摘要:

Variations in Atrial Flutter Cycle Length.Introduction: The purpose of this investigation was to study the mechanisms responsible for small variations in atrial flutter cycle lengths.Methods and Results: In a study group of 11 patients with common atrial flutter, atrial electrograms were recorded from an intraesophageal lead together with a surface lead (V1). Upon the onset of the QRS complex, atrial flutter intervals consistently increased by an average of 1.8% (SD± 0.9; P<0.01) and subsequently decreased by 2.1% (SD ± 0.8; P<0.01) before returning to the average flutter rate. Carotid sinus massage, which temporally prevented ventricular activation, markedly reduced the variations in atrial flutter intervals. Ventricular pacing at different rates clearly demonstrated that the pattern in atrial flutter intervals was coupled to the moment of ventricular contraction. The hypothesis was formulated that these periodic variations in atrial flutter intervals following a ventricular contraction were caused by the influence of stretch of the atrial myocardium on the conduction properties of a circulating impulse in the atrium. The secondary decrease in flutter rate could be explained if a partial excitable gap is assumed between head and tail of the circus movement. This hypothesis was tested in a simulation study, which revealed that the alternation in intervals as found in patients could only be reproduced if the excitable gap in the circus movement was partially excitable.Conclusion: In conclusion, the analysis of variations in atrial flutter cycle lengths points to a mechanism of circus movement with a partially excitable gap in common atrial flutte

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01337.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Activation Time Detection for Intraoperative Mapping.Introduction: Local activation determined from monopolar electrograms usually is marked at the time of the minimum slope. In bipolar recordings, the peak, the maximum absolute slope, the baseline crossing of the segment containing the maximum absolute slope, and morphological criteria have been used. The purpose of this work is: (1) to compare activation times determined using these algorithms with activation times corrected by electrophysiologists; and (2) to determine which computerized algorithm requires fewest operator correction of outliers.Methods and Results: Monopolar and bipolar electrograms were collected from the epicardium of subjects undergoing surgery for ventricular tachycardia and Wolff‐Parkinson‐White syndrome, and the above bipolar and monopolar algorithms were evaluated. The electrophysiologists viewed adjacent channels and evolving isochronal maps but not the computer markings. The morphological algorithm compared most favorably with times marked up by electrophysiologists having an overall average difference of 2.2 ± 3.1 msec. For monopolar data, a five point, least square fit, second‐order slope approximation algorithm most closely agreed with the electrophysiologist corrected algorithm (3.2 ± 4.0 msec). The morphological and least square algorithms also produced the fewest outliers (3.1% and 5.7%, respectively). When outliers were removed, bipolar and monopolar discrepancies were reduced to 1.8 ± 1.9 and 2.5 ± 2.3 msec, respectively.Conclusions: Thus, among those algorithms tested, an algorithm based on morphological criteria is best suited for computer determination of bipolar activation times and compares favorably to variations between electrophysiologist corrected and computer marked activation times determined traditionally by the largest negative slope in monopolar data. Identification of outliers using contextual and improved morphological algorithms may improve computerized mapping system pe

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01338.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

The Local Atrial Deflection.Introduction: As a wave front passes unfiltered bipolar recording electrodes, the point of local depolarization is marked by a maximal change in voltage, i.e., the intrinsic deflection. However, during electrophysiologic studies, the depolarization (A) on the lead recording the His‐bundle potential traditionally has been measured at the first rapid reproducible deflection on a filtered electrogram. This methodology permits considerable latitude for subjective interpretation. The purpose of this study was to assess the timing of the atrial electrogram using the intrinsic deflection of relatively unfiltered electrograms (0.1‐4.0 to 1,250 Hz) or the equivalent on filtered recordings.Methods and Results: To do this we studied 70 patients without evidence of atrial or atrioventricular (AV) nodal disease, documenting the difference in timing between the A wave as traditionally measured and as measured at its peak local deflection (AL) determined from simultaneously recorded filtered and relatively unfiltered electrograms. New ranges based on the ALwere established for timing of intra‐atrial and AV nodal conduction intervals. The P‐A (41 ± 11 msec) was significantly shorter than the P‐AL(55 ± 12) and the A‐H (80 ± 20) was longer than the AL‐H (66 ± 21 msec), both P<0.001. Interobserver differences in measurements were smaller when using the local (AL) rather than traditional criteria.Conclusions: Conventional measurement of the A deflection provides only a rough estimate of local depolarization of the atrium near the AV node. The criteria proposed in the present article may (1) provide a better estimate of the timing of local depolarization; (2) have application in computerized timing of intervals; and (3) decrease technical problems and

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01339.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Cardiac Output and Pacing Rate.Introduction: The purpose of this report is to determine the optimal pacing rate for an exercising patient.Methods and Results: From a review of the literature and from our own animal studies, the relationship between cardiac output and pacing rate and that between stroke volume and pacing rate are examined in resting and exercising animal and human subjects. With an adequately wide range of pacing rates, there exists a three‐phase relationship between cardiac output and pacing rate. Starting with a low pacing pacing rate, an increase in pacing results in an increase in cardaac output (phase 1), then little change in cardiac output (phase 2), after which there is a decrease in cardiac output (phase 3). However, the relationship between stroke volume and pacing rate does not typically exhibit characteristics that allow identification of the three phases. In resting subjects with impaired ventricles and in exercising subjects, phase 2 is narrow or absent, the cardiac output increasing, then decreasing with an increase in pacing rate. From the experimental data reviewed herein, a technique is proposed for identifying the starting point in selecting the best pacing rate for resting and exercising subjects. The technique relies on identification of the transitions in the three‐phase relationship between cardiac output and pacing rate.Conclusion: The best resting pacing rate is at the lower end of phase 2. A tentative first‐choice exercise rate is at the middle of the resting phase 2 region. However, a change in cardiac output with a change in pacing rate will allow refinement of this first‐choice exercise paci

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01340.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01341.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Electrophysiology of 9‐Deoxydoxorubicin.Introduction: The purpose of this investigation was to use standard microelectrode techniques to study the actions of the anthracycline antibiotic, 9‐deoxydoxorubicin (9‐DOD), on cellular electrophysiologic properties of canine Purkinje fibers and on ouabain‐induced ventricular tachycardia (VT) in intact dogs.Methods and Results: 9‐DOD, 1‐5μM, suppressed delayed afterdepolarizations and prolonged repolarization and the effective refractory period in Purkinje fibers. It had no effect on maximum diastolic potential, V̇maxof phase 0, or action potential overshoot through a 10μM concentration. Although 9‐DOD did augment early afterdepolarizations (EAD) induced by cesium, it did not induce EAD. In six of eight intact dogs with ouabain‐induced VT, 9‐DOD, 0.32‐1.28 mg/m2IV, brought conversion to sinus or junctional rhythm. In its cellular and intact animal antiarrhythmic actions, 9‐DOD is about 50 times more potent than the parent compound, doxorubicin. Like doxorubicin, it is highly selective for delayed afterdepolarization‐induced rhythms, suppressing these at concentrations lower than those required to reduce the rate of automatic rhythms. Moreover, it has a greater Class III action than doxorubicin and prolongs the duration of normal and calcium‐induced (slow response) action potentials. Hence, this subtle variation on the doxorubicin molecule adds greatly to the antiarrhythmic action of the drug.Conclusions: Although useful as an investigative tool, clinical development of 9‐DOD as an antiarrhythmic is not possible because the antitumor activity of the parent compound, which results in lipid peroxidatio

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01342.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Partial Reversal of Flecainide Toxicity by Isoproterenol.Introduction: Toxic levels of flecainide can cause life‐threatening electrophysiologic and hemodynamic changes. Isoproterenol is known to reverse therapeutic drug effects in patients with ventricular and supraventricular tachycardias. In a single cell preparation it appears that isoproterenol increases inward Na current and it is conceivable that isoproterenol may also be capable of decreasing the electrophysiologic effects of flecainide toxicity. This study was aimed at detailed characterization of the electrophysiologic changes induced by toxic levels of flecainide, the extent that isoproterenol may reverse these changes, and the effect of beta blockade on these changes.Methods and Results: In this experimental model, using the strength‐interval stimulation method, conduction time, and epicardial activation times, we defined the changes in conduction, refractoriness, and excitability caused by toxic levels of flecainide (>3μg/mL), during infusions of flecainide and isoproterenol, and lastly, these infusions and propranolol. In nine dogs, using atrial and ventricular stimulation at pacing rates of 120 and 210 beats/min, atrioventricular conduction, right ventricular refractoriness, and conduction changes were evaluated at baseline and following isoproterenol infusion (0.09μg/kg/min), flecainide infusion (4 mg/kg followed by 5 mg/kg/hr), flecainide combined with isoproterenol infusion, and lastly, flecainide, isoproterenol, and propranolol (0.2 mg/kg). Compared to baseline, toxic levels of flecainide (3.71‐3.86μg/mL) produced a 64% and 93% increase in the atrial‐His interval at pacing rates of 120 and 210 beats/minute, respectively. Isoproterenol reversed 15% and 55% of this prolongation. The His‐ventricular conduction was prolonged by 82% and 124% after flecainide at 120 and 210 beats/min, respectively. These changes were reversed by 29% and 53% with isoproterenol. With flecainide, the relative and effective refractory periods of the ventricular myocardium (during right ventricular pacing) were lengthened by 16% and 19%, respectively, and reversed to baseline values following isoproterenol. None of the ventricular electrophysiologic parameters altered by flecainide were significantly affected with increasing pacing rate. The QRS complex duration increased by 59% with flecainide, and isoproterenol reversed 30% of this increase. Left ventricular (LV) activation time during right ventricular (RV) pacing increased by 88% with flecainide, 59% of which was reversed by isoproterenol. Propranolol resulted in complete elimination of the isoproterenol‐produced partial reversal of flecainide toxicity. RV diastolic pacing threshold was raised by 61% with flecainide, but this effect was not reversed with isoproterenol.Conclusion: It is concluded that at least 30% of the toxic effects of flecainide can be reversed by isoproterenol. Such reversal may be useful in treating flecainide toxicity. Pacing threshold, however, does not improve with isoproterenol, and all the isoproterenol effects are abolished by propranolol. The electrophysiologic effects of toxic levels of flecainide were further aggravated with the addition

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01343.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Cardiovascular Reflexes and Electrophysiology.The autonomic nervous system mediates control of the heart and circulation for several sensors located throughout the cardiovascular system. Afferent signals originate from mechanoreceptors located in the carotid sinus, aorta, chambers of the heart, and great veins near the heart, and from chemoreceptors in the aortic arch and carotid sinus. Efferent signals are transmitted through the vagus and sympathetic nerves to the heart and vascular tree. Hemodynamic and electrophysiologic homeostasis is maintained by beat‐to‐beat regulation via these reflexes. Several cardiovascular diseases are often accompanied by abnormal function of these reflexes; moreover, abnormalities of reflex control of the circulation often contribute to the pathophysiology of many cardiovascular disea

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01344.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01345.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

Alcohol Ablation of Ventricular Tachycardia.Ventricular tachycardia that is refractory to medical management has been treated with surgical resection, catheter ablation, and antitachycardia pacemaker. In this case report we describe the use of transcoronary alcohol ablation to treat a patient's ventricular tachycardia. This is accomplished by using ethanol to destroy the site of origin or pathways used in ventricular tachycardia.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1991.tb01346.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY