Medical devices labelled for single use: the reuse of permanent cardiac pacemakers.
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Biomedical subjects
Publications and source records attributed to M Rosengarten.
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The electrophysiologic effects of intravenous propafenone were studied in 15 consecutive patients with accessory pathways. Thirteen patients had sustained orthodromic supraventricular tachycardia induced during baseline study, and two patients needed isoproterenol to render it sustained. In all except one patient, propafenone, 2 mg/kg given intravenously over a 10-minute period, was successful in converting the arrhythmia to sinus rhythm. Atrial fibrillation was inducible in 10 patients before propafenone, but was no longer inducible in seven of these patients after the drug. The HV interval (23 +/- 20 to 41 +/- 25 msec) and the anterograde (310 +/- 96 to 509 +/- 145 msec) and retrograde (256 +/- 30 to 334 +/- 105 msec) effective refractory periods of the bypass tract were all significantly prolonged after the drug. The pacing cycle length that produced conduction block over the bypass tract anterogradely (319 +/- 126 to 446 +/- 150 msec) and retrogradely (272 +/- 25 to 360 +/- 97 msec) was also increased. During orthodromic tachycardia, propafenone increased conduction time in both the anterograde and retrograde limbs of the tachycardia. Tachycardia terminated in the retrograde limb in 64% of the patients. We conclude that propafenone is very effective in terminating orthodromic tachycardia when given intravenously and that it should be considered in patients initially seen with atrial fibrillation and short refractory periods.
Pacemaker reimplantation in the same patient is common, and pacemaker transplantation or reuse in a second patient has been reported. No report prospectively compares the long term costs, the impact of reuse on the number of pacemakers implanted, the pacemaker related complications, the types of patients selected and the patient survival of those who receive new versus a refurbished pacemaker. The authors implanted 70 pacemakers of which 75% (52) were new and 25% (18) were refurbished. The refurbished pacemakers were implanted in older patients (P less than 0.02), with a mean +/- SD of 77 +/- 8 versus 69 +/- 13 years of age. During a follow-up period of 36 months, the rate of pacemaker related complications was the same in both groups, with no unusual or unexpected problems arising in the refurbished group. There were 12 (23%) complications in the new pacemaker group and four (22%) complications in the refurbished pacemaker group. There were no major pacemaker related complications, no pacemaker battery depletions and no pacemaker related deaths. The refurbished pacemakers saved $33,000. After three years the cumulative probability of survival in the new group tended to be higher (P = 0.08) with a mean (SE) of 0.62 (0.12) versus 0.44 (0.15). New and refurbished pacemakers are similar with respect to pacemaker related survival and complications. Refurbished pacemakers effect a major reduction in pacemaker costs while maintaining health care standards.
With the advent of the tined pacemaker electrode to improve endocardial fixation, increasing difficulty in extracting them when needed has resulted in reports of serious complications. The authors reviewed their experience between January 1975 and January 1985. During this 10 year period, 942 pacemakers were inserted and 73 were reoperated upon. In the reoperations, repositioning or removal of tined electrodes was attempted 28 times. Repositioning or removal was not possible in 12 of the 28 cases (43%). In 22 of 28, the attempts to remove tined leads were carried out more than one month after the original implantations and in this group the failure rate was 54.5% (12 of 22). All attempts of removal within one month of implantation were successful (six of six). No leads were retained during the period between January 1984 and January 1985. All 12 retained leads were followed-up for five years, five of which were retained in the presence of pacemaker pocket infections. After removal of the power pack and lead distal to the cephalic or subclavian vein inlet, control of infection was achieved in all five cases. One patient was noted to have the retained lead migrate into the right pulmonary artery but was asymptomatic at 35 months after catheter migration was detected. Until now, no thoracotomy for lead extraction has been required in this series.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiac pacing systems produce cardiac contractions by delivering electrical charges to the myocardium. Reliable cardiac pacing, and the longevity of pacemakers depends on the absence of electrical leaks. Electrical leaks often do not cause symptoms and if suspected, there are few methods which are able to identify their location and none suited to small or intermittent leaks. We surface mapped the pacemaker spike amplitudes over the pockets of 29 patients with unipolar pacemakers, several of which had suspected pacemaker leaks. For each patient, pacer voltage spikes were recorded with an optical ECG recorder from sixty-three positions on the skin over the pacemaker. The spike voltages were interpolated with a 2-D Fourier transform, contoured, and plotted by a computer. Electrical leaks were readily detected and their positions indicated by the resulting maps. The operative findings confirmed the map guided prediction in all six patients sent for pacemaker revision. Pacemaker spike amplitude surface mapping detects and locates pacing system insulation failures.
Theoretical considerations indicate that complex patterns of atrioventricular conduction produced by rapid atrial stimulation can be predicted from changes in atrioventricular conduction produced by premature stimulation of the atrium. The purpose of this study was to evaluate the validity of this theoretical approach in seven patients undergoing electrophysiologic investigation. The atrioventricular nodal recovery curve was determined at two different basic cycle lengths. Subsequently, periodic atrial stimulation was delivered for 30 sec periods over a range of frequencies giving 11, Wenckebach, reverse Wenckebach, and 21 rhythms. The recovery curve data was then used to compute the response to periodic stimulation by an iterative technique. The conduction patterns actually seen during periodic atrial stimulation showed close agreement with the computed patterns. This work thus provides a unified explanation for the appearance of Wenckebach, reverse Wenckebach, alternating Wenckebach, and high grade block rhythms.
The identification of a cardiac arrhythmia depends on the interpretation of both the QRS complexes and the P waves. P wave detection is unreliable and hence automated diagnostic systems are often imperfect. An alternative is a system which detects QRS only and which classifies the QRS events; the physician then has a detailed quantitated QRS analysis to aid in diagnosis. The ATREC system has an analog QRS detector, which suppresses the P wave and the T wave frequencies and feeds a minicomputer (Mitra 15/35) with signals for the RR interval, the QRS duration, and polarity. The computer classifies these signals as either narrow or wide complexes. The narrow complexes are analyzed for irregular rhythm, bradycardia, pauses, transient or continuous tachycardia, and fibrillation. The wide complexes are classed by their coupling interval, bi- or trigeminy, doublets, or salvos, and the number per hour. The system gives a trend of the 16 beat mean, and the minimum and maximum heart rate. The data is presented on several displays.
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22 patients with salvoes of ventricular tachycardia were investigated electrophysiologically and pharmacologically to determine the mechanism of the arrhythmia. The appearance of the ventricular complexes was suggestive of a septal origin. The arrhythmia appeared to occur and regress within precise limits of sinus rhythm. 24 hour ECG recording and endocavitary stimulation techniques showed its essentially variable character, but occasionally a fixed coupling interval with the first extrasystole was observed, suggesting the presence of an unprotected parasystolic focus. The repetition of the extrasystolic activity, which could be triggered and terminated at will, is explained by phenomena of delayed after potentials. The results of the systematic investigation of the effects of quinidine-like drugs, beta-blockers and verapamil do not invalidate these hypotheses and show a difference of degree but not of nature between the two populations A and B of patients classified according to the quantitative character of the extrasystolic activity over 24 hours (more or less than 1000/hour). The observation of intermediate forms with simple extrasystoles and other forms with sustained tachycardia extends the significance of these results to many forms of ventricular arrhythmia.
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The electrocardiograms of 100 patients with rapid and regular PP intervals during atrial arrhythmias (because of atrial tachycardia or flutter, or pacing) were examined for periods of irregular atrioventricular conduction. This irregular conduction corresponds to an alternating Wenckebach phenomenon, of a type that can be determined from simple rules. The different types of conduction encountered in different patients and the changes seen in the same patient suggest that the atrioventricular node functions physiologically with 3 levels of sequential block. The different prevalence of the 2 types of alternating Wenckebach block may reflect functional differences at the level of the atrioventricular node.
A 31-year-old female had recurring palpitations and black-outs for 13 years. Hyperthyroidism was diagnosed and electrocardiogram suggested ventricular preexcitation. Despite being treated for hyperthyroidism (which rendered the patient hypothyroid) and receiving propranolol for the arrhythmia, the palpitations persisted. Electrophysiologic testing identified the patient's arrhythmia, and demonstrated that it improved with intravenous propafenone, a new type 1C antiarrhythmic medication. After two days of oral propafenone, this initially good response was followed by episodes of Torsade de pointes ventricular tachycardia with repeated cardiac arrest. Lidocaine and isoproterenol failed to control the rhythm, and the patient was stabilized by electrical cardioversions, atrial pacing and withdrawing the propafenone. Propafenone has been used to treat Torsade de pointes, but we show that it may also cause Torsade de pointes.
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