Onset Of Paroxysmal Atrial Fibrillation Research Articles

Simultaneous catheter mapping of the pulmonary veins in focal atrial fibrillation: significance of rapid focal activation, effectiveness for catheter ablation.

Most focal atrial fibrillation (AF) is initiated by premature beats from the pulmonary veins (PV), and ablation of these foci can effectively cure AF. We investigated the efficacy of focal ablation and the role of rapid focal activation (RFA) in the maintenance of AF using simultaneous multisite catheter mapping in four PVs. Forty-two patients with frequent attacks of paroxysmal AF were included in the study population. Bipolar electrograms were simultaneously recorded from all four PVs. RFA was determined at AF onset, during sustained AF, or just before the spontaneous termination of AF. RFA was continuously observed not only at a triggered PV, but also at all sites including an opposite non-triggered PV, coronary sinus and high right atrium in sustained AF (>10 minutes), whereas RFA was observed only in the triggered PV and not at the other sites in nonsustained AF. Once RFA ceased, AF terminated immediately. After a mean follow-up of 21 months, focal ablation had eliminated AF without drugs in 24 patients (57%). The technique of simultaneous mapping of the PV using microcatheters is a feasible and effective method for mapping and ablation of focal AF originating from the PV. RFA arising from PVs is important not only as a trigger of onset, but also in the maintenance of AF.

Pharmacologic management of atrial fibrillation: Current therapeutic strategies

Background Atrial fibrillation (AF), the most common form of sustained arrhythmia, is associated with a frightening risk of embolic complications, tachycardia-related ventricular dysfunction, and often disabling symptoms. Pharmacologic therapy is the treatment used most commonly to restore and maintain sinus rhythm, to prevent recurrences, or to control ventricular response rate. Methods This article reviews published data on pharmacologic treatment and discusses alternative systems to classify AF and to choose appropriate pharmacologic therapy. Results AF is either paroxysmal or chronic. Attacks of paroxysmal AF can differ in duration, frequency, and functional tolerance. In the new classification system described, 3 clinical aspects of paroxysmal AF are distinguished on the basis of their implications for therapy. Chronic AF usually occurs in association with clinical conditions that cause atrial distention. The risk of chronic AF is significantly increased by the presence of congestive heart failure or rheumatic heart disease. Mortality rate is greater among patients with chronic AF regardless of the presence of coexisting cardiac disease. The various options available for the treatment of chronic AF include restoration of sinus rhythm or control of ventricular rate. Cardioversion may be accomplished with pharmacologic or electrical treatment. For patients in whom cardioversion is not indicated or who have not responded to this therapy, antiarrhythmic agents used to control ventricular response rate include nondihydropyridine calcium antagonists, digoxin, or β-blockers. For patients who are successfully cardioverted, sodium channel blockers or potassium channel blockers such as sotalol, amiodarone, or a pure class III agent such as dofetilide, a selective potassium channel blocker, may be used to prevent recurrent AF to maintain normal sinus rhythm. Conclusions The ultimate choice of the antiarrhythmic drug will depend on the presence or absence of structural heart disease. An additional concern with chronic AF is the risk of arterial embolization resulting from atrial stasis and the formation of thrombi. In patients with chronic AF the risk of embolic stroke is increased 6-fold. Therefore anticoagulant therapy should be considered in patients at high risk for embolization. Selection of the appropriate treatment should be based on the concepts recently developed by the Sicilian Gambit Group (based on the specific channels blocked by the antiarrhythmic agent) and on clinical experience gained over the years with antiarrhythmic agents. For example, termination of AF is best accomplished with either a sodium channel blocker (class I agent) or a potassium channel blocker (class III agent). In contrast, ventricular response rate is readily controlled by a β-blocker (propranolol) or a calcium channel blocker (verapamil). Alternatively, antiarrhythmic drug therapy may be chosen based on the Vaughan-Williams classification, which identifies the cellular electrophysiologic effects of the drug. (Am Heart J 2001;141:S15-21.)

Prediction of paroxysmal atrial fibrillation in patients with congestive heart failure: a prospective study

OBJECTIVESWe sought to prospectively determine whether patients with congestive heart failure (CHF) at risk for paroxysmal atrial fibrillation (PAF) could be identified by clinical and study variables including the P-wave signal-averaged electrocardiogram (P-SAECG).BACKGROUNDAlthough it is important to assess the risk of developing PAF in patients with CHF, it still remains difficult to predict the PAF appearance in patients with CHF clinically.METHODSThe study group consisted of 75 patients in sinus rhythm without a history of PAF, whose left ventricular ejection fraction, as measured by radionuclide angiography, was <40%. These patients underwent P-SAECG, echocardiography and 24-h Holter monitoring; in addition, the plasma concentration of atrial natriuretic peptide (ANP) was measured at study entry.RESULTSAn abnormal P-SAECG was found at study entry in 29 of 75 patients. In the follow-up period of 21 ± 9 months, the PAF attacks documented on the ECG significantly more frequently occurred in patients with (32%) rather than without an abnormal P-SAECG (2%) (p = 0.0002). The plasma ANP level was significantly higher in patients with rather than without PAF attacks (75 ± 41 vs. 54 ± 60 pg/ml, p = 0.01), although there were no significant differences in age, left atrial dimension or high grade atrial premature beats between the groups. The multivariate Cox analysis identified that the variables significantly associated with PAF development were an abnormal P-SAECG (hazard ratio 19.1, p = 0.0069) and elevated ANP level ≥60 pg/ml (hazard ratio 8.6, p = 0.018).CONCLUSIONSAn abnormal P-SAECG and elevated ANP level could be predictors of PAF development in patients with CHF.

Mode of Onset of Paroxysmal Atrial Fibrillation during 24 hour Holter Monitoring

Mode of Onset of Paroxysmal Atrial Fibrillation during 24 hour Holter Monitoring

Classification system of atrial fibrillation.

A number of publications and clinical trials on the management of atrial fibrillation (AF) deal with this arrhythmia as if it represents a single entity. As a result, advances made in recent years have not affected the way AF patients are treated in general practice except, perhaps, for the use of warfarin in anticoagulation. Therefore, there is a need for a classification system and for uniformity in the nomenclature used. The two terms currently used to describe AF, paroxysmal and chronic, require a time frame. It is proposed that if an AF episode lasts longer than 7 days, the condition should be considered chronic. For the first symptomatic, non-self-terminating episode that is fewer than 7 days long, the term recent onset AF may be used, or recent discovery if the AF is asymptomatic or if the duration cannot be determined. Attacks of paroxysmal AF may differ in their duration, frequency, and functional tolerance. In the classification system described, three clinical aspects of paroxysmal AF were isolated in such a way as to have implications for therapy. This classification system was found to be useful for characterizing different subsets of patients with AF.

Altered complexity and correlation properties of R-R interval dynamics before the spontaneous onset of paroxysmal atrial fibrillation.

Trigger mechanisms for the onset of paroxysmal atrial fibrillation (AF) in patients without structural heart disease are not well established. New analysis methods of heart rate (HR) variability based on nonlinear system theory may reveal features and abnormalities in R-R interval behavior that are not detectable by traditional analysis methods. The purpose of this study was to reveal possible alterations in the dynamics of R-R intervals before the spontaneous onset of paroxysmal AF. Traditional time and frequency domain HR variability indices, along with the short-term scaling exponent alpha(1) and approximate entropy (ApEn), were analyzed in 20-minute intervals before 92 episodes of spontaneous, paroxysmal AF in 22 patients without structural heart disease. Traditional HR variability measures showed no significant changes before the onset of AF. A progressive decrease occurred both in ApEn (1.09+/-0.26 120 to 100 minutes before AF; 0.88+/-0.24 20 to 0 minutes before AF; P<0.001) and in alpha(1) (1.01+/-0.28 120 to 100 minutes before AF, 0.89+/-0.28 20 to 0 minutes before AF; P<0.05) before the AF episodes. Both ApEn (0. 89+/-0.27 versus 1.02+/-0.30; P<0.05) and alpha(1) (0.91+/-0.28 versus 1.27+/-0.21; P<0.001) were also lower before the onset of AF compared with values obtained from matched healthy control subjects. A decrease in the complexity of R-R intervals and altered fractal properties in short-term R-R interval dynamics precede the spontaneous onset of AF in patients with no structural heart disease. Further studies are needed to determine the physiological correlates of these new, nonlinear HR variability measures.

Circadian variation of symptomatic paroxysmal atrial fibrillation. Data from almost 10 000 episodes.

To determine the circadian rhythm of paroxysmal atrial fibrillation in a very large outpatient population. We reviewed all emergency telephone calls received in Shahal (a medical service covering 44 000 subscribers), from 1987 to 1997. Patients were included if new-onset atrial fibrillation was recorded. During this study period, 9989 episodes of paroxysmal atrial fibrillation were recorded. The time of onset was not uniformly distributed throughout the 24 h period. Instead, the distribution of arrhythmic episodes showed a double peak, with a significant increase in the number of episodes in the morning and a second rise in the evening (P<0.001). A non-uniform weekly distribution of events was also noted, with substantially fewer episodes on Saturdays (P<0.001). Finally, more arrhythmias occurred during the last months of each year (P<0.001). The onset of paroxysmal atrial fibrillation does not occur randomly. The large patient population in the present study suggests that the circadian rhythm of paroxysmal atrial fibrillation is similar to that described for other cardiovascular diseases, with clustering of events in the morning and (to a lesser degree) late in the evening. Weekly and yearly circadian patterns are also prominent.

Use of an advanced mode switching algorithm in Inos 2 CLS and Logus dual chamber pacemakers

Background: According to literature, 30–60 % of pacemaker patients suffer from paroxysmal atrial fibrillation (PAF). As rapid tracking of PAF may cause severe symptoms in patients with dual chamber pacemakers, refined algorithms providing AV synchronous pacing during periods of sinus rhythm and preventing high ventricular rates during PAF are highly desirable. Aim and method: This comprehensive paper introduces a new mode switching (MS) algorithm which uses either a fixed (Inos2CLS) or programmable (Logos) number of short intervals out of 8 consecutive atrial intervals to detect PAF. If the MS criterion is fulfilled, a switch from AV synchronous pacing to nontracking mode is automatically performed. The algorithm is described together with a discussion on optimization of the programming of parameters which may indirectly influence the MS sensitivity and specificity. Results: This MS concept maintains the high sensitivity and fast reactivity towards PAF of the “mode conversion” in Actros and Kairos pacemaker systems, preventing a long time delay between onset of PAF, detection of the arrhythmia, and switch to nontracking mode. In addition, adequeate sensing and short blanking periods in the new MS concept enable reliable MS. The occurrence of atrial oversensing should be tested, as it may lead to inappropriate MS. Programmability of the MS algorithm may be advantageous for individual programming with respect to the patients' arrhythmia rate and atrial sensing performance, but the use of very restrictive or very liberal criteria should be avoided as both may lead to mode oscillations. Finally, examples of stored diagnostic data are presented to assess MS reliability, identify possible problems, and optimize MS function during follow-up.

Heart Rate Variability to Assess Changes in Cardiac Vagal Modulation Prior to the Onset of Paroxysmal Atrial Fibrillation in Patients With and Without Structural Heart Disease

Background and Objectives: In patients with paroxysmal lone AF, clinical data indicate a predominance of vagal modulation preceding attacks of the arryhthmia. Systematic data derived from time‐domain analysis of HRV evaluating changes in autonomic modulation prior to AF onset are sparse, both in patients without and with evidence for structural heart disease. This study evaluated changes in autonomic modulation prior to the onset of AF in patients with and without structural heart disease.Methods and Results: In 26 consecutive patients with at least one episode of paroxysmal AF preceded by a period of sinus rhythm of at least 8 hours duration documented on Holter monitoring, the time‐domain parameters SDNN, rMSSD, and pNN5O were analyzed at different time points between 8 hours and 10 minutes prior to the onset of AF. Fourteen patients had AF associated with structural heart disease, whereas 12 patients had paroxysmal lone AF. Analysis of HRV changes before onset of AF revealed significant differences between the two patient groups: In patients without heart disease, pNN5O and rMSSD increased from 10 ± 3 to 15 ± 4% (P=0.003) and from 38 ± 7 to 53 ± 9 ms (P=0.035). No significant change in HRV was observed in patients with structural heart disease (pNN5O 5 ± 3 vs. 6 ± 2 % and rMSSD 25 ± 4 vs. 28 ± 6 ms).Conclusions: In patients with lone AF, there is a significant shift of autonomic modulation towards a vagal predominance prior to the onset of paroxysmal AF as compared to patients with structural heart disease. Analysis of HRV prior to attacks of AF is useful in determining these triggering mechanisms.

Changes of autonomic tone before the onset of paroxysmal atrial fibrillation

The relationship between autonomic nerve system and the onset of paroxysmal atrial fibrillation (PAF) is still controversial. Furthermore, no prior studies have compared heart rate variability (HRV) between PAF patients with (organic) or without (idiopathic) underlying cardiac diseases. The purpose of this study was to assess the alteration of autonomic tone by analyzing HRV immediately before the onset of atrial fibrillation. This study included 57 patients (M/F: 34/23, 66±22 years) with frequent attacks of PAF. All cases underwent 24-h ambulatory Holter monitoring; each patient had one or more episodes of sustained PAF (>30 s). A period of sinus rhythm 40 min was allowed for accurate assessment of HRV over these periods. Spectral HRV was expressed as low (0.04–0.15 Hz) and high (0.15–0.40 Hz) frequency components (LF, HF), and L/H ratio at 2-min intervals over a 40-min period before the onset of PAF. According to HRV, three subtypes were classified; onset of PAF accompanied with increased HF component and decreased L/H ratio was designated as vagal type; decreased HF component and increased L/H ratio was designated as sympathetic type, and the other episodes which did not belong to vagal or sympathetic type were designated as non-related type. In group I (idiopathic PAF, n=30): 63 episodes of PAF were found and vagal type was predominant (41/63, 63.5%); HF increased significantly before the onset of AF. In group II (organic PAF, n=27): 58 episodes of PAF were found and sympathetic type was predominant (39/58, 67.2%); L/H ratio increased before AF onset. None of the three subtypes showed significant circadian distributions in group I and II patients. Changes of HRV before the onset of PAF were not universal; most of the patients with idiopathic PAF were vagal dependent and most of the patients with organic PAF were sympathetic dependent.

Analysis of the cardiac rhythm preceding episodes of paroxysmal atrial fibrillation

Aims: This study seeks to elucidate whether there was a common mode of initiation of paroxysmal atrial fibrillation (PAF) episodes that might suggest new therapies. Methods: A library of 177 digitized and analyzed 24-hour Holter recordings from PAF pharmacotherapy trials was studied. All noise-free PAF episodes ≥0.5 minutes were identified. PAF episodes and the preceding 2 minutes of sinus rhythm were printed as tachograms and visually inspected. Heart rate and ectopic beat behavior were used to characterize modes of PAF onset by comparing half-minute segments of the final 2 minutes of sinus rhythm. Results: Thirty-four recordings (from 19 patients, aged 61.7 ± 11.5 years) provided 231 PAF episodes suitable for analysis. No patients had a consistent mode of PAF onset. This was confirmed by systematic analysis of the five patients with the most episodes. Overall, a highly significant increase in ectopic beats, from 1.34 to 6.52 min -1 (p < 0.001) was found, but heart rate did not significantly change (mean heart rate at onset = 64 beats/min). PAF was initiated by a solitary ectopic beat in more than half of the cases. No consistent evidence for short-long-short sequences, seen in ventricular arrhythmias, was found. Conclusion: The mode of onset of atrial fibrillation is inconsistent, both across a population with PAF and within individuals. This has implications for understanding the mechanisms of atrial fibrillation onset in human beings and for the treatment of the disorder. (Am Heart J 1998;135:1010-9.)

Atrial Ectopics Prior to Atrial Fibrillation Onset

Background: This study examined the possible role of atrial ectopics and short runs of atrial tachycardia in the initiation of episodes of paroxysmal atrial fibrillation (PAF).Methods: Holter recordings from patients participating in pharmacotherapy trials for the prevention of PAF were examined. Treatment comprised placebo, digoxin, disopyramide, or atenolol. The frequency of atrial ectopic beats during each 30 seconds over the 5 minutes prior to PAF and whether this was also associated with atrial tachycardia (3 or more ectopics in succession) was calculated.Results: The mean number of ectopics was 4.1 in the final minute, but patients receiving disopyramide or atenolol had significantly more ectopics than those on placebo (P &gt; 0.05 for both). Those on digoxin had a similar number of ectopics to placebo patients. There was no relationship between heart rate at PAF onset and ectopic frequency, nor any association between the presence of one or more episodes of atrial tachycardia and ectopic frequency.Conclusion: Atrial ectopics increase in frequency prior to PAF onset, and this study suggests that antiarrhythmic therapy may increase the number of ectopics required to initiate PAF.

Alternating short cycles before the onset of paroxysmal atrial fibrillation

Alternating short cycles before the onset of paroxysmal atrial fibrillation

Alternating Short Cycles Before the Onset of Paroxysmal Atrial Fibrillation

Alternating Short Cycles Before the Onset of Paroxysmal Atrial Fibrillation

Diurnal Fluctuations in the Mode of the Onset of Paroxysmal Atrial Fibrillation

Diurnal Fluctuations in the Mode of the Onset of Paroxysmal Atrial Fibrillation

A relationship between fluctuations in heart rate and the duration of subsequent episodes of atrial fibrillation.

A relationship between autonomic tone and the onset of paroxysmal atrial fibrillation in some patients is recognised. Episodes of PAF may vary enormously in duration, however, from a few beats to many hours. Whether autonomic tone influences the duration of the episodes has been less well investigated. From a database of Holter recording taken from patients with symptomatic PAF, we identified all episodes of at least 30 seconds duration which were preceded by noise free sinus rhythm. This study examined the heart rate prior to AF onset, the change in heart rate over the final minute of sinus rhythm and the time of AF onset, and compared the data from those episodes of AF of more than 5 minutes duration to the shorter ones. Heart rate was slower before long episodes of AF, but this was found to predominantly represent data from separate recordings. A highly significant rise in heart rate was detected prior to long AF episodes compared to shorter ones. Daytime AF episodes were slightly longer than nocturnal ones. The most important finding was that longer AF episodes were typified by a heart rate acceleration. This suggests that, regardless of underlying aetiology, and increase in sympathetic tone may be important in the sustenance of episodes of PAF.

Diurnal fluctuations in the mode of the onset of paroxysmal atrial fibrillation

Diurnal fluctuations in the mode of the onset of paroxysmal atrial fibrillation

Alcohol and paroxysmal atrial fibrillation

Alcohol is accepted as a cause of paroxysmal atrial fibrillation (PAF), supraventricular tachycardia and other cardiac arrhythmias1 but the effect is usually attributed to abuse rather than simple use.2 Abuse of alcohol – if this means the constant consumption in excess of 21-28 units a week for a man – is not always necessary in the initiation and prolongation of attacks of PAF, as my personal history indicates. Much lesser amounts may be responsible. I am over 70 years old and have been hypertensive for about 20 years and on various therapeutic regimens, mostly beta-blockers and thiazides at first, but more recently a combination of captopril, doxazosin and indapamide. My blood pressure, originally about 180/110, is now around 150/80 and my left ventricular T waves, at first flat or slightly inverted, are now normal. About 15 years ago I developed non-insulin dependent diabetes mellitus, now well controlled with a no-sugar diet, metformin 500 mg b.d. and chlorpropamide 100 mg a day. My ‘normal’ alcohol consumption was about 20-30 units per week as wine, with occasional excesses. About 12 years ago, after a reunion with a considerable intake of alcohol, I had my first attack of atrial fibrillation starting about 5 a.m. and lasting some four hours. Attacks thereafter were occasional at first, but gradually became more frequent, even with the accepted safe limit of alcohol intake. In 1993, I thought I was having some benefit from diuretics,3 and probably still do, but I am on indapamide for hypertension anyway (7.5 mg daily) and do not wish to experiment by leaving it off. About a year or so ago, attacks of atrial fibrillation were occurring three or four times a week and lasting up to 24 hours. Some attacks were followed by supraventricular tachycardia and one lasted four and a half days, being cut short only by sotalol. The prospect of a permanent supraventricular arrhythmia was then daunting. On the whole, antiarrhythmics were not much help. Continuous beta-blockers (atenolol or labetalol) and flecainide did not prevent attacks. In August 1996, I started experimenting by stopping all alcohol for some weeks, thereafter trying occasional amounts and assessing the effect. Two things quickly became apparent. Firstly, the effect of any alcohol consumption lasted for about five days; and secondly, the amount precipitating an attack did not need to be large – even one unit was enough. I am now virtually teetotal and limited to tasting wine and letting my friends drink it! Without alcohol I am not completely free from attacks but only have one every seven to 10 days or so; they last from one to three hours and never overnight. I could list about half a dozen precipitating factors. On the whole, the medical textbooks are gloomy about the prognosis of PAF, suggesting there is an inevitable natural progression to permanent atrial fibrillation. However, Paul Wood in the 1960s4 recognised that PAF was still paroxysmal four times out of five after an average of 10 years and that age was an important factor in its aetiology; but he did not even mention alcohol as a causative factor. It would be interesting to know how many people with PAF and taking an accepted safe amount of alcohol would benefit from either a drastic reduction in their intake or total abstinence. Most have probably not tried and are unlikely to be asked to do so by their medical attendants in view of the current belief that alcohol is safe in amounts of up to 28 units per week for a man and 21 units for a woman.

Prediction of paroxysmal atrial fibrillation attacks by use of the P wave signal-averaged ECG in patients with WPW syndrome after catheter ablation

Prediction of paroxysmal atrial fibrillation attacks by use of the P wave signal-averaged ECG in patients with WPW syndrome after catheter ablation

The incidence of asymptomatic paroxysmal atrial fibrillation in patients treated with propranolol or propafenone

Anti-arrhythmic therapy for paroxysmal atrial fibrillation leads to complete symptomatic relief in a number of patients. The elimination of symptoms may be associated either with a complete elimination of arrhythmia or with a conversion of symptomatic atrial fibrillation into asymptomatic episodes of arrhythmia. The aim of the study was to evaluate the occurrence of asymptomatic paroxysmal atrial fibrillation in 52 patients treated with propafenone (35 drug trials) or propranolol (34 drug trials) by means of ambulatory ECG Holler monitoring. Propafenone was clinically effective (complete relief of symptoms) in 26 (74%) patients. However, in 7 cases (27%) asymptomatic episodes of arrhythmia were still recorded when awake. In patients treated with propranolol clinical symptoms were absent in 18 (53%). However, in 4 (22%) patients attacks of paroxysmal atrial fibrillation were present. The mechanism of drug-induced conversion of symptomatic episodes of atrial fibrillation into asymptomatic spells of arrhythmia was a marked shortening in duration of episodes in 7 patients (from 2215 ± 3843 s to 16 ± 10 s, N.S.) or by a significant slowing of ventricular response during atrial fibrillation in 4 patients (from 125 ± 27 to 84 ± 8 beats/min, P = 0.05). In conclusion, in a significant proportion of patients with symptomatic paroxysmal atrial fibrillation asymptomatic episodes of arrhythmia may occur while on anti-arrhythmic drug therapy. Some of these patients, particularly those with other risk factors for stroke such as advanced age or the presence of organic heart disease, may require anti-coagulant therapy or change in anti-arrhythmic treatment, and can be selected on the basis of ambulatory ECG monitoring.