Effects of enhanced parasympathetic tone on atrioventricular nodal conduction during atrioventricular nodal reentrant tachycardia.

The effects of various physiologic and pharmacologic stimuli on the anterograde slow pathway in patients with atrioventricular nodal reentrant tachycardia are well characterized. We sought to further characterize the nature of anterograde and retrograde conduction during tachycardia and to define the differential input of the parasympathetic nervous system to these pathways. A custom-made neck suction collar was placed to stimulate the carotid body baroreceptors during supraventricular tachycardia. Neck suction at -60 mm Hg was applied and changes in tachycardia cycle length, AH, and ventriculoatrial intervals were measured in 20 patients. These measurements were repeated after intravenous administration of 10 mg of edrophonium to enhance vagal tone. We observed a 15 +/- 6 ms increase in tachycardia cycle length from baseline (p <0.0001) and a 14 +/- 6 ms increase in AH interval (p <0.0001), but no change in the VA interval with neck suction alone. The tachycardia cycle length prolonged 26 +/- 55 ms (p <0.0001) with edrophonium and an additional 12 +/- 43 ms (p <0.001) with neck suction after edrophonium. There was no change in the VA interval before or after edrophonium during neck suction. There were 10 tachycardia terminations in 8 patients during anterograde slow pathway block during neck suction, with tachycardia cycle length prolongation and mean AH prolongation before termination of 45 +/- 37 ms (vs 15 +/- 7 ms increase in AH interval without tachycardia termination, p = 0.10). There were 12 tachycardia terminations in 4 patients with retrograde block during neck suction, only after edrophonium, without any preceding change in tachycardia cycle length during 11 episodes. We conclude that anterograde slow pathway demonstrates gradual conduction slowing with parasympathetic enhancement, whereas retrograde fast pathway responds with abrupt block.

Selective slow pathway ablation does not alter enhancement of vagal tone on sinus and atrioventricular nodal function.

We studied the effects of edrophonium on sinus cycle length, atrioventricular (AV) nodal fast pathway refractoriness, and AV nodal Wenckebach cycle length in 21 patients with AV nodal reentrant tachycardia (AVNRT) who received edrophonium, and 8 patients who received phenylephrine before and after selective slow pathway ablation. Changes in sinus cycle length, fast pathway conduction, and refractoriness were not altered by radiofrequency ablation of the slow pathway, suggesting that parasympathetic denervation does not occur after slow pathway ablation of AVNRT.

Late occurrence of incessant atrial tachycardia following the maze procedure.

We report a patient with incessant atrial tachycardia and AV nodal reentrant tachycardia tachycardia and AV nodal reentrant tachycardia beginning almost 18 months following a successful maze procedure. Both tachycardias were cured by radiofrequency ablation. We speculate that the right atrial tachycardia may have been related to the maze procedure. Finally, we believe this report should emphasize the importance of careful and long-term follow-up of all patients undergoing the maze procedure. Proper evaluation of the place of this therapy greatly depends on reporting of all short- and long-term complications of this new procedure.

Safety of pacemaker implantation in patients with transvenous (nonthoracotomy) implantable cardioverter defibrillators.

While several reports have documented the safety of implantation of transvenous pacemakers in patients with epicardial patch-based implantable cardioverter defibrillators (ICDs), the implantation of transvenous pacemakers in patients with transvenous (nonthoracotomy) ICDs has not been well-described. We present three patients with transvenous ICDs who subsequently underwent implantation of transvenous pacemakers without complication. Technical considerations and a testing, protocol for detection of pacemaker-ICD interactions are discussed.

Radiofrequency catheter ablation of sinus node reentrant tachycardia.

Sinus node reentrant tachycardia is a relatively uncommon (5%-15%) form of recurrent paroxysmal supraventricular tachycardia (SVT). We describe a case of symptomatic sinus node reentrant tachycardia in a 67-year-old male with ischemic heart disease, congestive heart failure, and depressed ventricular function. Adenosine administered during an electrophysiology study caused prolongation of the tachycardia cycle length due to atrial cycle length prolongation (without atrio-His prolongation) prior to tachycardia termination. Right atrial mapping revealed the earliest site of atrial activation in the high lateral right atrium just below the superior vena cava. Low energy (10 and 20 W) radiofrequency lesions were applied at this site with termination of the tachycardia within 3 seconds of radiofrequency energy delivery. Tachycardia could not be reinduced after delivery of the radiofrequency lesions. The sinus node function immediately and 6 weeks after radiofrequency catheter ablation remained normal and the patient was without clinical recurrence of SVT. Mapping of sinus node reentrant tachycardia and elimination of the reentrant circuit with radiofrequency catheter ablation is possible without causing sinus node dysfunction. Adenosine causes prolongation of the atrial cycle length followed by termination of sinus node reentrant tachycardia.

The effect of left ventricular intracavitary volume on the unipolar electrogram.

In order to examine the effects of ventricular distention on the unipolar electrogram (UEG), an isolated rabbit heart modified Langendorff preparation was utilized. Left ventricular (LV) volume was adjusted using ionically permeable (PB = 9 hearts) or ionically impermeable balloons (IB = 4 hearts). LV UEGs, LV end-diastolic pressure (EDP), and LV minor axis dimension (MAD), as measured by ultrasonic transducers, were recorded. Three hundred twenty-five electrograms were digitized and analyzed with custom-designed software. In the PB group, a significant inverse linear relationship was found between UEG amplitude and changes in MAD (P < 0.0001). For each animal, this relationship had an R value > 0.8 and a P value < 0.0001. There was also a significant inverse linear relationship between UEG slope and changes in MAD (P < 0.01). UEG amplitude and slope also exhibited a significant inverse relationship to changes in LV EDP, which were best described by a third order polynomial function. In the IB group, no significant relationship was found between either UEG amplitude or slope and MAD or EDP. In this study, intracavitary volume exerted a profound and significant influence on UEG amplitude and slope. This effect was due to increases in conductive intraventricular volume and not to myocardial stretch.

Electrophysiological consequences of hypothermic hyperkalemic elective cardiac arrest.

While the development of pharmacological cardioplegic solutions for myocardial protection during cardiopulmonary bypass (CPB) have significantly lengthened the safe operating time for cardiac surgical procedures, the introduction of hypothermic hyperkalemic cardioplegia (CPG) has markedly increased the incidence of postoperative arrhythmias and conduction abnormalities. Using a customized modification of a computerized mapping system, we have developed a large animal porcine model of CPB that is exquisitely sensitive to the electrophysiological (EP) derangements imposed by ischemia and cardiac arrest. This model is able to measure spatial and temporal parameters of ventricular activation with high resolution, using an array of up to 84 epicardial electrodes that can be reproducibly placed on the surface of the heart utilizing known epicardial anatomical markers (e.g., coronary arteries). With this system we have measured the spectrum of clinically observed EP disturbances caused by CPG, from slowed intraventricular conduction to complete heart block. Compared to the control group of hypothermia alone, 2 hours of crystalloid CPG arrest had a significant slowing effect on ventricular activation (p < 0.05). CPG was accompanied, in each animal, by profound changes in the spatial distribution of ventricular activation and persistent slowing of ventricular activation. Traditional EP parameters of effective refractory period and pacing threshold were unchanged by CPG. Smaller temporal and spatial changes were observed in the control group, but were always reversed by 90 minutes of warm reperfusion. We conclude that CPG induces injury of the specialized conducting system and, to a lesser degree, the myocardium. This model will afford us the opportunity to test new methods of CPG to further improve myocardial preservation during CPB.

Differentiation between monomorphic ventricular tachycardia and sinus tachycardia based on the right ventricular evoked potential.

The differentiation between ventricular tachycardia (VT) and sinus tachycardia (ST) is problematic in some patients with implantable defibrillators and/or antitachycardia pacemakers. The integral of the ventricular endocardial evoked response, or paced depolarization integral (PDI), has been demonstrated to undergo characteristic changes with a variety of stimuli including catecholamines, pacing rate, and exercise. We hypothesized that the PDI recorded from a unipolar transvenous right ventricular endocardial catheter would differentiate VT from ST. The PDI was calculated from a unipolar pacing stimulus, delivered via a cathode in the right ventricular apex, and the reference electrode, a quadripolar catheter positioned in the superior vena cava. PDIs were measured in 22 patients during VT and sinus rhythm. The PDI measured during sinus rhythm was 579 +/- 240 microV-sec and the PDI during VT was 894 +/- 411 microV-sec (P < 0.001). In a subset of seven patients, PDIs were measured during VT, sinus rhythm, and ST induced by catecholamine infusion or exercise. In this subset, the PDI during sinus rhythm was 645 +/- 295 microV-sec, during ST 588 +/- 308 microV-sec (9% decrease from sinus, P = 0.05), and during VT 863 +/- 342 microV-sec (33.9% increase, P = 0.01). These data indicate that the measurement of the PDI is potentially useful in differentiating VT from ST.