摘要:

Coronary Sinus Ostium.Introduction: The purpose of this study was to perform a quantitative fluoroscopic analysis of the coronary sinus ostium and its relationship to the His bundle in patients with and without AV nodal reentrant tachycardia. Sites of slow pathway ablation are often near the coronary sinus ostium, which can be located within a few millimeters of the His bundle. Whether such close proximity of the coronary sinus ostium to the His bundle is unique to patients with AV nodal reentrant tachycardia is unknown.Methods and Results: Fifty consecutive patients (mean age 39 ± 14 years) with no structural heart disease underwent electrophysiologic testing and radiofrequency ablation. The study group consisted of 28 patients with inducible AV nodal reentrant tachycardia or dual AV nodal physiology and 22 patients in the control group. A coronary sinus venogram was performed in each patient. The coronary sinus ostium was similar in size in the study group (11.4 ± 4.5 mm) and in the control group (10.5 ± 3.6 mm, P = 0.2). The coronary sinus ostium was funnel shaped in half of the study patients and in half of the control patients (P = 1.0). The mean distance from the upper lip of the coronary sinus ostium to the tip of the His bundle catheter was 9.7 ± 5.5 mm in the study group and 10.4 ± 5.1 mm in the control group (P = 0.7). The mean distance from the lower lip of the coronary sinus ostium to the tip of the His‐bundle catheter in the study group was 20.1 ± 6.1 mm and 19.5 ± 5.6 mm in the control group (P =0.7).Conclusion: This study demonstrates a wide range of normal coronary sinus ostium diameters, morphology, and anatomic relationships with surrounding structures, with no demonstrable correlation to the presence or absence of dual AV node physiology or AV nodal reentrant tac

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00444.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Dofetilide and Ventricular Tachyarrhythmias.Introduction: Dofetilide is a new antiarrhythmic agent with potent Ikblocking properties in vitro. We developed a dose‐ranging, placebo‐controlled study design to define the range of effective doses and to evaluate the clinical electrophysiology of intravenous dofetilide in patients in whom sustained ventricular tachycardia or fibrillation was reproducibly inducible at baseline electrophysiologic testing.Methods and Results: The initial four patients received low doses that were increased in subsequent groups of four if adverse effects were absent. In each group of four patients, one patient was randomly assigned to placebo (double blind). Twenty‐four patients were studied at six incremental loading and maintenance infusion regimens. Dofetilide (0.1 to 8.0 ng/ml.) produced concentration‐related increases in the %δ of QT (r = 0.79, P<0.001). QTc(r = 0.60, P =0.02), RR (r = 0.62, P<0.02), and right ventricular effective refractory period (cycle length 600 msec; r = 0.68, P = 0.04). Placebo produced no changes in any of these measurements. Sustained ventricular tachycardia or ventricular fibrillation was no longer inducible in 1 of 6 patients receiving placebo and 8 of 18 receiving dofetilide (4 to 13 sec nonsustained ventricular tachycardia was induced in 4 of these 8). One patient developed torsades de pointes at a high concentration (5.3 ng/mL).Conclusions: We conclude that: (1) dofetilide produces concentration‐related Igblocking effects in patients: (2) an incremental dose‐ranging study design aids in identifying the range of doses demonstrating electrophysiologic effects and efficacy; (3) a concomitant placebo group provides important data to assess reproducibility of results over time; and (4) further studies of dofetilide's efficacy and toxicity should

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00445.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Long RP Tachycardia.Introduction: The purpose of this study is to describe a simple and reliable diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long KP tachycardia. Long RP tachycardias may he caused by atypical AVNRT, orthodromic reciprocating tachycardia (ORT) involving a slowly conducting retrograde accessory pathway, or atrial tachycardia. The differentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium.Methods and Results: Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventional criteria were enrolled In this study. The atrial‐His (AH) interval was measured at the His‐bundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 msec ± 50 msec (± SD) longer during high right atrial pacing than during the tachycardia (P<0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the AH interval measured during the tachycardia. In contrast, in patients with ORT or atrial tachycardia, the differences in AH interval between atrial pacing and tachycardia were never more than 20 and 10 msec, respectively.Conclusion: The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of differentiating atypical AVNRT from other types of long RP tachyca

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00446.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Influence of Slow Pathway Ablation on Atrial Fibrillation.Introduction: The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well‐defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.Methods and Results: In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1‐week follow‐up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P<0.01), 673 ± 161 (P<0.01), and 535 ± 98 msec (P<0.01), respectively. These effects remained stable during follow‐up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P<0.05) immediately and to 400 ± 56 msec (P<0.01) at 1‐week follow‐up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P<0.05), respectively.Conclusion: This study shows a decrease in ventricular response to pacing‐induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of poster

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00447.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Antiarrhythmic Drugs and DFT.Introduction: Class III antiarrhythmics have been reported to lower defibrillation threshold (DFT); however, the mechanism(s) of this effect is unknown. Recent evidence suggests that DFT strength DC shocks may terminate reentrant arrhythmias through prolongation of action potential duration and refractory periods. Since Class III antiarrhythmic drugs prolong repolarization, we examined the hypothesis that these drugs enhance shock‐induced action potential duration extension (APDE), which might contribute to lowering of DFT.Methods and Results: In order to investigate the specificity of drug effects on action potential repolarization following a shock, an optical enantiomer with mixed β‐blocking and Class III effects (CK‐4000) and its enantiomer with “pure” Class III antiarrhythmic effects (CK‐4001) were compared against placebo in a canine defibrillation model (n = 8 per group). At the 3 mg/kg dose, the enantiomers nonstereoselectively lowered DFT voltage by 19 ± 15% (CK‐4000, P<0.05 compared to placebo) and 25 ± 12% (CK‐4001, P<0.05 compared to placebo), indicating that Class III antiarrhythmic actions alone were sufficient for this effect. Similarly, CK‐4000 and CK‐4001 at 3 mg/kg enhanced APDE (P<0.01 compared to placebo) by 20 ± 11% and 24 ± 17%, respectively. APDF prolongation significantly correlated with reduction in DFT voltage for both CK‐4000 (r = ‐0.55, P<0.03) and CK4001 (r = ‐0.63, P<0.01). At 3 mg/kg, the enantiomers stereoselectively prolonged action potential duration (APD75) by an average of 37 ± 14% (CK‐4000, P<0.001) and 23 ± 14% (CK‐4001, P<0.001), and ventricular effective refractory period (VERP) by 38 ± 15% (CK‐4000, P<0.01) and 27 ± 13% (CK‐4001, P<0.05). Prolongations of APD75and VERP did not correlate with reductions of DFT in individual dogs.Conclusions: These results show that Class III antiarrhythmics and DFT strength shocks additively delay repolarization, which suggests that drug enhancement of A

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00448.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Effects of Cocaine on Triggered Activity.Introduction: Cocaine has been shown to have broad cardiovascular effects that could be life threatening. Most of the reported electrophysiologic effects of cocaine have been studied in normal but not infarcted myocardium.Methods and Results: Using microelectrode techniques, we investigated the eletrophysiologic effects of cocaine on endocardial canine Purkinje fibers that survived 1 day of myocardial infarction. In quiescent infarcted preparations, stimulated trains were followed by subthreshold delayed afterdepolarizations (DADs), in the presence of propranolol (1 μ M). Cocaine (10 μ M) decreased the amplitude of DADs from 6.1 ± 1.8 mV to 3.0 ± 1.3 mV (P<0.05, n = 6). When stimulated preparations (n = 23) showing no triggered activity during control (+propranolol) were superfused with a low concentration of caffeine (1 mM) or high extracellular Ca2+(8.1 mM), triggered activity was induced. Subsequent cocaine (10 μ M) superfusion prevented the induction of caffeine‐ and high Ca2+‐induced triggered activity. Cocaine's effects were reversible upon washout. In preparations that showed triggered activity during control conditions (+propranolol), the mean cycle length of triggered activity was 755 ± 45 msec. Cocaine (10 μ M) superfusion lengthened the cycle length to 1030 ± 141 msec and terminated triggered activity with a subthreshold DAD (n = 12). In addition, cocaine and ryanodine (10 μ M) suppressed triggered activity in a similar manner when tested in the same preparations (n = 4). During control conditions, cocaine did not cause any significant change on the rate of rise of action potential upstroke (from 55.6 ± 24.3 to 54.5 ± 28.6 V/sec, n = 8) and maximum diastolic potential (from ‐58.4 ± 4.3 to 56.6 ± 6.5 mV, n = 8). In the absence of propranolol, 50 μ M but not 10 μ M cocaine induced early afterdepolarizations in 62% of the preparations exhibiting triggered activity during control conditions.Conclusion: The results suggest that cocaine modulates DADs and triggered activity in infarcted endocardial fibers via direct inhibition of cyclic release of Ca2+from sarcoplasmic reticulum (SR) independently from a local anesthetic or sympathomimetic effect. This SR inhibition could account for the myocardial depressant effect of cocaine. However, while cocaine suppressed DADs, its induction of EADs can precipitate malignant ventricular arrhythmias in the setting of cocaine ove

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00449.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Optimal Monophasic and Biphasic Waveforms.Introduction: The truncated exponential waveform from an implantable cardioverter defibrillator can be described by three quantities: the leading edge voltage, the waveform duration, and the waveform time coastant (τs). The goal of this work was to develop and test a mathematical model of defibrillation that predicts the optimal durations for monophasic and the first phase of biphasic waveforms for different τsvalues. In 1932, Blair used a parallel resistor‐capacitor network as a model of the cell membrane to develop an equation that describes stimulation using square waves. We extended Blair's model of stimulation, using a resistor‐capacitor network time constant (τm), equal to 2.8 msec, to explicitly account for the waveform shape of a truncated exponential waveform. This extended model predicted that for monophasic waveforms with τsof 1.5 msec, leading edge voltage will be constant for waveforms 2 msec and longer; for τsof 3 msec, leading edge voltage will be constant for waveforms 3 msec and longer; for τsof 6 msec, leading edge voltage will be constant for waveforms 4 msec and longer. We hypothesized that the best phase 1 of a biphasic waveform is the best monophasic waveform. Therefore, the optimal first phase of a biphasic waveform for a given τsis the same as the optimal monophasic waveform.Methods and Results: We tested these hypotheses in two animal experiments. Part I: Defibrillation thresholds were determined for monophasic waveforms in eight dogs. For τsof 1.5 msec, waveforms were truncated at 1, 1.5, 2, 2.5, 3, 4, 5, and 6 msec. For τsof 3 msec, waveforms were truncated at 1, 2, 3, 4, 5, 6, and 8 msec. For τsof 6 msec, waveforms were truncated at 2, 3, 4, 5, 6, 8, and 10 msec. For waveforms with τs, of 1.5, leading edge voltage was not significantly different for the waveform durations of 1.5 msec and longer. For waveforms witb τsof 3 msec, leading edge voltage was not significantly different for waveform durations of 2 msec and longer. For waveforms with τsof 6 msec, there was no significant difference in leading edge voltage for the waveforms tested.Part II: Defibrillation thresholds were determined in another eight dogs for the same three τsvalues For each value of τs, six biphasic waveforms were tested: 1/1, 2/2, 3/3, 4/4, 5/5, and 6/6 msec. For waveforms with τsof 1.5 msec, leading edge voltage was a minimum for the 2/2 msec waveform. For waveforms with τsof 3 msec, leading edge voltage was a minimum for the 3/3 msec waveform. For waveforms with τsof 6 msec, leading edge voltage was a minimum and not significantly different for the 3/3, 4/4, 5/5, and 6/6 msec waveforms.Conclusions: The model predicts the optimal monophasic duration and the first phase of a biphasic waveform to within 1 msec as τsvaries from 1.5 to 6 msec: for τsequal to 1.5 msec, the optimal monophasic waveform duration and the optimal first phase of a biphasic waveform is 2 msec, for τsequal to 3.0 msec, the optimal duration is 3 msec, and for τsequal to 6 msec, the optimal duration is 4 msec. For both monophasic and biphasic waveforms, optimal waveform duration shortens as the wavefo

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00450.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Cardiac Pacing and Neurocardiogenic Syncope. Head‐up tilt testing is increasingly being used as a diagnostic modality in patients with unexplained syncope who are thought to have neurocardiogenic (vasovagal) mechanisms of syncope. Although large‐scale placebo‐controlled trials are still awaited, pharmacologic therapy is usually effective in preventing syncope or presyncope in this patient population. However, the role of permanent pacemaker therapy remains controversial. Because hypotension is usually associated with paradoxical bradycardia and occasionally asystole, it has been argued that permanent pacemaker therapy may be useful in preventing syncope and, thus, injury, in the so‐called “malignant vasovagal cardioinhibitory response” in which the onset of syncope is thought to be abrupt. The onset of hypotension, however, usually precedes bradycardia during neurocardiogenic syncope, and pacing may thus not prevent syncope or presyncope in these patients. The role of cardiac pacing in patients with neurocardiogenic syncope

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00451.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY

摘要:

Baroreflex Sensitivity. Baroreflex sensitivity (BRS) has rapidly gained considerable attention as a result of multiple experimental and clinical reports on its prognostic value after a myocardial infarction. This article reviews the several aspects related to the use and significance of BRS. The methodology of baroreflex testing in man is described. The complex pathophysiology underlying BRS and the hypotheses proposed to explain its frequent reduction after a myocardial infarction are discussed. The section on experimental data also provides a rationale to understand the relation between increased vagal activity and reduced propensity for ventricular fibrillation. The article focuses largely on the clinical studies relating BRS and risk of cardiac mortality and also discusses the several attempts to modify this marker of reflex vagal activation.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1995.tb00452.x

出版商:Blackwell Publishing Ltd    

年代:1995

数据来源: WILEY