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Triggered Activity (triggered + activity)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Beta-Adrenergic Stimulation of Pig Myocytes with Decreased Cytosolic Free Magnesium Prolongs the Action Potential and Enhances Triggered Activity

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2002
SHAO-KUI WEI M.D.
Beta-Adrenergic Stimulation and Repolarization.Introduction: Heart failure results in chronic beta-adrenergic stimulation, repolarization lability, and arrhythmias associated with early afterdepolarizations (EADs) and delayed afterdepolarizations (DADs). Having described a significant reduction in intracellular free magnesium ([Mg2+]i) in experimental heart failure, we asked whether a reduction in [Mg2+]i would delay repolarization or facilitate EADs and/or DADs. Methods and Results: Left ventricular myocytes were isolated from Yorkshire swine. Cytosolic free [Mg2+] was set at 0.12 mM (LoMg) or 1.2 mM (HiMg) through pipette dialysis. Action potentials (AP), Ca current (ICa), and sodium/calcium exchange current (INCX) were measured in the presence or absence of isoproterenol (2 ,M) at 37°C. Under basal conditions (0.1-Hz stimulation, 2 mM external [Ca2+]), reducing [Mg2+]i had no effect on AP duration and ICa but did significantly enhance INCX. In contrast, during superfusion with isoproterenol, reduced [Mg2+]i caused a significant increase in AP duration at both 50% and 90% repolarization (APD50 and APD90) compared with HiMg (P < 0.05). LoMg cells manifested a high incidence of triggered activities, including spontaneous AP, EADs, and DADs (83.3% in LoMg, n = 12 vs 38.3% in HiMg, n = 13; P < 0.05). ICa and INCX were significantly increased in LoMg cells compared with HiMg cells (P < 0.05). Conclusion: Decreased cytosolic free magnesium prolongs AP duration and increases the incidence of triggered activity during beta-adrenergic stimulation. These effects may be due to increased ICa and INCX in the presence of reduced intracellular [Mg2+]. A magnesium-dependent increase in triggered activity coupled with delayed repolarization during beta-adrenergic stimulation could contribute to the arrhythmogenic substrate in heart failure. [source]

Electrophysiologic characteristics and radiofrequency ablation of focal atrial tachycardia arising from para-Hisian region

INTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 3 2007
Y. Zhou
Summary This study describes the electrophysiologic characteristics and radiofrequency ablation of focal atrial tachycardia (AT) arising from para-Hisian region in 14 (6.0%) patients of a consecutive series of 224 patients patients. Inverted or biphasic P wave in V1 and uncharacteristic P wave in inferior leads were observed during tachycardia, suggesting that there isn't a characteristic P-wave morphology for para-Hisian AT. During electrophysiological study, tachycardia could be induced with programmed atrial extrastimuli in 11 patients while a spontaneous onset and offset with ,warm-up and cool-down' phenomenon were seen in other three patients. Moreover, the tachycardias were sensitive to intravenous administration of adenosine triphosphate in all patients. On the basis of these findings, the mechanism is suggestive of triggered activity or micro-reentry, but automaticity cannot be conclusively excluded. Radiofrequency energy was delivered to the earliest site of atrial activation during AT. Ablating energy was carefully titrated, starting at 5 W and increasing gradually upto a maximum of 40 W, to achieve the ceasing of tachycardia. The long-term outcome was a 100% success rate in these 14 patients and there were no irreversible complications associated with ablation. Thus, the mapping and ablation of focal AT arising from para-Hisian region is safe and effective, delivery of radiofrequency energy in a titrated manner and continuous monitoring of atrioventricular (AV) conduction advocated to minimise the risk of damage to the anterograde AV conduction. [source]

Idiopathic Ventricular Tachycardia Originating from the Posteroseptal Mitral Annulus: A Case Report

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2006
KEIICHI ASHIKAGA M.D.
We describe a 71-year-old man with a ventricular tachycardia (VT) originating from the mitral annulus. A sustained VT was induced by exercise or an isoproterenol administration, but not by pacing. Frequent premature ventricular contractions (PVCs) with the same QRS as the VT were transiently suppressed by an adenosine triphosphate injection, suggesting that it was due to cyclic-AMP mediated triggered activity. The PVCs and VT were all abolished by radiofrequency catheter ablation guided by the earliest activation and a perfect pace map, which was located at the posteroseptal mitral annulus. The patient has been free from any symptoms for 2 years. [source]

Focal Origin of Atrial Tachycardia in Dogs with Rapid Ventricular Pacing-Induced Heart Failure

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2003
GUILHERME FENELON M.D.
Introduction: Dogs with rapid ventricular pacing-induced congestive heart failure (CHF) have inducible atrial tachycardia (AT), with a mechanism consistent with delayed afterdepolarization-mediated triggered activity. We assessed the hypothesis that AT has a focal origin. Methods and Results: Twenty-one CHF dogs undergoing 3 to 4 weeks of ventricular pacing at 235 beats/min were studied. Biatrial epicardial mapping of 20 sustained AT episodes (cycle length [CL], 175 ± 53 msec) in 5 dogs revealed an area of earliest activation in the right atrial (RA) free wall (13 episodes), RA appendage (4 episodes), or between the pulmonary veins (3 episodes). Total epicardial activation time during AT (73 ± 19 msec) was similar to that during sinus rhythm (72 ± 13 msec) and on average was <50% of the AT CL. Higher-density mapping of the RA free wall during 30 sustained AT episodes (163 ± 55 msec) in 9 dogs identified a site of earliest activation along the sulcus terminalis most frequently as a stable, focal activation pattern from a single site. Endocardial mapping of 49 sustained AT episodes (156 ± 27 msec) in 10 dogs revealed multiple sites of AT origin arising along the crista terminalis and pulmonary veins. Right and left ATs were terminated with discrete radiofrequency ablation, but other ATs remained inducible. A rapid, left AT generating an ECG pattern of atrial fibrillation was ablated inside the pulmonary vein. Conclusion: AT induced in this CHF model after 3 to 4 weeks of rapid ventricular pacing has an activation pattern consistent with a focal origin. Sites of earliest activation are distributed predominately along the crista terminalis and within or near the pulmonary veins. (J Cardiovasc Electrophysiol, Vol. 14, pp. ***-***, October 2003) [source]

Beta-Adrenergic Stimulation of Pig Myocytes with Decreased Cytosolic Free Magnesium Prolongs the Action Potential and Enhances Triggered Activity

Pathophysiology of the Pulmonary Vein as an Atrial Fibrillation Initiator:

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7p2 2003
From Bench to Clinic
The basic electrophysiologic studies have proved the arrhythmogenic mechanisms of the pulmonary vein as an atrial fibrillation initiator; the mechanisms include enhanced automaticity, triggered activity, and microreentry from myocardial sleeves inside pulmonary veins. Immunohistology study has proved the conduction characteristics of pulmonary vein myocardium, and further study of ionic currents are important for understanding atrial fibrillation initiation from the pulmonary vein. (PACE 2003; 26[Pt. II]:1576,1582) [source]