Accuracy and clinical utility of transtelephonic pacemaker follow-up.

The diagnostic accuracy of transtelephonic pacemaker monitoring (TTM) has been quantified in a retrospective study involving 369 patients in three U.S. cardiac centers. Using existing medical records, TTM findings in a total of 413 reports were judged for equivalence to the findings of subsequent physical examinations in pacemaker clinics. This study found TTM follow-up testing to have a sensitivity of 94.6%, specificity of 98.5%, positive predictive value of 93.3%, and negative predictive value of 98.8%. The study also documents the clinical utility of TTM in identifying various modes of pacemaker malfunctions and instances of significant arrhythmia.

Innovative methods of cardiac defibrillation.

Sudden death caused by fatal cardiac arrhythmias represents a major health care problem in New Jersey. The use of a remote transtelephonic defibrillator, a technique undergoing development, is an interesting new approach to provide prompt restoration of cardiac rhythm and function.

Halothane antagonizes ouabain toxicity in isolated canine Purkinje fibers.

Standard intracellular microelectrode techniques were used to study the effects of halothane on ouabain-induced delayed after depolarizations (DAD) in canine Purkinje fibers. Free running Purkinje fibers were superfused with 2 X 10(-7)M ouabain in Krebs-Henseleit buffer for 30-50 min until DAD appeared. Purkinje fibers were then paced for 20 beats at cycle lengths between 1,000 ms and 200 ms, and the amplitude of the DAD and coupling interval between the DAD and last paced beat were determined. Halothane (0.5, 1, and 2%) was then administered and measurements repeated. Halothane produced dose-related decreases in DAD amplitude without changing DAD coupling interval. The ability of calcium to antagonize the effects of halothane was evaluated by doubling buffer calcium concentration to 5 mM in the presence of halothane 2%. Doubling buffer calcium concentration to 5 mM antagonized the reduction of DAD amplitude caused by halothane. In several preparations, dysrhythmias occurred during ouabain superfusion. Halothane reversibly terminated these arrhythmias. Halothane antagonizes DAD and dysrhythmias induced in vitro by ouabain toxicity. This effect, in part, may account for the apparent effectiveness of halothane against ouabain-induced dysrhythmias in vivo.

A comparison of the electrophysiologic effects of acute and chronic amiodarone administration on canine Purkinje fibers.

The electrophysiologic effects of acutely and chronically administered amiodarone on canine Purkinje fibers were assessed using microelectrode techniques to record intracellular action potentials. Chronically treated dogs received amiodarone for 3 weeks (serum levels, 0.91 +/- 0.09 microgram/ml or 1.42 X 10(-6) M). Acute studies were performed using fibers from untreated dogs superfused for 1 h with 5 X 10(-5) M amiodarone (32 micrograms/ml) in Tyrode's solution (KCl = 4 mM). Acute superfusion shortened the action potential duration to 50 and 90% repolarization by 41 and 8%, respectively (p less than 0.01), and decreased Vmax of phase 0 from 418 +/- 20 to 309 +/- 23 V/s (p less than 0.01) (paced cycle length of 500 ms). Prominent use-dependent depression of Vmax was noted. Acute exposure of fibers from untreated dogs to blood from dogs chronically treated with amiodarone using the blood cross-perfusion technique decreased the action potential duration to 50% repolarization and Vmax, similar to acute exposure in Tyrode's solution. Blood cross-perfusion was used to study fibers from treated dogs superfused with blood from another amiodarone-treated dog. Chronic amiodarone prolonged the action potential duration to 90% repolarization by 13% (p less than 0.02) and did not change Vmax when compared to control studies using fibers obtained from untreated dogs superfused with blood from untreated dogs. Thus, the effects of acutely superfused amiodarone on action potentials of canine Purkinje fibers differ from the effects of chronically administered amiodarone.

Chronotropic response of an activity detecting pacemaker compared with the normal sinus node.

We compared the rate responsiveness of an activity-detecting multiprogrammable, single chamber pacemaker (Medtronic Activitrax) to rate responsiveness of the normal sinus node. This pacemaker changes its basic pacing rate in response to physical activity. The rate responsiveness is programmable by selecting one of three activity thresholds, and one of 10 rate response settings. The study included a group of six normal volunteers and 12 patients implanted with Activitrax to examine the similarity of the pacemaker rate to normal sinus rhythm during acceleration and deceleration. The pacemaker was set to Activity mode, at a basic rate of 60 bpm. In volunteers, the device was externally secured on the chest wall and tested at two programmed settings. When programmed at a high threshold of activity and high rate response in volunteers, there was no significant difference in maximum normal sinus rates and pacemaker rates during arm waving, jumping in place, and walking during stress testing. At a medium activity threshold, the only significant difference occurred during submaximal stress testing, when the maximum sinus rate achieved was 141 +/- 19 bpm and the maximum pacing rate was 105 +/- 8 bpm (p less than .02). The pacemaker behaved in a similar manner in patients, successfully simulating the typical fast acceleration and slow deceleration of a normal sinus node in exercise testing. There was no difference in pacer response when implanted in abdominal or infraclavicular locations. The implanted units have functioned normally over a follow-up period of nine to 22 months. Activitrax can be programmed to achieve physiologic pacing rates in response to normal daily activities with appropriate programming.

Electrophysiologic effects of halothane and quinidine on canine Purkinje fibers: evidence for a synergistic interaction.

The authors studied possible interactions between halothane and quinidine on the action potentials of canine Purkinje fibers superfused with Tyrode's solution. Using standard microelectrode techniques and a physiologic pacing rate (2 Hz), halothane in concentrations from 0.5% to 2% decreased the action potential duration to 50% repolarization (ADP50). Total ADP (APD100), in contrast, increased after 1% and 2% halothane. Resting membrane potential (RMP) and action potential amplitude (APamp) increased after 0.5% halothane, but returned to control with higher halothane levels. Conduction time (CT) increased at each halothane level. Pacing at faster (3 Hz) or slower (1 Hz) rates did not markedly alter the effects of halothane. Quinidine 1 X 10(-5)M decreased the phase O upstroke (Vmax) and prolonged APD100 and CT. When halothane was added, RMP and APamp decreased, Vmax decreased further, and APD100 and CT were markedly prolonged. This resulted in conduction block or inexcitability, especially at faster pacing rates (3 Hz). Synergistic interactions between halothane and quinidine were found on RMP, APamp, APD100, and CT. Effects on Vmax, APD50, and action potential duration to 90% repolarization (APD90) were additive. It is concluded that quinidine and halothane act synergistically to decrease action potential amplitude, lower RMP, and prolong conduction. Severe depression of conduction often progressed to conduction block or inexcitability when halothane, 2%, was administered during superfusion with therapeutic concentrations of quinidine.

Simultaneous appearance of endocardial late potentials and ability to induce sustained ventricular tachycardia after procainamide administration.

We describe a patient in whom procainamide induced the appearance of late potentials during intraoperative sinus rhythm electrogram mapping. Only nonsustained ventricular tachycardia (VT) could be induced while off all antiarrhythmic drugs. After administration of the procainamide, programmed stimulation induced sustained VT coincident with the appearance of late potentials during sinus rhythm. The late potential was recorded from the same site, during normal sinus rhythm, where mid to late diastolic activation during VT was recorded, and where cryotermination occurred during cryomapping. We hypothesize that procainamide slowed conduction, manifested as prolongation or appearance of late potentials in sinus rhythm, and facilitated induction of sustained reentrant ventricular tachycardia.

Correlates of prolonged HV conduction in aortic stenosis.

Forty-eight patients with predominant aortic stenosis underwent His bundle electrography (HBE) at the time of diagnostic catheterization. Patients were divided into four groups based upon severity of calcification of the aortic valve fluoroscopically as judged independently by three angiographers. Of 48 patients, three had no calcification, 11 had mild, 18 had moderate, and 16 had severe aortic valve calcification. No correlation was found between HV interval and severity of aortic valve calcification. Significant correlation was found between HV interval prolongation and aortic valve area (p less than 0.02), history of congestive heart failure (p less than 0.02), and increasing left ventricular end-diastolic pressure (p less than 0.05). Left ventricular ejection fraction less than 45% had greater likelihood of HV interval prolongation (p less than 0.01). No correlation was established between HV interval and age, aortic valve gradient, left ventricular peak systolic pressure, syncope, and coronary artery disease. Aortic valve area was the most significant independent predictor of HV prolongation, with history of congestive heart failure second. We conclude that HV interval prolongation in aortic stenosis with calcified valves is best predicted by evidence of declining left ventricular function rather than severity of aortic valve calcification.

Esophageal P-synchronous pacing.

An esophageal electrode can be employed to provide atrial sensing which then can be used to change from temporary right ventricular (VVI) pacing to P-synchronous (VAT) pacing. Two cases of postoperative aortic valve replacement, each with new complete heart block (CHB) and dopamine dependency, are presented. In both cases, establishment of P-synchronous pacing resulted in improved hemodynamic status characterized by successful weaning from dopamine and maintenance of adequate cardiac output (CO).

Cryothermal mapping of recurrent ventricular tachycardia in man.

Intraoperative reversible cryothermal mapping of recurrent ventricular tachycardia was performed in seven patients with left ventricular aneurysms with use of a 0 degrees C ice probe. A single, reproducible cryotermination site was found in each patient. The cryotermination site was uniformly located in an area where local electrograms obtained during ventricular tachycardia showed electrical activation during the diastolic portion of the surface electrocardiogram, and was different than the site of activation coincident with the onset of the QRS complex on the surface electrocardiogram (earliest reactivation site or ERS) by 4.5 +/- 2.7 cm (mean +/- SD) in five of seven patients. Sinus rhythm late potentials were recorded at the cryotermination site in five of six patients and from the ERS in one. In five patients, extensive subendocardial resection including both the ERS and cryotermination sites was performed. In two patients only the cryotermination site was excised. In six survivors, including one in whom only the cryotermination site was excised, ventricular tachycardia could not be induced 2 weeks after surgery and has not recurred during the follow-up period of 7 to 17 months (12 +/- 4.5 months, mean +/- SD). Reversible cryothermal mapping may provide additional important information not obtained by standard electrogram mapping of ventricular tachycardia that may help guide surgical therapy of recurrent ventricular tachycardia.

Radionuclide angiography in the quantitation of mitral regurgitation.

First pass radionuclide angiography (RA) was used to assess its ability to detect and quantitate the presence of left-sided regurgitation due to isolated mitral regurgitation (MR). In this study the nuclear regurgitant fraction (NRF) obtained from first pass RA was correlated with the results of contrast ventriculography (CV) in 50 patients, 18 with and 32 without MR. The correlation between CV and RA in the confirmation and quantification of isolated MR revealed a sensitivity of 100 percent and a specificity of 97 percent in patients with LVEF greater than or equal to 35 percent.

Emergency guide wire pacing: new methods for rapid conversion of a cardiac catheter into a pacemaker.

We developed a new electrode to convert rapidly a previously inserted pulmonary artery or left ventricular catheter into a pacemaker. One method of doing this is by withdrawal of the pulmonary artery catheter from the pulmonary artery to the right ventricle by pressure control, and a Teflon-coated guide wire, stripped of 5 mm of insulation at its tip, is advanced through the catheter to contact the endocardium. In the second method, the pacing electrode is advanced through the distal lumen of the catheter while it is positioned within the pulmonary artery and withdrawn into the right ventricle while pacing. Finally, a third method involves advancement of the guide wire electrode into the left ventricle through a pigtail catheter. To pace, the guide wire electrode is connected to the cathode of a pacemaker referenced to a skin electrode. We paced 10 of 10 right heart cardiac catheterization, intra- and postoperative surgery patients by methods 1 and 2, and 4 of 4 left heart catheterization patients by method 3. Thresholds (mean +/- SEM) for guide wire pacing were: right ventricle 1.52 +/- 0.4 mA; left ventricle 1.33 +/- 0.1 mA. Guide wire pacing is rapid, reliable, and requires little operator skill. Our indications for guide wire pacing are: 1) emergency right ventricular pacing in operative or intensive care unit patients with unexpected bradyarrhythmias who have an indwelling pulmonary artery catheter; and 2) emergency left ventricular pacing in left heart cardiac catheterization patients with contrast-induced bradyarrhythmias.

Dissociation of the site of origin from the site of cryo-termination of ventricular tachycardia.

We performed conventional electrogram mapping and cryomapping in dogs with one-week-old experimentally-induced myocardial infarctions and programmed stimulation-induced sustained ventricular tachycardias to assess whether there is a correlation between the "site of origin" and site of cryo-termination of ventricular tachycardia (VT). Electrogram maps showed that 4 of 8 induced sustained VTs were due to macro- and 4 of 8 to microre-entry. Local cooling of the site of origin terminated 4 of 4 microre-entrant VTs, but only 1 of 4 macrore-entrant VTs. In the other 3 macrore-entrant VTs, the sites of cryo-termination were 2, 2.5, and 4 cm distant from the sites of origin. In contrast, cooling of the mid-to-late diastolic portions of the re-entry loops terminated all 8 VTs. These data demonstrate a dissociation of the site of origin from the site of cryo-termination of macrore-entrant VT.

Localization and mechanism of ventricular tachycardia by ice mapping 1 week after the onset of myocardial infarction in dogs.

We developed a new technique of "ice mapping" to localize the site of termination of ventricular tachycardia in dogs 4 to 8 days after the onset of myocardial infarction. During programmed stimulation-induced ventricular tachycardia, the epicardium was mapped by moving an ice probe with a 1 cm tip over the infarct, lateral border, and normal areas. In 31 of 46 morphologically distinct sustained ventricular tachycardias, a specific area could be found that reproducibly terminated ventricular tachycardia. During ventricular tachycardia, bridging or late diastolic electrical activity was recorded from ice termination sites. In vitro microelectrode studies of 10 ice termination sites revealed slow conduction, but no spontaneous or triggered automaticity or delayed afterdepolarizations. Conduction slowed to complete block when the Tyrode perfusate was cooled from 37 degrees to 27 degrees C. We conclude that ice mapping can physiologically localize a site responsible for maintenance of ventricular tachycardia by termination of the arrhythmia, and that the presence of bridging or late diastolic electrical activity, slow conduction with cooling-induced block, and absence of spontaneous or triggered automaticity or delayed afterdepolarizations suggest that local cooling terminates ventricular tachycardia by slowing or blocking conduction in a reentrant loop.

A new device and method for rapid emergency pacing: clinical use in 10 patients.

A new multipurpose transthoracic pacing device is described that will simultaneously enable transthoracic electrode insertion, intracardiac drug infection, and blood sample removal for blood gas determination, all via a single myocardial needle insertion. The device proved efficacious and safe in trials in an animal model. In clinical use in 10 emergency room patients with brady-asystolic cardiac arrest, pacing was achieved in all 10 with one short-term survivor. Median insertion time was 30 seconds. Median threshold in 6 patients was 2.5 mA (1 to 6). This new device enables reliable and rapid emergency treatment of brady-asystolic cardiac arrest.