
The success of an implanted cardiac pacemaker is dependent upon the establishment of a harmonious relationship between the artificial pacemaker and the human receiver. Failure of a pacemaker system may arise from an electronic or mechanical defect within the pacemaker, a physiologic problem, or from a poor relationship between the normal function of both. Such malfunctions may necessitate the repair, replacement, or repositioning of a pacemaker component or removal of a source of external interference. True pacemaker malfunctions must be clearly distinguished from pseudo-malfunctions, where there is no pacemaker system defect. These situations may, variously, require the repair of faulty testing equipment, reassessment of falsely interpreted test data, or treatment of the patient for an unrelated disorder. This paper outlines a system for investigating patients with suspected pacemaker malfunction. For simplicity, only malfunctions associated with the ventricular inhibited pacing system will be discussed.
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A new balloon-tipped ventricular endocardial electrode for permanent artificial cardiac pacing is described. Following transvenous insertion of the electrode to the right ventricular apex, the distal balloon is inflated with contrast material in order to wedge the electrode tip between or beneath trabeculae and prevent displacement. fifty-nine electrodes were implanted, including a second generation type incorporating a wedge tip as well as the balloon. The incidence of displacement was 17% with 10% of cases being early, and 7% late. Early in the series, 50% Urografin was used to inflate the balloon and this resulted in premature deflation and early electrode displacement in two of the nine patients. When the concentration of Urografin was reduced, the balloon remained inflated for a longer period and the incidence of early displacement was reduced to 8%. However, there was still a late displacement of 8%. Only one wedge-tipped balloon electrode displaced. This electrode had a faulty sealing mechanism and the balloon could not be adequately inflated. There was a 3% incidence of early and a 3% incidence of late threshold problems with the electrode. However, name of the wedge-tipped balloon electrodes exhibited this problem. It was concluded that this new electrode did not fulfill its objectives. The total electrode failure rate, including displacements and episodes of high threshold was approximately 24%.
The diagnosis of right ventricular perforation by an endocardial pacemaker electrode should be suspected when failure of pacing occurs without electrode displacement. Although a number of changes occur on the standard electrocardiogram (ECG), none of these are diagnostic. The intracardiac electrogram performed during electrode withdrawal is not only diagnostic of perforation but can also aid in electrode positioning. Two case reports highlight these changes in the intracardiac electrogram. The first case also illustrates that, with electrode perforation, the ability to sense the intrinsic intracardiac electrical activity may be retained.
An unusual case is described of primary oxalosis with renal failure and cardiac involvement with complete heart block. Although cardiac involvement rarely occurs, it nevertheless requires evaluation because of the therapeutic implications.
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Described is an unusual complication occurring during right-sided cardiac catheterization using a 7F flow-directed balloon catheter. During an attempt to direct the catheter from the main pulmonary artery into the pulmonary wedge position, the tip became entangled in a loop of catheter and knotted. Initially, all attempts to unknot or remove the catheter failed. A movable core guide wire was passed through the major lumen of the catheter, resulting in the immediate unknotting of the catheter, thus allowing its withdrawal.