Biomedical subjects
Publications and source records attributed to J A Matos.
Many problems remain to be solved before implanted pacers can assume a major role in the treatment of ventricular tachycardia. Case histories are cited to illustrate some of the difficulties to be overcome. Possible mechanisms for the success and failure of antitachycardia pacing are reviewed. Prospects for antitachycardia pacing will increase with the advent of cardioverter/defibrillator back-up.
15 AICD (automatic implantable cardioverter-defibrillator) Model B units were implanted in 10 patients. The median sternotomy is our preferred surgical approach using a right atrial patch electrode, a left ventricular apex patch electrode, and two closely placed epicardial sensing electrodes. Follow-up is 109 patient months and all patients are alive. AICD units discharged for ventricular tachycardia, ventricular flutter, and ventricular fibrillation. Discharges also occurred for sinus tachycardia and atrial fibrillation above the rate limit in three units. Premature pulse generator depletion has occurred in four AICD-B units 3 to 18 months postimplant and appears due to a defect in original battery design. Discharge of the AICD for supraventricular tachycardia is a problem that will remain until a better means of differentiating supraventricular tachycardia from ventricular tachyarrhythmias is found. The AICD appears to prevent sudden death from ventricular tachyarrhythmias.
Over a 39 month period, 143 patients with coronary artery disease had programmed stimulation (PES) for recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF). Twenty-two patients underwent operations. Ages ranged from 40 to 71 years; 20 of the 22 were men. All patients had coronary artery disease and 11 had left ventricular aneurysms. The mean ejection fraction was 31% (16% to 50%). Eighteen of the 22 patients underwent operations for drug-resistant ventricular arrhythmias (more than six different drugs plus drug combinations tested per patient). Nineteen patients had intraoperative mapping, endocardial resection, and/or an encircling endocardial ventriculotomy. Three patients with ischemia-related VT had coronary artery bypass (CABG) alone. The 30 day operative mortality was 14%. Thirteen of 19 (68%) operative survivors were effectively controlled with operation alone or a combination of operation and previously ineffective drug therapy. Of the six patients whose VT was inducible postoperatively, three have experienced episodes of sustained VT and one patient died suddenly. Three of these patients have the automatic implantable defibrillator. Operation guided by endocardial mapping is effective alone or in combination with drugs in this select group of patients. If the patients' VT was uninducible postoperatively with or without the addition of antiarrhythmic therapy, late deaths (3/19) were due to poor myocardial reserve and coronary artery disease, not the reemergence of sustained ventricular arrhythmias during a mean follow-up of 15 months.
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Termination of ventricular tachycardia (VT) with single programmed extrastimuli or slow underdrive competitive pacing is often possible. The usefulness of these techniques is limited because the zone in the cardiac cycle during which programmed stimuli are effective may be narrow, with significant time elapsing until termination of the VT, and the zone may vary markedly between episodes, rendering preset extrastimuli ineffective. Ultrarapid trains of stimuli beginning during the refractory period and of a duration sufficient to cause only a single capture should terminate all tachycardias whose termination zone begins just after the refractory period. To test this hypothesis, 21 patients with 371 well-tolerated episodes of VT had single programmed extrastimuli and trains of 10 bipolar stimuli at 25, 50, and 100 Hz. VT was terminated 1 or more times in 18 of the 21 patients with programmed extrastimuli or trains, or both. Forty-eight percent of 290 episodes were terminated with programmed stimulation, compared with 56% of 120 episodes with trains (difference not significant). In 98 episodes, the effects of trains and programmed stimulation could be matched (same patient, date, tachycardia morphology, rate, and drug therapy); the results were concordant (both techniques either terminated the VT or failed) in 92 and discordant in 6. With only 2 possible exceptions, the termination zone always began just after the refractory period; thus, for tachycardias terminating with single captures, the first train to achieve capture was effective, minimizing the duration of the VT.
In addition to providing basic physiologic information, knowledge of the maximal rate of sinus tachycardia development may be helpful in developing algorithms permitting new generations of antitachycardia pacemakers to distinguish accurately between sinus and ventricular tachycardia. To determine the maximal rate of sinus tachycardia development, 50 normal subjects rushed up 100 stairs as rapidly as possible, with continuous electrocardiographic monitoring. During the first second of exercise, the mean cardiac cycle length shortened from 709 to 570 ms, equivalent to an increase in heart rate from 85 to 105 beats per minute, or 20 beats per minute per second. Thereafter, a more gradual decrease in cycle length occurred. Differences between men and women, smokers and non-smokers, and sedentary compared to active subjects were all insignificant. Analysis of 50 spontaneous episodes of ventricular tachycardia also revealed a sequential but more abrupt decrease in the cycle length during the first second from 757 to 360 ms, equivalent to a rate increase from 79 to 167 beats per minute, or 88 beats per minute per second. After approximately 1 1/4 seconds, the ventricular tachycardia cycle length remained virtually constant. Baseline cycle lengths were similar in the sinus and ventricular tachycardia groups, but differed in all subsequent beats, although overlap for individual subjects did occur.
Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia for several minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2-3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 +/- 19 vs. 1.33 +/- 24 (p less than 0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely to prove useful in the long-term treatment of many patients with recurrent ventricular tachycardia.
The effectiveness of pacing techniques for termination of ventricular tachycardia is well established, and of great value in the electrophysiologic laboratory, and, to a more limited degree, for chronic therapy using implanted anti-tachycardia devices. Although it appears that most clinical ventricular tachycardias are due to reentrant mechanisms, responses to antitachycardia pacing have often been difficult to understand. In this paper, clinical observations are correlated with hypothetical constructs and considerations, in an attempt to derive some general principles related to the success and failure of pacing for ventricular tachycardia. In these analyses, it appears that properties of conductivity and refractoriness in the myocardium are as important as the properties of the tachycardia circuit. Programmed extrastimuli or rapid pacing result in shortening of the effective refractory period of the myocardium, together with depressed conduction velocity of the stimulated wavefront. However, the changes in wavefront conductivity do not occur in step with changes in the effective refractory period; as a result, the stimulated wavefront arrives at the tachycardia circuit in a pattern which differs from the stimulation pattern. In general, it appears that termination of the tachycardia is favored when the stimulated wavefront arrives at the tachycardia circuit at a point when it cannot enter the circuit in an antegrade direction. These conditions are favored by a refractory period in the circuit which is moderately long compared to that of the myocardium. Constructions explaining the observation of a tachycardia termination zone are presented, together with explanations for failure to achieve termination, and for various patterns of acceleration.
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Implanted pacemakers can provide a viable alternative to pharmacologic therapy or surgical management of patients with recurrent ventricular tachycardia. An increasing variety of pacemaker techniques are proving useful for preventing, controlling the effective rate of or terminating ventricular tachycardia. To assess the role of permanent pacing in the treatment of ventricular tachycardia, a consecutive series of 160 patients undergoing electrophysiologic testing for recurrent ventricular tachycardia were analyzed. Thirty-nine patients received implantable pacemakers, of which 13 were intended for bursts of rapid ventricular pacing. No adverse responses were attributed to these burst pacemakers, but concern for possible acceleration of tachycardia and appropriate identification of the arrhythmia were among factors limiting more widespread use of antitachycardia pacing. Some of these limitations may be resolved with further advances in electrophysiologic understanding of arrhythmias combined with strides in medical electronics, which will permit the development of new generations of highly sophisticated antitachycardia pacemakers.
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A previously unrecognized beneficial drug interaction is described. Without affecting the antiarrhythmic properties of disopyramide, a sustained-release form of pyridostigmine (a cholinesterase inhibitor) was shown to prevent completely anticholinergic side effects in a study population (17 patients), whereas side effects occurred in 26 of 89 patients (29%) in a control group (p less than 0.025). Pyridostigmine also diminished or abolished disopyramide-induced anticholinergic side effects in each of 10 patients in whom they were already present. Pyridostigmine allowed an increase in tolerated disopyramide blood levels (4.53 +/- 1.59 micrograms/ml versus 3.85 +/- 1.78 micrograms/ml) and a significant increase in disopyramide dosages (224 +/- 68 mg versus 188 +/- 68 mg every 6 h) (p less than 0.02). No patients suffered side effects from pyridostigmine. These data suggest that pyridostigmine can be used to prevent as well as to treat the anticholinergic side effects of disopyramide. The usefulness of disopyramide has previously been limited by these anticholinergic side effects. Further investigation is in progress to determine what role pyridostigmine can play in making disopyramide therapy available to patients who otherwise could not benefit from its use.