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Atrioventricular Conduction (atrioventricular + conduction)
Selected AbstractsIntermittent Impairment of Atrioventricular Conduction: What is the Mechanism?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2009MAREK JASTRZEBSKI M.D., Ph.D. No abstract is available for this article. [source] Spontaneous Transition of 2:1 Atrioventricular Block to 1:1 Atrioventricular Conduction During Atrioventricular Nodal Reentrant Tachycardia:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2003Evidence Supporting the Intra-Hisian or Infra-Hisian Area as the Site of Block Introduction: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. Methods and Results: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 ± 0.25 mV vs 0.16 ± 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 ± 19 ms) compared with 2:1 AV block (44 ± 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 ± 6 ms, P < 0.01). Conclusion: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1337-1341, December 2003) [source] Transvenous Parasympathetic Nerve Stimulation in the Inferior Vena Cava and Atrioventricular ConductionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2000PATRICK SCHAUERTE M.D. Parasympathetic Stimulation in the Inferior Vena Cava. Introduction: In previous reports, we demonstrated a technique for parasympathetic nerve stimulation (PNS) within the superior vena cava, pulmonary artery, and coronary sinus to control rapid ventricular rates during atrial fibrillation (AF). In this report, we describe another vascular site, the inferior vena cava (IVC), at which negative dromotropic effects during AF could consistently he obtained. Moreover, stimulation at this site also induced dual AV nodal electrophysiology. Methods and Results: PNS was performed in ten dogs using rectangular stimuli (0.1 msec/20 Hz) delivered through a catheter with an expandable electrode basket at its tip. Within 3 minutes and without using fluoroscopy, the catheter was positioned at an effective PNS site in the IVC at the junction of the right atrium. AF was induced and maintained by rapid atrial pacing. During stepwise increase of the PNS voltage from 2 to 34 V, a graded response of ventricular rate slowing during AF was observed (266 ± 79 msec without PNS vs 1,539 ± 2,460 msec with PNS at 34 V; P = 0.005 by analysis of variance), which was abolished by atropine and blunted by hexamethonium. In three animals, PNS was performed during sinus rhythm. Dual AV nodal electrophysiology was present in 1 of 3 dogs in control, whereas with PNS, dual AV nodal electrophysiology was observed in all three dogs. PNS did not significantly change sinus rate or arterial blood pressure during ventricular pacing. Conclusion: Stable and consistent transvenous electrical stimulation of parasympathetic nerves innervating the AV node can be achieved in the IVC, a transvenous site that is rapidly and readily accessible. The proposed catheter approach for PNS can be used to control ventricular rate during AF in this animal model. [source] Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing RatePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000IVAN ILIEV ILIEV The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source] Effects of Direct Sympathetic and Vagus Nerve Stimulation on the Physiology of the Whole Heart , A Novel Model of Isolated Langendorff Perfused Rabbit Heart with Intact Dual Autonomic InnervationEXPERIMENTAL PHYSIOLOGY, Issue 3 2001G. André Ng A novel isolated Langendorff perfused rabbit heart preparation with intact dual autonomic innervation is described. This preparation allows the study of the effects of direct sympathetic and vagus nerve stimulation on the physiology of the whole heart. These hearts (n= 10) had baseline heart rates of 146 ± 2 beats min,1 which could be increased to 240 ±11 beats min,1 by sympathetic stimulation (15 Hz) and decreased to 74 ± 11 beats min,1 by stimulation of the vagus nerve (right vagus, 7 Hz). This model has the advantage of isolated preparations, with the absence of influence from circulating hormones and haemodynamic reflexes, and also that of in vivo preparations where direct nerve stimulation is possible without the need to use pharmacological agents. Data are presented characterising the preparation with respect to the effects of autonomic nerve stimulation on intrinsic heart rate and atrioventricular conduction at different stimulation frequencies. We show that stimulation of the right and left vagus nerve have differential effects on heart rate and atrioventricular conduction. [source] Predictors of Complete Heart Block After Alcohol Septal Ablation for Hypertrophic Cardiomyopathy and the Timing of Pacemaker ImplantationJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2007F.R.A.C.P., SEIFEDDIN S. EL-JACK M.B.B.S. Catheter-based alcohol septal ablation has recently been introduced for the treatment of left ventricular outflow tract obstruction in hypertrophic obstructive cardiomyopathy. It is associated with various conduction disturbances and may lead to transient or persistent complete heart block (CHB). Electrocardiographic (ECG) changes and predictors of developing CHB and the timing of permanent pacemaker implantation have been variable among the different studies. Among 50 patients studied, we found that a new right bundle branch pattern was the most common new ECG change after septal ablation and that baseline left bundle branch block was strongly associated with the development of CHB (P = 0.004); 9 patients (18%) required permanent pacemaker implantation of whom 7 (78%) remained pacemaker dependent at 14 days with no delayed recovery of atrioventricular conduction. This favors an early pacemaker implantation strategy. [source] Sunao Tawara: A Father of Modern CardiologyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2001KOZO SUMA SUMA, K.: Sunao Tawara: A Father of Modern Cardiology. Knowledge of the conduction system of the heart was greatly advanced by Tawara's work carried out in Aschoff's laboratory in Marburg at the beginning of this century. In his monograph, The Conduction System of the Mammalian Heart, published in 1906, Tawara indicated that the treelike structure of specific muscle fibers comprising the atrioventricular node, His bundle, bundle branches, and Purkinje fibers served as the pathway for atrioventricular conduction of excitation in the mammalian heart. From his own anatomic and histological findings of the conduction system, he assumed precisely that the conduction velocity of excitation in the system, except in the atrioventricular node, would be fast and that contraction as the result of excitation would take place at the various sites of the ventricles almost simultaneously. According to Tawara, a long pathway to each contracting unit and a fast conduction velocity of excitation would be a prerequisite for the effective contraction of the ventricles. Tawara's findings and assumptions provided Einthoven the theoretical basis for interpreting the electrocardiogram, resulting in rapid popularization of electrocardiography. This century has witnessed the rapid progress of cardiology, including cardiac pacing and its related sciences. This progress has its roots in the discovery of the conduction system and the development of electrocardiography that took place almost in the same period at the beginning of this century. Tawara's pioneering work on the conduction system still serves as an invaluable reference for basic and clinical research. [source] Electrocardiographic Alterations during Hyperinsulinemic Hypoglycemia in Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2008Tomi Laitinen M.D. Background: We evaluated the arrhythmogenic potential of hypoglycemia by studying electrocardiographic (ECG) changes in response to hyperinsulinemic hypoglycemia and associated sympathoadrenal counterregulatory responses in healthy subjects. Methods: The study population consisted of 18 subjects, aged 30,40 years. Five-minute ECG recordings and blood samplings were performed at baseline and during the euglycemic and hypoglycemic hyperinsulinemic clamp studies. PR, QT, and QTc intervals of electrocardiogram and ECG morphology were assessed from signal-averaged ECG. Results: Although cardiac beat interval remained unchanged, PR interval decreased (P < 0.01) and QTc interval (P < 0.001) increased in response to hyperinsulinemic hypoglycemia. Concomitant morphological alterations consisted of slight increases in R-wave amplitude and area (P < 0.01 for both), significant decreases in T-wave amplitude and area (P < 0.001 for both), and moderate ST depression (P < 0.001). Counterregulatory norepinephrine response correlated with amplification of the R wave (r =,0.620, P < 0.05) and epinephrine response correlated with flattening of the T wave (r =,0.508, P < 0.05). Conclusions: Hyperinsulinemic hypoglycemia with consequent sympathetic humoral activation is associated with several ECG alterations in atrioventricular conduction, ventricular depolarization, and ventricular repolarization. Such alterations in cardiac electrical function may be of importance in provoking severe arrhythmias and "dead-in-bed" syndrome in diabetic patients with unrecognized hypoglycemic episodes. [source] | ||||||||||