摘要:

Pacing During Supraventricular Tachycardia.Introduction:Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism.Methods and Results:Fifty‐three patients with paroxysmal Supraventricular tachycardia were studied. Twenty‐two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15‐beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P<0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing.Conclusions:Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachyc

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01227.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Sustained Bundle Branch Reentrant Tachycardia.introduction:The clinical, electrophysiologic features and follow‐up of 48 patients with inducible bundle branch reentrant (BBR) tachycardia are presented.Methods and Results:Forty‐eight patients were identified in whom a diagnosis of BBR tachycardia was made during electrophysiologic evaluation. The clinical presentation was syncope or sudden death in 38 patients, and sustained palpitations during wide QRS complex tachycardia in 5 patients. Electrophysiologic studies were performed in 5 additional patients for various other reasons. Structural heart disease was present in 45 patients. Idiopathic dilated cardiomyopathy and coronary artery disease were the anatomical substrates in 19 (39%) and 24 (50%) patients, respectively, severe aortic regurgitation was present in 2 patients, and no organic heart disease was identified in 3. All 48 patients had evidence of His‐Purkinje system disease. BBR tachycardia with left and right bundle branch block morphologies was induced in 46 and 5 patients, respectively, and interfascicular BBR tachycardia was initiated in 2 patients. Ventricular tachycardia of a myocardial origin was induced in 11 patients. Management of BBR tachycardia included transcatheter bundle branch ablation in 28 patients, and antiarrhythmic drug therapy in 16 patients. Four patients were treated with implantablc defibrillators. After a mean follow‐up of 15.8 months in 42 patients, there were 13 deaths due to congestive heart failure, 4 sudden cardiac deaths, 3 nonsudden cardiac deaths, and 3 noncardiac related deaths.Conclusion:Sustained BBR, a form of monomorphic ventricular tachycardia, is a highly malignant arrhythmia usually seen in patients with structural heart disease. Three different types of BBR tachycardia are described. If distinguished from ventricular tachycardia of a myocardial origin, catheter ablation of the right bundle branch can be easily performed and effectively eliminates BBR. During follow‐up, congestive heart failure is the most common cause of death in this p

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01228.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01229.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

d‐Sotalol and Atrial Reentry.Introduction:In the chronically instrumented animal and the isolated blood perfused heart, atrial reentry via a fixed path around an anatomical obstacle has been described and is terminated by the Class III antiarrhythmic agent, d‐sotalol. The precise mechanism by which d‐sotalol terminates this arrhythmia is not known.Methods and Results:In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart during episodes of sustained flutter (n = 7) and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. D‐sotalol was effective in terminating atrial reentry in this model. In all episodes, block of the excitatory impulse in a specific region of the reentrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described.Conclusion:The Class III antiarrhythmic agent d‐sotalol can terminate atrial reentry in several ways. In one mode, complete conduction block of he reentering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original reentrant circuit occurs when there is failure of a lateral boundary. Often in this latter case, interruption of the original circuit is by an extra impulse that is secondary to a change in the path of the impulse. In both modes cycle length oscillations are

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01230.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Retrograde Right Bundle Branch Activation. A 40‐year‐old man undergoing electro‐physiologic study for recurrent palpitations was found to have a right bundle branch block during sinus rhythm and right bundle potentials occurring after ventricular activation. The sequence of activation of the proximal and distal right bundle potentials was suggestive of a retrograde invasion of the right bundle during sinus rhythm. This transseptal activation of the right bundle via the left bundle exhibited decremental conduction characteristics during atrial as well as ventricular stimulation. Observations made in this case may provide some important information concerning the electrophysiologic behavior of transseptal imp

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01231.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Sarcolemmal Phospholipid Alterations and Arrhythmogenesis. Myocardial ischemia in vivo is associated with dramatic electrophysiologic alterations that occur within minutes of cessation of coronary flow and are rapidly reversible with reperfusion. This suggests that subtle and reversible biochemical alterations within or near the sarcolemma may contribute to the electrophysiologic derangements. Our studies have concentrated on two amphipathic metabolites, long‐chain acylcarnitines and lysophosphatidylcholine (LPC). which have been shown to increase rapidly in ischemic tissue in vivo and to elicit electrophysiologic derangements in normoxic tissue in vitro. Incorporation of these amphiphiles into the sarcolemma at concentrations of 1 to 2 mole %, elicits profound electrophysiologic derangements analogous to those observed in ischemic myocardium in vivo. The pathophysiological effects of the accumulation of these amphiphites are thought to be mediated by alterations in the biophysical properties of the Sarcolemmal membrane, although there is a possibility of a direct effect upon ion channels. Inhibition of carnitine acyltransferase I (CAT‐I) in the ischemic cat heart was found to prevent the increase in long‐chain acylcarnitines and LPC and to significantly reduce the incidence of malignant arrhythmias including ventricular tachycardia and fibrillation. This review focuses on the electrophysiologic derangements that are observed during early ischemia and presents data supporting the concept that accumulation of these amphiphiles within the sarcolemma contributes to these changes. The potential contribution of these amphiphiles to the increases in extracellular potassium and intracellular calcium are examined. Finally, recent data pertaining to the accumulation of long‐chain acylcarnitines on cell‐to‐cell uncoupling are presented. In addition to the events reviewed here, there are many other alterations that occur during early myocardial ischemia, but the results from multiple studies over the past two decades indicate that the accumulation of these amphiphiles contributes importantly to arrhythmogenesis and that development of specific inhibitors of CAT‐I or phospholipase A may be a promising therapeutic strategy to attenuate the incidence of lethal arrhythmias associated with ischemic heart d

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01232.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Aggravation of Arrhythmia. Aggravation of arrhythmia, denned as worsening of a preexisting arrhythmia or the occurrence of a new arrhythmia, is a common complication of antiarrhythmic drug therapy. Although it is largely an unpredictable event, patients at greatest risk are those with a history of congestive heart failure due to systolic dysfunction who present with a sustained ventricular tachyarrhythmia. As a rule, aggravation of arrhythmia is an early event, occurring within the first few days of initiating therapy. However, in the Cardiac Arrhythmia Suppression Trial (CAST), the increased sudden death mortality due to drug therapy, which was a result of arrhythmia aggravation, occurred throughout the entire duration of the trial, suggesting that arrhythmia aggravation can also be a late complication of therapy. Also disturbing was the fact that patients in CAST were low risk and did not have congestive heart failure or a serious ventricular tachyarrhythmia. This suggests that another important risk factor is myocardial ischemia and its potentially dangerous interaction with antiarrhythmic drugs. In patients with heart disease, especially those with coronary artery disease, antiarrhythmic drugs must therefore be used cautiously. Close and continuous follow‐up is mandator

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01233.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

“Supernormal” Conduction and Excitability. Electrocardiograph manifestation of “supernormal” conduction is defined as conduction that is more rapid than expected or presence of conduction when block is anticipated. It is not supernormal in the sense of being more rapid than normal. Therefore, the term relative supernormality or “supernormality” is more appropriate. The mechanism of “supernormal” conduction is conduction during a period of supernormal excitability and conduction associated with altered membrane potential. Some of the more common phenomena that are not dependent on conduction during the supernormal period but manifest better than expected conduction, thus simulating “supernormal” conduction, include dual AV nodal conduction, the “gap” phenomenon, “peeling back” of the refractory period, summation of subthreshold responses, diastolic phase 4 depolarization, and

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01234.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Cardiac Arrhythmias and the Autonomic Nervous System. The multiple facets of cardiac arrhythmias and their relationship with the autonomic nervous system can be investigated by studying the spontaneous heart rate behavior through ambulatory ECG recordins, an approach that complements the limitations of invasive electrophysiologic investigations. Information obtained from heart rate behavior is more reliable in the absence of structural heart disease and ventricular hypertrophy/failure, during which compensatory mechanisms involving the autonomic nervous system tend to limit reflex changes in heart rate. Thus, in such situations, less marked sinus rhythm variations preceding the arrhythmia onset do not imply a more limited influence of the autonomic nervous system, and the sensitivity of the electrophysiologic substrate may otherwise vary. These two factors may combine to form the basis of the adrenergic paradox11that implies that the more marked the autonomic nervous system dependence of tachyarrhythmias, the less obvious its evidence. Assessment of the QT interval dynamicity may also allow one to evaluate the modulation of autonomic neural effects on the ventricular tissues. Finally, it may be difficult to distinguish clearly autonomic nervous system dependence from rate dependence: the latter frequently conditions the behavior of the trigger whereas the former mainly concerns the electrophysiologic substrate. There are many examples of the importance of the autonomic nervous system as a determinant of cardiac arrhythmias. In the atrium, either limb of the autonomic nervous system, particularly the parasympathetic limb, can generate atrial fibrillation. The absence of structural heart disease defines pure electrophysiologic substrates responsible for benign forms of ventricular tachycardia as welt as potentially lethal tachyarrhythmias of the long QT syndrome and its variants. In both, the role of the autonomic nervous system is essential, although the therapeutic consequences are crucial only in the latter. In the presence of heart disease and, in particular, heart failure, the autonomic nervous system behavior is more difficult to assess than in the absence of structural heart disease. This does not mean that its role is less crucial. In this situation the beneficial effects of beta blockers may be as important as in normal hearts although physicians should be more cautious when heart failure is present.

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01235.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY

摘要:

Idiopathic Ventricular Tachycardia and Fibrillation. Important data have recently been added to our understanding of sustained ventricular tachyarrhythmias occurring in the absence of demonstrable heart disease. Idiopathic ventricular tachycardia (VT) is usually of monomorphic configuration and can be classified according to its site of origin as either right monomorphic (70% of all idiopathic VTs) or left monomorphic VT. Several physiopathological types of monomorphic VT can be presently individualized, according to their mode of presentation, their relationship to adrenergic stress, or their response to various drugs. The long‐term prognosis is usually good. Idiopathic polymorphic VT is a much rarer type of arrhythmia with a less favorable prognosis. Idiopathic ventricular fibrillation may represent an underestimated cause of sudden cardiac death in ostensibly healthy patients. A high incidence of inducibility of sustained polymorphic VT with programmed ventricular stimulation has been found by our group, but not by others. Long‐term prognosis on Class IA antiarrhythmic medications that are highly effective at electrophysiologic study appears excellentJfyCardiovasc Electrophysiol, Vol. 4, pp. 356–368, June

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1993.tb01236.x

出版商:Blackwell Publishing Ltd    

年代:1993

数据来源: WILEY