Repetitive ICD discharges during an ambulance ride: an unusual pacemaker-ICD interaction.
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Biomedical subjects
Publications and source records attributed to M Ezri.
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The possible interference of drugs with the function of implanted electrical cardiac devices in two patients is described, and the literature on the interaction between these drugs and devices is reviewed. A 59-year-old woman had a permanent pacemaker implanted after diagnosis of tachycardia-bradycardia syndrome, and her drug regimen of digoxin, verapamil, and warfarin was supplemented with flecainide to prevent paroxysmal atrial fibrillation. A Holter monitor recording performed after five days of flecainide therapy showed the pacemaker was sensing and pacing normally. Approximately three weeks after pacemaker implantation and initiation of flecainide therapy, a Holter monitor recording showed high-grade atrioventricular block and failure of the pacemaker to capture. A chest roentgenogram showed that the pacemaker lead was properly placed. The pacemaker's pulse amplitude and pulse width were increased, and the device again functioned reliably. Six months later the pacing threshold was noted to have returned to normal. A 64-year-old man had a history of aborted sudden cardiac death from ventricular tachyarrhythmias. The patient received an automatic implanted cardioverter-defibrillator (AICD); at that time, a 15-J discharge was required to terminate induced ventricular fibrillation (VF). Three years later, the AICD was replaced; the energy required for VF termination with the new unit was 16 J. Seven months after implantation of the new unit, the patient had several episodes of ventricular tachycardia (VT). Moricizine therapy was initiated. An electrophysiologic study (EPS) three days later showed that a larger shock (28 J) was required to terminate VF and that the pacing threshold had increased.(ABSTRACT TRUNCATED AT 250 WORDS)
A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.
Subendocardial left ventricular aneurysmectomy relieved previously intractable ventricular tachycardia in a 68-year-old man with severe coronary artery disease. Staphylococcal septicemia developed postoperatively; an infected venoclysis site may have provided the portal of entry. Autopsy confirmed staphylococcal abscess at the epicardial aspect of the ventriculotomy, constituting the first reported case, to our knowledge, of this complication following endocardial surgery.
Thirteen patients with syncope and bifascicular block were evaluated by electrophysiologic study (EPS) including programmed stimulation. The mean age was 62 years. Six patients had coronary artery disease, three had cardiomyopathy, and four showed no evidence of organic heart disease. Holter monitoring and neurologic evaluation were nondiagnostic in all patients prior to EPS. EPS demonstrated inducible ventricular tachycardia (VT) in four patients, an HV interval greater than or equal to 70 msec in four, intra- and infra-His block with atrial pacing in one, and was nondiagnostic in four patients. Four of six patients with an HV interval greater than or equal to 70 msec or pacing-induced infranodal block were treated with permanent pacemakers, four of four patients with VT received antiarrhythmic therapy, and three of four patients with nondiagnostic studies received no therapy (one patient received a permanent pacemaker). During a mean follow-up period of 19 months (range 3 to 60 months) all but three patients have been free of syncope. One patient with VT did not take prescribed antiarrhythmic therapy, another patient with VT died suddenly; the remaining patient had a normal study and basilar migraines were subsequently diagnosed. We conclude that: (1) ventricular tachycardia may be a significant cause of syncope in patients with bifascicular block and was induced by programmed stimulation in approximately one third of patients studied; (2) EPS including programmed stimulation is helpful in delineating both the etiology of syncope and appropriate treatment in patients with bifascicular block. A negative study may also be of prognostic value.