摘要:

Electrophysiologic Substrate of Long QT Syndrome.Introduction:The mechanisms of T wave abnormalities and arrhythmias in patients affected by the long QT syndrome (LQTS) are unclear, as are the reasons why a high‐risk subgroup (20%) continues to have syncope during therapy with beta blockers but is protected after left cardiac sympathetic denervation (LCSD). Afterdepolarizations, both early (EAD) or delayed (DAD), have been implicated as likely electrophysiologic substrates for the ECG abnormalities and arrhythmias in LQTS. To test this hypothesis, we analyzed nine Hotter recordings of a LQTS patient typical of the high‐risk subgroup.Methods and Results:We applied to the ECG rules derived from previous in vitro and in vivo studies, which relate the coupling intervals of the dysrhythmic beats to the preceding cycle lengths, to discriminate among arrhythmia mechanisms. In the absence of therapy, the patient's ECG showed peaked T waves, with a notched second component accentuated by sinus pauses. The amplitude of the notches increased directly with the preceding RR interval (r = 0.58, P<0.05), as it is observed with EAD. Therapy with the beta blocker propranolol did not modify the notches, which maintained their amplitude and their relationship with the preceding RR (r = 0.62, P<0.05). Moreover, during beta‐blocker therapy, ventricular premature beats, couplets, and runs of ventricular tachycardia (VT) occurred. The coupling intervals of ventricular premature beats and couplets were not influenced by the preceding RR intervals. By contrast, the coupling interval of the first beat of VT decreased as the preceding RR shortened, as it occurs with DAD‐induced triggered activity. After LCSD, T wave notch amplitude was reduced (P<0.05) and was no longer influenced by the preceding RR (r = 0.31, P = 0.22). The same was true when the calcium entry blocker verapamil was administered.Conclusion:In this patient, T wave abnormalities and some ventricular arrhythmias had the behavior observed in vitro for EAD and the consequent triggered activity. However, the cycle length dependence of VT manifested the behavior observed in vitro for DAD and the related triggered activity. The fact that these phenomena were accentuated by beta blockade and disappeared after LCSD suggests that the alpha‐adrenergic receptor‐effector system may be a modulator of T wave abnormalities and arrhythmias in some patients unresponsive to beta blockade and protected by LCSD. (J Cardiovasc Electrophysiol, Vol. 3, pp. 295–305

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00975.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Effects of Flunarizine on Impulse Initiation.Introduction:The calcium channel blocker, flunarizine, selectively blocks accumulation of intracellular calcium during conditions of calcium overload. It has been reported to selectively terminate delayed after depolarization‐induced arrhythmias in intact dogs.Methods and Results:Using standard microelectrode techniques, we studied the effects of flunarizine on the transmembrane action potential and various arrhythmogenic mechanisms in canine Purkinje fibers. Flunarizine significantly decreased the fast response action potential duration at 50% repolarization in a concentration‐dependent manner (10‐8to 10‐5M), but had no effect on maximum diastolic potential, overshoot, maximum upstroke velocity (Vmax), or APD at 90% repolarization. For Ca2+‐induced slow response action potentials, flunarizine decreased the overshoot, and prolonged action potential duration at both 50% and 90% repolarization. It had no effect on automaticity of Purkinje fibers exposed to solutions containing either low [K+] or barium chloride. Flunarizine, 10‐5M, inhibited the development of both ouabain‐induced and calcium‐ and catecholamine‐induced delayed after depolarizations. It did not inhibit the development of cesium‐induced early afterdepolarizations.Conclusions:Thus, in vitro, flunarizine selectively suppresses delayed after depolarizations and has no effects on early afterdepolarizations or normal or abnormal automaticity. Hence, its utility in intact animal models of triggered arrythmias is borne out mechanistically in these isolated tissue studies. (J Cardiovasc Electrophysiol, Vol. 3, pp. 3

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00976.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Epicardial Ectopics.Introduction:Ventricular ectopic beats demonstrating: (1) depolarization in ischemically‐injured anterior epicardium preceding His‐Purkinje activation by more than 25 msec; (2) initial delta waves on the anterior chest leads of the surface ECG coincident with presystolic epicardial activation; and (3) a left bundle branch block morphology were observed in 46 of 256 anesthetized dogs evaluated 18–24 hours following anterior descending coronary artery occlusion.Methods and Results:In 18 experiments, endocardial and epicardial recordings, and signal‐averaged recordings from the left ventricle were used to determine the earliest activation time/site for epicardial ectopic beats. In these ventricular ectopic beats, early epicardial activation was coupled to the preceding beat by a constant, fixed coupling interval. Electrical activity during the interectopic interval was not detected with composite or multiple bipolar recordings, or with signal averaging from the heart. The mean coupling interval was prolonged by lidocaine from 385 ± 24to 409 ± 45 msec (P<0.01), and was decreased by epinephrine (364 ± 7 msec) and D‐600 (324 ± 32 msec)(P<0.05). Spontaneous ventricular beats of epicardial origin could be reversibly suppressed by epicardial lidocaine administration or permanently suppressed with intracoronary latex injection, eliminating presystolic potentials. Histologic examination of the epicardium revealed surviving tissue bands (0.5–2.0 mm) distributed throughout transmural infarcted epicardium.Conclusion:The present experiments demonstrate constant‐coupled ectopic ventricular beats of epicardial origin, 18–24 hours following myocardial infarction. The ventricular ectopic beats may result from abnormal automaticity or electrotonic excitation from an initiating beat across an unexcitable gap with slow conduction from the “site of origin’ to reactivate the left ventricle. (JCardiovasc Electrophysiol, Vol. 3, p

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00977.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Pacemaker Current if. Since the hyperpolarization‐activated current, if, was originally associated with the diastolic depolarization phase of action potential in the sinoatrial (SA) node in 1979, its central role in the generation and control of pacemaker activity has become increasingly clear through a series of experimental findings, some of which have substantially modified the pre‐existing theories of cardiac pacemaking and its modulation by the autonomic transmitters. Thus, the pacemaker current of Purkinje fibers, formerly described as a deactivating pure potassium (K) current, was found to be in fact, like the nodal if, inward and activating on hyperpolarization. Furthermore, in SA node cells, as well as mediating rhythm acceleration induced by catecholamines, if was found to underlie the slowing effect of low acetylcholine (ACh) concentrations, in contrast with the generally accepted hypothesis that activation of a K conductance is the main process responsible for cardiac slowing. A final, atypical property of if recently demonstrated concerns the activating action exerted on if by intracellular cAMP. Unlike that on other voltage‐gated, cAMP‐modulated cardiac channels, this action is independent of phosphorylation and involves a direct binding of cAMP to if channels. (J Cardiovasc Electrophysiol, Vol. 3, pp. 334–344, Au

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00978.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Current Status of Lasers for Arrhythmia Ablation. Wavelength specific effects and mode of laser operation allow either photocoagulation or tissue removal as a means of approaching arrhythmia ablation. Successful intraoperative ablation of ventricular tachycardias has been performed with the Nd: YAG laser (photocoagulation) and argon laser (tissue vaporization). The argon laser has been used intraoperatively for transection of accessory pathways. Experimental studies indicate a strong theoretical potential for Nd:YAG laser catheter ablation of ventricular tachycardia. Laser energy has been used experimentally to evaluate the possibility of AV junctional ablation/modification and accessory pathway ablation. Adaption of laser energy to effective catheter systems for arrhythmia ablation requires solutions to problems inherent in all catheter systems and some unique to laser energy. (J Cardiovasc Electrophysiol, Vol. 3, pp. 345–353, August 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00979.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Alcohol Ablation for Tachycardia Therapy. Selective administration of ethanol into branches of the coronary arterial circulation has been proposed as a means of ablating cardiac fibers that give rise to cardiac arrhythmias, no matter where in the heart they might be located. In patients with uncontrollable ventricular rates in the setting of atrial fibrillation or atrial flutter, ethanol has been infused into the atrioventricular (AV) nodal artery in order to abolish or modify AV nodal conduction. Such a procedure is technically feasible in approximately 80% of patients and is successful in 70%–80% of individuals who are treated. Many of these patients require permanent pacemaker implantation because of chronic complete AV block. Intracoronary ethanol ablation has also been used to treat patients with AV nodal reentrant supraventricular tachycardia and ectopic atrial tachycardia, but there is scant clinical experience with the technique in these arrhythmias. Among patients with incessant or recurrent ventricular tachycardia (VT), intracoronary ethanol ablation has abolished clinical recurrences of arrhythmia in 78% of treated individuals. However, inability to identify a VT‐related arterial branch and other technical considerations may limit application of ethanol ablation to fewer than 50% of potential candidates with VT. Ethanol ablation is generally well tolerated, but significant complications have occurred, including ethanol‐induced occlusion of nontarget coronary arteries leading to unintended myocardial infarction. Procedure‐related death has also occurred. Ethanol ablation shows promise as a method for abolishing intractable tachycardias but further study is required to improve the safety of the technique and to define more precisely which patients are the best candidates in whom to consider this approach. (J Cardiovasc Electrophysiol, Vol. 3, pp. 354–364, Au

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00980.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Wide QRS Complexes. Wide QRS complex tachycardia is a commonly encountered arrhythmia and its appropriate diagnosis often poses a challenge to most physicians. The origin of a wide QRS complex is either supraventricular with abnormal ventricular activation or ventricular. This review addresses the main electrophysiologic mechanisms involved in the genesis of a wide QRS complex and its maintenance as a sustained arrhythmia. (J Cardiovasc Electrophysiol, Vol. 3, pp. 365–393, August 199

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00981.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Cardiac Electrophysiology in Duchenne Muscular Dystrophy. Duchenne muscular dystrophy is an X‐linked recessive neuromuscular disorder that involves striated muscle fibers (skeletal, cardiac), smooth muscle Fibers (vasculature), and nervous system (neurons of central brain and cortex). The Duchenne dystrophy gene has been identified on the Xp21 locus of the short arm of the X chromosome. Dystrophin, the protein product of the gene, is present on and limited to myogenic cells in every tissue tested except the central nervous system, and is absent or nearly so in Duchenne dystrophy. However, the function of dystrophin and the pathogenesis of Duchenne dystrophy remain unclear. There is convincing morphological (gross, histologic, ultrastructural) and metabolic evidence (positron emission tomography) that myocardial involvement is found initially in the posterobasal left ventricular wall (cardiac phenotype). This regional localization of myocardial dystrophy is believed to account for the distinctive 12‐lead scalar electrocardiogram (ECG). Abnormalities of cardiac rhythm and conduction have been reported in Duchenne muscular dystrophy, but the pathogenesis of the electrophysiologic disturbances has not been established. Two variables are relevant to cardiac electrophysiologic involvement in Duchenne dystrophy: (1) the small vessel coronary arteriopathy (medial hypertrophy, luminal narrowing); and (2) abnormalities that might originate in the specialized cardiac tissues. The role of the coronary arteriopathy is presently speculative, and it is not currently known whether dystrophin is normally present on the cell membrane of normal cardiac specialized tissues, and if so, whether those tissues are dystrophin deficient in Duchenne dystrophy. Animal models (mouse, cat, dog) have shed light on the pathogenesis of skeletal muscle and myocardial involvement, less so on involvement of cardiac specialized tissues. The determinants of calcium homeostasis in dystrophin‐deficient myogenic cells (skeletal or cardiac) is unclear, and the relationship between dystrophin deficiency, calcium homeostasis, cellular response and phenotypic expression in skeletal muscle and myocardium is imperfectly understood. The purpose of this report is to bring together current genetic, molecular biological, biochemical, histopathological, and clinical information from human Duchenne dystrophy and from animal models bearing on the electrophysiologic expressions of the neuromuscular disease. (J Cardiovasc Electrophysiol, Vol. 3, pp. 394–409, Augu

ISSN:1045-3873    

DOI:10.1111/j.1540-8167.1992.tb00982.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY