Shortening Of Atrial Refractory Period Research Articles

Circulation : Clinical Summaries

<i>Circulation</i> : Clinical Summaries

Atrial fibrillatory rate in the clinical context: natural course and prediction of intervention outcome.

Shortening of atrial refractory period during atrial fibrillation has been considered a hallmark of atrial electrical remodelling. The atrial fibrillatory cycle length, which is intimately related to the atrial fibrillatory rate (AFR), is generally accepted as a surrogate marker for local refractoriness. The value of using AFR to monitor the progress of atrial ablation therapy has been demonstrated and gradual slowing of AFR has consistently been observed to precede arrhythmia termination during paroxysmal or permanent atrial fibrillation ablation. Today, AFR is the key characteristic of the fibrillatory process, repeatedly validated against intracardiac recordings and extensively studied in clinical contexts. This paper provides an overview of clinical data accumulated since the method was introduced in 1998, and to present the current state of knowledge regarding ECG-derived AFR: its time course and dynamics, clinical factors affecting AFR, and available evidence of its value in the clinical context. We conclude that AFR is a promising, easily available AF characteristic that can be derived from the conventional surface ECG. It is clearly a useful tool for monitoring drug effects. Reference values for predicting intervention effect, however, are likely to be population- and context-specific and related to age, clinical types of atrial fibrillation, as well as to presence and advancement of underlying structural heart disease. Prospective studies in homogeneous patient populations are still needed to establish the clinical value of AFR.

Paradoxical Change in Atrial Fibrillation Dominant Frequencies with Baroreflex‐Mediated Parasympathetic Stimulation with Phenylephrine Infusion

Parasympathetic stimulation is known to promote atrial fibrillation (AF) through shortening of atrial refractory periods. We hypothesized that baroreflex-mediated parasympathetic stimulation via phenylephrine (PE) infusion would increase AF rate as measured by dominant frequency (DF). The protocol was performed in 27 patients (24 M, 59 ± 1 years old) prior to AF ablation. For 10 patients in AF, PE was infused until systolic blood pressure increased ≥30 mmHg. Electrograms were recorded in the left atrium before and after PE. DFs of each recording were calculated offline. Atrial effective refractory periods (ERPs) were measured before and after PE in 11 patients who were in sinus rhythm during the procedure. DFs were also measured in 6 patients in AF before and after complete parasympathetic blockade with atropine (0.04 mg/kg). PE resulted in increased RR intervals during sinus rhythm (1,170 ± 77 to 1,282 ± 85 ms, P = 0.03) and AF (743 ± 32 to 826 ± 30 ms, P = 0.03), consistent with parasympathetic effect on the sinus and AV nodes, respectively. DFs were decreased by PE in the left atrium (6.2 ± 0.2 to 6.0 ± 0.2 Hz, P = 0.004). Correspondingly, atrial ERPs significantly increased from 218 ± 13 to 232 ± 11 ms (P = 0.04). Atropine resulted in a decreasing trend in DF in the left atrium (5.9 ± 0.1 to 5.8 ± 0.1 Hz, P = 0.07). Despite baroreflex-mediated parasympathetic effect, PE produced a slowing of AF along with lengthening of ERP, while parasympathetic blockade also slowed DF. It is therefore likely that the direct and indirect adrenergic effects of PE on atrial electrophysiology are more prominent than its parasympathetic effects.

Pathophysiology and Treatment Strategy for Atrial Fibrillation In Patients with Impaired LV Function

A variety of pathophysiological factors contribute to the development of atrial fibrillation in heart failure. More specifically, the elevated left atrial pressure, stretching and dilatation of atrial muscle, activation of the sympathetic nervous system and neurohumoral factors, atrial muscle hypertrophy, ischemia, fibrosis, etc., associated with impaired left ventricular function promote electrophysiological changes, such as shortening of atrial refractory period, and conduction disorders, leading to reentrant tachyarrhythmias.

Long-term changes in sequence of atrial activation and refractory periods: No evidence for “atrial memory”

The purpose of this study was to test whether the spatial distribution of the atrial refractory period (AERP) and the vulnerability to atrial fibrillation (AF) are altered by long-term changes in the sequence of atrial activation. The spatial distribution of the AERP plays an important role in AF. Changes in the activation sequence have been postulated to modulate atrial repolarization ("atrial memory"). Six goats were chronically instrumented with epicardial atrial electrodes to determine activation time and AERP at 11 different areas of the right (RA) and left (LA) atrium and the Bachmann bundle. Activation time and AERP were measured during sinus rhythm and during prolonged RA and LA pacing (1 week RA pacing, 2 weeks LA pacing, 1 week RA pacing; 150 bpm). Inducibility of AF was determined by the number of atrial sites where single premature stimuli induced AF paroxysms >1 second. During sinus rhythm (106 +/- 4 bpm), AERP was longest at the Bachmann bundle and shortest at the LA free wall (185 +/- 6 ms and 141 +/- 5 ms, P < .001). In five of six goats, an inverse correlation between local activation time and AERP was found during sinus rhythm (r = -0.53 +/- 0.05; P < .05). The increase in atrial rate during RA and LA pacing caused an overall shortening of AERP from 167 +/- 6 ms to 140 +/- 6 ms (P < .001). However, a switch between long-term RA and LA pacing did not significantly change AERP at any of the 11 atrial regions and had no significant effect on AF inducibility. During sinus rhythm, an inverse relationship exists between the sequence of atrial activation and the local refractory period. However, long-term changes in the sequence of atrial activation do not alter the spatial distribution of AERP or the inducibility of AF.

Electrical Remodeling in Human Atrial Fibrillation Influences Post-Cardioversion Atrial Mechanical Dysfunction and Early Relapse

Background:It has been demonstrated that atrial fibrillation (AF induces shortening of atrial refractory period, which was known as electrical remodeling, resulting in an increased vulnerability for reinduction of AF. Atrial mechanical function does not restore immediately after cardioversion, atrial stunning exists during this period in chronic AF. We hypothesized that electrical remodeling in chronic AF determines the atrial mechanical dysfu- nction after cardioversion and early relapse of AF. Method:Patients with chronic atrial fibrillation (CAF, n =17 who have been done transthoracic DC cardioversion, paroxysmal AF (PAF, n=11, and normal control (CON, n=5 were studied. Using MAP (monophasic action potential catheter, MAP duration 90% repolari- zition (MAPD90 and atrial effective refractory period (AERP were measured at 9 different sites in the right atrium. Magnitude of dispersion of these parameters was calculated by SD 2 (variance. Assessment of mitral inflow variables (peak velosities of A, E wave, and A/E ratio was performed at immediately after DC cardio- version, 1st day, 3rd days, 1 week, 4 weeks and 8 weeks by transthoracic pulse wave Doppler. Result:MA- PD90 significantly shortened in patients with CAF (235.4±38.1 ms compared with that of PAF (270.9±45.2 ms and control (274.0±51.9 ms, whereas AERP did not show significant differences. The magnitude of dispersion of MAPD90 and AERP was not different among the groups. AF recurred in 9 of 17 (53% patients with CAF particularly in whom A/E ratio was 0.4(250.9±52.9 ms, p=0.05. Conclusion:Electrical remodeling in chronic human AF characterized by shortening of monophasic action potential duration is one of the main factors that determines the atrial mechanical dysfunction after cardioversion and early relapse into AF. (Korean Circulation J 1999;29(8 :788-795

Myocardial infarction related atrial fibrillation: role of endogenous adenosine.

Exogenous administration of adenosine induces atrial fibrillation in up to 7.0% of patients. Animal studies affirm endogenous adenosine released in response to tissue hypoxia may play a mechanistic role in...

Synergistic nonuniform shortening of atrial refractory period induced by autonomic stimulation

We investigated the nonuniform effects of autonomic nerve stimulation of the effective refractory period (ERP) of the right atrium in the anesthetized dog. Stimulation of the discrete intracardiac sympathetic nerves to the sinoatrial (SA) nodal region uniformly shortened ERPs at three sites in the right atrium after administration of atropine. Right ansa subclavia (RS) stimulation similarly shortened ERPs in the absence of atropine. Stimulation of the discrete intracardiac parasympathetic nerves to the SA nodal region (SAP stimulation) shortened ERPs of the right atrium in a nonuniform manner. Simultaneous RS and SAP stimulation additively shortened ERPs at each site and decreased sinus rate much more than SAP stimulation alone. Shortening of ERP induced by SAP stimulation was greater than that induced by RS stimulation at similar absolute changes in heart rate. These results suggest that simultaneous activation of sympathetic and parasympathetic nerves nonuniformly shortens the ERP in the right atrium as the algebraic sum of the individual responses to each stimulation. However, parasympathetics exert the principal neural control over atrial ERP.

Electrophysiologic effects of atropine on human sinus node and atrium

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (± standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 ± 26.4 versus 647 ± 20.0 ( P <0.001); sinus nodal recovery time 1,029 ± 37 versus 774 ± 36 ( P <0.001); mean calculated sinoatrial (S-A) conduction time 103 ± 5.7 versus 58 ± 3.9 ( P <0.001); mean P-A interval 34 ± 1.5 msec versus 31 ± 1.5 ( P < 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 ±11.3 versus 238 ± 7.9 and 331 ± 11.6 versus 280 ± 8.6, respectively ( P <0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 ± 7.7 versus 213 ± 7.4 and 277 ±11.4 versus 245 ± 9.5, respectively ( P <0.001 for both). In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.

Conversion of atrial flutter to sinus rhythm after stimulation of carotid sinus

Electrophysiologic studies were conducted in 17 patients without apparent sinus node disease before and after intravenous administration of 1 to 2 mg of atropine. Mean values in milliseconds (± standard error of the mean) before and after administration of atropine were as follows: sinus cycle length 846 ± 26.4 versus 647 ± 20.0 (P <0.001); sinus nodal recovery time 1,029 ± 37 versus 774 ± 36 (P <0.001); mean calculated sinoatrial (S-A) conduction time 103 ± 5.7 versus 58 ± 3.9 (P <0.001); mean P-A interval 34 ± 1.5 msec versus 31 ± 1.5 (P < 0.05); mean atrial effective and functional refractory periods during sinus rhythm 285 ±11.3 versus 238 ± 7.9 and 331 ± 11.6 versus 280 ± 8.6, respectively (P <0.001 for both); mean atrial effective and functional refractory periods measured at equivalent driven cycle length 239 ± 7.7 versus 213 ± 7.4 and 277 ±11.4 versus 245 ± 9.5, respectively (P <0.001 for both).In conclusion, atropine shortened sinus cycle length, sinus nodal recovery time and calculated S-A conduction time. The shortening of atrial refractory periods with atropine implies that vagotonia prolongs atrial refractoriness in man.