Background-The mechanisms of the atrial contractile dysfunction induced by atrial fibrillation (AF) are not completely understood. In particular, the relation between the atrial dysfunction and electrical remodeling has not yet been studied. Methods and Results-Seven goats were chronically instrumented with electrodes sutured to the atria and with ultrasonic piezoelectric crystals to record the atrial diameters. A pressure transducer was implanted in the right atrium. After 5 minutes, 3 hours, and throughout the first 5 days of artificially maintained AF, atrial contractile function was measured and the atrial effective refractory period (AERP) was monitored for comparison. Also, the positive inotropic effects of the L-type Ca 2ϩ -channel agonist BayY5959 and short trains of rapid atrial pacing were studied. After resumption of sinus rhythm, the recovery of atrial contractile function was followed. After 5 minutes of AF, atrial contractility was decreased by Ϸ55% but recovered completely within 10 minutes. Five days of AF nearly completely abolished the atrial contractile function, and recovery took 2 days. During the first days of AF, the development of the contractile dysfunction followed the same time course as the shortening of AERP (electrical remodeling). In remodeled atria, BayY5959 increased atrial contractility to the same extent as it prolonged AERP. The inotropic effect of short trains of rapid atrial pacing was similar in normal and remodeled atria. Conclusions-Depending on the duration of AF, different mechanisms contribute to the AF-induced atrial hypocontractility. Atrial contractile remodeling during several days of AF goes hand in hand with electrical remodeling and might be caused by a reduction of the L-type Ca

Introduction: Atrial dilation plays an important role in the development and persistence of atrial fibrillation (AF). The mechanisms by which atrial dilation increases the vulnerability to AF are not fully understood. Methods and Results: In 11 isolated rabbit hearts, the right atrium was acutely dilated by increasing the intra‐atrial pressure from 2 to 9 and 14 cm H2O. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium. The atrium was paced from four different sites at intervals of 240 and 125 msec. At normal atrial pressure (2 cm H2O), conduction was uniform in all directions with an anisotropy ratio between 1.5 and 1.7. Increasing the pressure to 9 cm H2O decreased the normalized conduction velocity during rapid pacing by 18%. The incidence of areas of slow conduction and conduction block increased from 6.6% and 1.6% to 10.2% and 3.3%. At 14 cm H2O, conduction velocity decreased by 31% and the percentage of slow conduction and block further increased to 11.5% and 6.6% (P < 0.001). The appearance of lines of intra‐atrial block was largely dependent on the pacing site. Whereas during pacing at the cranial part of the crista terminalis no increase in conduction delays occurred, pacing from the low right atrium unmasked several lines of block oriented parallel to the major trabeculae and the crista terminalis. In an additional series of six hearts the left atrium also was mapped. The effect of dilation of the left atrium was comparable to that of the right atrium. Increasing the atrial pressure to 14 cm H2O increased the amount of intra‐atrial conduction block threefold to fourfold. Conclusion: Acute atrial dilation results in slowing of conduction and an increase of the amount of intra‐atrial conduction block. The increase in spatial heterogeneity in conduction was related to the anisotropic properties of the atrial wall. (J Cardiovasc Electrophysiol, Vol. 14, pp. 269‐278, March 2003)

Background-Atrial dilatation is an important risk factor for atrial fibrillation (AF). In the present study, we monitored the electrophysiological changes during progressive atrial dilatation in chronically instrumented goats. Methods and Results-In 8 goats, 2 screw-in leads with piezoelectric crystals were implanted transvenously in the right atrium. After 2 weeks, atrial diameter and effective refractory period were measured. AF paroxysms were induced by burst pacing to determine the baseline AF cycle length and stability of AF. After His-bundle ablation, the above measurements were repeated once a week. After 4 weeks of complete AV block, the free wall of the right atrium was mapped and the atrium was fixed in formalin for histological analysis. After His-bundle ablation, the ventricular rate decreased from 113.8Ϯ4.8 to 44.6Ϯ2.5 bpm. Right atrial diameter increased gradually by 13.5Ϯ3.9% during 4 weeks of AV block (PϽ0.01). The duration of induced AF paroxysms increased from 4.6 seconds to 6.4 minutes (PϽ0.05). Atrial effective refractory period and AF cycle length remained constant. Spontaneous paroxysms of AF were not observed. Atrial mapping during rapid pacing revealed that slow conduction (Ͻ30 cm/s) was present in 3.7Ϯ1.0% of the mapped area (control, 0.9Ϯ0.5%, PϽ0.05). Histological analysis showed hypertrophy without atrial fibrosis. Connexin40 and connexin43 expression was unchanged. Conclusions-Chronic

In a goat model of chronic atrial dilation, AF-induced electrical remodeling was unchanged. However, AFCL no longer shortened during electrical remodeling. Thus, in dilated atria a wider excitable gap exists during AF, probably caused by intra-atrial conduction defects and a higher contribution of anatomically defined re-entrant circuits.

The progressive loss of efficacy of Class IC drugs to cardiovert AF of longer duration is not due to a decrease in the sensitivity of remodeled atrial myocardium for Class IC drugs. Failure of cardioversion was due to an increase in the critical AF cycle length required for pharmacological cardioversion.

In dilated atria, blockade of the rapid sodium channels caused a higher degree of local conduction delay and intra-atrial conduction block than in nondilated atria.

Allessie. Loss of atrial contractility is primary cause of atrial dilatation during first days of atrial fibrillation. Am J Physiol Heart Circ Physiol 287: H2324 -H2331, 2004. First published July 15, 2004 doi: 10.1152/ajpheart.00581.2004.-Atrial fibrillation (AF) induces a progressive dilatation of the atria which in turn might promote the arrhythmia. The mechanism of atrial dilatation during AF is not known. To test the hypothesis that loss of atrial contractile function is a primary cause of atrial dilatation during the first days of AF, eight goats were chronically instrumented with epicardial electrodes, a pressure transducer in the right atrium, and piezoelectric crystals to measure right atrial diameter. AF was induced with the use of repetitive burst pacing. Atrial contractility was assessed during sinus rhythm, atrial pacing (160-, 300-, and 400-ms cycle length), and electrically induced AF. The compliance of the fibrillating right atrium was measured during unloading the atria with diuretics and loading with 1 liter of saline. All measurements were repeated after 6, 12, and 24 h of AF and then once a day during the first 5 days of AF. Recovery of the observed changes after spontaneous cardioversion was also studied. After 5 days of AF, atrial contractility during sinus rhythm or slow atrial pacing was greatly reduced. During rapid pacing (160 ms) or AF, the amplitude of the atrial pressure waves had declined to 20% of control. The compliance of the fibrillating atria increased twofold, whereas the right atrial pressure was unchanged. As a result, the mean right atrial diameter increased by ϳ12%. All changes were reversible within 3 days of sinus rhythm. We conclude that atrial dilatation during the first days of AF is due to an increase in atrial compliance caused by loss of atrial contractility during AF. Atrial compliance and size are restored when atrial contractility recovers after cardioversion of AF. stunning; remodeling; atrial tachyarrhythmias A RELATIONSHIP between atrial size and atrial fibrillation (AF) was first proposed by Fraser and Turner in 1955 (1), who showed that AF was more common in patients with enlarged atria than in patients with normal atrial size. In the 1990s, large prospective trials established left atrial enlargement as an independent risk factor for the development of AF (13,14). Today, it is generally accepted that AF is not only a consequence but also a cause of atrial dilatation. In patients with "lone AF," Sanfilippo et al. (9) demonstrated that AF resulted in progressive atrial dilatation, which in turn, might contribute to the self-perpetuating nature of the arrhythmia.The mechanism of atrial dilatation related to AF is still unclear. It has been proposed that mild impairment of ventricular pump function due to the high ventricular rate during AF might increase end-diastolic ventricular and atrial pressures (12). An alternative explanation might be that the pronounced atrial contractile dysfunction of the atria induced by AF (6, 7, 10) underlies the dilatation of ...

Background Atrial fibrillation is commonly associated with obesity. Observational studies have shown that weight loss is associated with improved prognosis and a decrease in atrial fibrillation frequency and severity. However, despite these benefits, nonadherence to lifestyle programs is common. Objective In this study, we evaluated adherence to and feasibility of a multidisciplinary lifestyle program focusing on behavior change in patients with atrial fibrillation and obesity. Methods Patients with atrial fibrillation and obesity participated in a 1-year goal-oriented cardiac rehabilitation program. After baseline assessment, the first 3 months included a cardiac rehabilitation intervention with 4 fixed modules: lifestyle counseling (with an advanced nurse practitioner), exercise training, dietary consultation, and psychosocial therapy; relaxation sessions were an additional optional treatment module. An advanced nurse practitioner monitored the personal lifestyle of each individual patient, with assessments and consultations at 3 months (ie, immediately after the intervention) and at the end of the year (ie, 9 months after the intervention). At each timepoint, level of physical activity, personal goals and progress, atrial fibrillation symptoms and frequency (Atrial Fibrillation Severity Scale), psychosocial stress (Generalized Anxiety Disorder–7), and depression (Patient Health Questionnaire–9) were assessed. The primary endpoints were adherence (defined as the number of visits attended as percentage of the number of planned visits) and completion rates of the cardiac rehabilitation intervention (defined as performing at least of 80% of the prescribed sessions). In addition, we performed an exploratory analysis of effects of the cardiac rehabilitation program on weight and atrial fibrillation symptom frequency and severity. Results Patients with atrial fibrillation and obesity (male: n=8; female: n=2; age: mean 57.2 years, SD 9.0; baseline weight: mean 107.2 kg, SD 11.8; baseline BMI: mean 32.4 kg/m2, SD 3.5) were recruited. Of the 10 participants, 8 participants completed the 3-month cardiac rehabilitation intervention, and 2 participants did not complete the cardiac rehabilitation intervention (both because of personal issues). Adherence to the fixed treatment modules was 95% (mean 3.8 sessions attended out of mean 4 planned) for lifestyle counseling, 86% (mean 15.2 sessions attended out of mean 17.6 planned) for physiotherapy sessions, 88% (mean 3.7 sessions attended out of mean 4.1 planned) for dietician consultations, and 60% (mean 0.6 sessions attended out of mean 1.0 planned) for psychosocial therapy; 70% of participants (7/10) were referred to the optional relaxation sessions, for which adherence was 86% (mean 2 sessions attended out of mean 2.4 planned). The frequency of atrial fibrillation symptoms was reduced immediately after the intervention (before: mean 35.6, SD 3.8; after: mean 31.2, SD 3.3), and this was sustained at 12 months (mean 24.8, SD 3.2). The severity of atrial fibrillation complaints immediately after the intervention (mean 20.0, SD 3.7) and at 12 months (mean 9.3, SD 3.6) were comparable to that at baseline (mean 16.6, SD 3.3). Conclusions A 1-year multidisciplinary lifestyle program for obese patients with atrial fibrillation was found to be feasible, with high adherence and completion rates. Exploratory analysis revealed a sustained reduction in atrial fibrillation symptoms; however, these results remain to be confirmed in large-scale studies.