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Atrial Refractory Period (atrial + refractory_period)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Automatic Mode Switching Variants: Dual Demand Pacing, Retriggerable Atrial Refractory Periods, Automatic Mode Adaptation, and Pseudomode Switching.

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7 2000
Enlightenment or Obfuscation?
No abstract is available for this article. [source]

Dietary Fish Oil Protects Against Stretch-Induced Vulnerability to Atrial Fibrillation in a Rabbit Model

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2005
DANIEL M. NINIO M.B.B.S.
Introduction: Dietary fish oil is thought to reduce sudden cardiac death by suppressing ventricular arrhythmias but little is known about its impact on atrial arrhythmias. We examined the effect of dietary fish oil on the rabbit model of stretch-induced vulnerability to atrial fibrillation (AF). Methods and Results: Six-week-old rabbits were fed standard rabbit pellets supplemented with 5% tuna fish oil (n = 6) or supplemented with 5% sunflower oil (n = 6) for 12 weeks. Six rabbits raised on the standard diet were used as controls. In Langendorff-perfused hearts intraatrial pressures were increased in a stepwise manner and rapid burst pacing applied to induce AF at increasing intraatrial pressures until AF was sustained (>1 minute). Atrial refractory periods were recorded at each pressure. Increased atrial pressure resulted in a reduction in atrial refractory period and a propensity for induction of sustained AF. Higher pressures were needed to induce and sustain AF in the fish oil group compared with the sunflower oil and control groups. The stretch-induced drop in refractory period was also less marked in the fish oil group. Red blood cell, atrial, and ventricular omega-3 fatty acid levels were significantly higher in the fish oil group. The ratio of atrial n-6/n-3 polyunsaturated fatty acids was 13 ± 0.9 with sunflower oil and 1.5 ± 0.01 with fish oil (P < 0.001). Conclusions: Incorporation of dietary omega-3 fatty acids into atrial tissue reduces stretch-induced susceptibility to AF. [source]

Effect of Chronic Amiodarone Therapy on Excitable Gap During Typical Human Atrial Flutter

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004
PHILIPPE MAURY M.D.
Introduction: Class I antiarrhythmic drugs increase duration of the excitable gap (EG) during typical atrial flutter whereas intravenous class III drugs decrease the EG. The effect of chronic oral amiodarone therapy on the EG is unknown. Methods and Results: EG was prospectively determined by introducing a premature stimulus and analyzing the response pattern during typical atrial flutter in 30 patients without antiarrhythmic drugs and in 20 patients under chronic oral amiodarone therapy. EG was calculated by the difference between the longest coupling interval leading to resetting and the effective atrial refractory period (EARP). A fully EG was defined by the portion of EG where the response curve of the return cycles was flat. A partially EG was defined by the portion of EG where the return cycle increases while coupling interval decreases. A resetting response curve was constructed by plotting the duration of the return cycle against the value of the coupling interval. Cycle length (CL; 222 ± 17 vs 267 ± 20 msec, P < 0.0001), EARP (128 ± 16 vs 152 ± 18 msec, P < 0.0001), and EG (54 ± 19 vs 70 ± 21 msec, P = 0.01) were significantly longer in patients taking amiodarone than in controls. Compared to CL, the relative part of the EARP (57 ± 7 vs 57 ± 6%, P = 0.96) and EG (24 ± 7 vs 26 ± 8%, P = 0.41) were comparable in both groups. The fully EG was larger in patients under chronic amiodarone therapy than in controls (39 ± 21 vs 26 ± 20 msec, P = 0.03). Neither duration of the partially EG (28 ± 15 vs 31 ± 15 msec, P = 0.42) nor slope of the ascending portion of the resetting response curve (1.15 ± 0.5 vs 1.13 ± 0.4 msec/msec, P = 0.71) differed between the two groups. Conclusion: EG in patients under chronic amiodarone therapy is significantly larger than in controls, mainly because of a longer fully EG. This observation may be explained by opposite effects on conduction velocity and refractoriness. [source]

Inhibitors of the Na+/H+ Exchanger Cannot Prevent Atrial Electrical Remodeling in the Goat

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2004
YURI BLAAUW M.D.
Introduction: It has been suggested that blockade of the Na+/H+ exchanger (NHE1) can prevent atrial fibrillation (AF)-induced electrical remodeling and the development of AF. Methods and Results: AF was maintained by burst pacing in 10 chronically instrumented conscious goats. Intravenous and oral dosages of two NHE1 blockers (EMD87580 and EMD125021) resulted in plasma levels several magnitudes higher than required for effective NHE1 blockade. Shortening of atrial refractoriness immediately after 5 minutes of AF was not prevented by NHE1 blockade. In remodeled atria, increasing dosages of EMD87580 and EMD125021 did not reverse shortening of the atrial refractory period or reduce the duration of AF episodes. The cycle length during persistent AF also was not affected. Oral pretreatment with EMD87580 (8 mg/kg bid) starting 3 days before AF could not prevent electrical remodeling. After 24 and 48 hours of remodeling, the duration of AF paroxysms was 47 ± 32 seconds and 135 ± 63 seconds compared to 56 ± 17 seconds and 136 ± 52 seconds in placebo-treated animals (P > 0.8), respectively. Conclusion: In the goat model of AF, the Na+/H+ exchanger inhibitors EMD87580 and EMD125021 did not prevent or revert AF-induced electrical remodeling. This indicates that activation of the Na+/H+ exchanger is not involved in the intracellular pathways of electrical remodeling. This does not support the suggestion that blockers of the Na+/H+ exchanger may be beneficial for prevention and treatment of AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 440-446, April 2004) [source]

Impact and Prevention of Far-Field Sensing in Fallback Mode Switches

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003
PIERRE BORDACHER
BORDACHAR, P., et al.: Impact and Prevention of Far-Field Sensing in Fallback Mode Switches.Far-field oversensing (FFOS) promoted by high atrial sensitivity and short atrial refractory periods induces false positive mode switches. We evaluated the incidence of ventricular FFOS in a population of DDD paced patients. Methods: One hundred thirty-seven patients (71 ± 10years, 76 men) implanted with a Talent DR pacemaker were studied. Before discharge, an analysis of internal data stored in the memories of the PM was performed by the specific software incorporated in the programmer in parallel with a 24-hour Holter recording. Data were validated by a panel of experts. One and 4 months follow-up was based only on the data stored in the PM memories. Results: Pacing indications were atrioventricular block(n = 75), sinus node dysfunction(n = 57), and other(n = 5). Sustained far-field oversensing was observed in 12/137 patients (9%). Out of a total of 3,511 triggered mode switch episodes, FFOS accounted for 20% and 7% of a 311 days cumulative time in mode switch. Inappropriate mode switch episodes induced by far-field were more numerous but shorter than episodes prompted by atrial arrhythmias. Atrial sensitivity was increased in eight patients, successfully in four. Reprogramming of the atrial refractory period(156 ± 11 ms)was successful in five of six patients. Conclusions: A 9% rate of ventricular FFOS was observed in an unselected population, easily and automatically diagnosed using the internal memory function and the automatic analysis provided by the programmer. Prolongation of the atrial refractory period was more effective than resetting of the atrial sensitivity in eliminating FFOS. (PACE 2003; 26[Pt. II]:206,209) [source]

Electrocardiograms from the Turtle to the Elephant that Illustrate Interesting Physiological Phenomena

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2002
L.A. GEDDES
GEDDES, L.A. Electrocardiograms From the Turtle to the Elephant that Illustrate Interesting Physiological Phenomena. This article describes a collection of ECGs from many species obtained over the past 50 years. Presented are ECGs of species in which the pacemaker is a separate contractile chamber with its own action and recovery potentials. In such species, pacemaker atrial and AV block can be produced. Shortening of the atrial refractory period and the negative inotropic effect can be produced by vagal stimulation. The cardiac electrogram and stroke volume are recorded from the turtle heart. The ECG and respiration were recorded from the snake. ECG records were obtained from the anesthetized and decapitated housefly. ECG records of the rabbit show slowing when the nose encountered irritating vapors. Records from a dog with atrial fibrillation exhibit rhythmic fibrillation frequency changes correlated with respiration. In addition, in a morphinized dog with atrial fibrillation, impulses crossed the AV node only during inspiration. The ECGs of a cow and camel exhibit long P-R intervals and biphasic P waves. Finally the elephant ECG shows a clear U wave following the T wave. [source]