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Atrial fibrillation is commonly associated with a structural heart disease such as valvular disease, coronary artery disease, or dilated cardiomyopathy. Lone atrial fibrillation may be defined as a form of paroxysmal, persistent, or permanent atrial fibrillation with a “pure” electrophysiological substrate. But, does a pure lone atrial fibrillation really exist? To answer this question, it is important to investigate carefully both the anatomic and the electrophysiologic substrates, including all modulating factors that may increase the probability of induction of atrial fibrillation.

Atrial fibrillation (AF) shortens life expectancy in patients with cardiovascular disease. Lone atrial fibrillation is not associated with an excess in mortality. However, lone atrial fibrillation decreases life expectancy when associated with comorbidities during its evolution.

In this issue of the Journal , Stiles et al. ([1][1]) publish a report titled “Paroxysmal Lone Atrial Fibrillation Is Associated With an Abnormal Atrial Substrate: Characterizing the ‘Second Factor’.” In 25 patients with paroxysmal lone atrial fibrillation (AF), atrial electrophysiological

Although the clinical phenotype of atrial fibrillation (AF) has multiple causes, the most prevalent cause in the Western world is hypertensive heart disease caused by the high prevalence of hypertension. Change in hemodynamic status by an increase in blood pressure has many direct effects on left

Atrial fibrillation (AF) is a possible complication of sport in middle-aged athletes. When sinus rhythm has been restored, at what time is deformation restored too? This question has never been answered. We studied an one 47-year old cyclist and runner with acute lone atrial fibrillation. A day before, he trained hard intervals and felt at the next day an irregular rhythm, training was not possible. He told this would occure 2 times a year , but after the light training the irregular puls will disappear. At the chest-pain unit we performed echocardiography inclusive strain measurements of the right and left ventricle during atrial fibrillation and immediately after the recovery of the sinus rhythm. He recovered to sinus rhythm during the exercise test. Global strain was at the moment of atrial fibrillation – 11.8%, direct after the recovery of the sinus rhythm -17,2%, and -20.5% at the next day, even though the normalized diastolic function directly after conversion from AF. It seems to be that the heterogenity of the deformation need time to recovery after the conversion to the sinus rhythm, even though the diastolic function seems to be normalized. The further endurance training should be continued only after normalization of deformation values.

A giant ball-thrombus was found in the left atrium in 78 year-old female with non-valvular lone atrial fibrillation. Intraoperative echocardiography revealed the thrombus was floating freely inside the left atrium. The thrombus was sometimes scarcely entrapped into the mitral annulus and bounded back toward the left atrium. The removed thrombus was 45×35×20mm in size.

BackgroundRecent community-based research has linked aortic stiffness to the development of atrial fibrillation. We posit that aortic stiffness contributes to adverse atrial remodeling leading to the persistence of atrial fibrillation following catheter ablation in lone atrial fibrillation patients, despite the absence of apparent structural heart disease. Here, we aim to evaluate aortic stiffness in lone atrial fibrillation patients and determine its association with arrhythmia recurrence following radio-frequency catheter ablation.MethodsWe studied 68 consecutive lone atrial fibrillation patients who underwent catheter ablation procedure for atrial fibrillation and 50 healthy age- and sex-matched community controls. We performed radial artery applanation tonometry to obtain central measures of aortic stiffness: pulse pressure, augmentation pressure and augmentation index. Following ablation, arrhythmia recurrence was monitored at months 3, 6, 9, 12 and 6 monthly thereafter.ResultsCompared to healthy controls, lone atrial fibrillation patients had significantly elevated peripheral pulse pressure, central pulse pressure, augmentation pressure and larger left atrial dimensions (all PConclusionAortic stiffness is an important risk factor in patients with lone atrial fibrillation and contributes to higher atrial fibrillation recurrence following catheter ablation procedure.

Atrial fibrillation (AF) is the most common arrhythmia seen in clinical practice in all its presentation forms: paroxysmal, recurrent and chronic. Though usually associated with organic heart disease, it is also found in the absence of any structural cardiac abnormality in a substantial number of cases. Its clinical significance, prognosis, and management are largely dependent on underlying or associated heart disease; understanding the electrophysiologic (EP) mechanisms and modulating factors, such as the autonomic nervous system, is of utmost importance in the clinical management of AF patients.

Clinical factors such as tall stature, lean body mass, obstructive sleep apnea, alcohol or caffeine, smoking, endurance sports, and genetic factors are proposed as risk factors for lone atrial fibrillation (LAF). The KORAF (KORean Atrial Fibrillation) study is a retrospective multicenter registry that enrolled 3,570 consecutive atrial fibrillation (AF) patients. Data on risk factors were available for 2,133 patients, of whom 398 (18.7%) were identified as having LAF. In univariate analysis, patients with LAF were more likely to be men (82.4% vs 59.8%, P < 0.001) and current smokers (25.9% vs 15.6%, P < 0.01), alcohol drinkers (55.3% vs 31.2%, P < 0.01) and frequent consumers of caffeinated beverages (> 2 cups/day) (31.7% vs 19.3%, P < 0.01), and have a family history of AF (9.0% vs 2.6%, P < 0.001) than the non-LAF patients. Multivariate analysis showed that male gender (OR, 2.30; 95% CI, 1.61-3.27, P < 0.01), family history of AF (OR, 3.12; 95% CI, 1.91-5.12, P < 0.01), current alcohol use (OR, 2.01; 95% CI, 1.46-2.76, P < 0.01), and frequent caffeinated beverage consumption (OR, 1.66; 95% CI, 1.20-2.29, P < 0.01) were independently associated with LAF. In Korean patients, LAF is more closely associated with male gender, family history of AF, current alcohol and frequent caffeinated beverage consumption than non-LAF.

Background Recent genome-wide association studies suggested that SCN10A common variants modulate PR and QRS duration. SCN10A encodes the sodium channel NaV1.8, initially cloned from dorsal root ganglion (DRG) neurons but more recently identified in the heart. We identified 3 rare variants (417delK, A1886V, R814H) that associated with lone atrial fibrillation and slow ventricular rates. We hypothesized that these mutations affect NaV1.8 biophysics, thus providing a mechanism for the associated disease. Here we functionally characterized these variants. Methods Site-directed mutagenesis was used to generate the mutants and whole-cell patch-clamp experiments were performed to study the biophysics of the variants transiently expressed in ND7/23 cells. Whole-cell currents were recorded 48 hours after transfection at 37°C. Results Compared with wild-type (WT) channel, A1886V displayed a larger peak INa (103 ± 16.6 pA/pF vs 43 ± 4.8 pA/pF, P Conclusions All 3 variants studied showed significantly increased INa-L, which supports the idea that they are causative for the variable cardiac conduction. Partially rescued 417delK INa after incubation at 28°C might be explained by rescue of a trafficking defect that prevented delivery of the channel to plasma membrane. Additional parameters for SCN10A WT and rare variants Additional parameters for SCN10A WT and rare variants WT (37°C) WT (28°C) 417delK (37°C) 417delK (28°C) A1886V (37°C) R814H (37°C) Peak INa (pA/pF) –43 ± 4.8 –41 ± 3 –7.5 ± 1.4 (P –21 ± 3.1 (P –103 ± 16.6 (P –187.1 ± 22.6 (P Voltage-to-peak INa (mV) +3.6 ± 1.4 +5 ± 3.4 +6.2 ± 1.8 +3.8 ± 1.4 +7.5 ± 1.6 +15.9 ± 1.2 (P Late INa (INa-L) (% INa) 6.1 ± 0.9 6 ± 1 17.5 ± 4.1 (P 8.7 ± 0.4 (P 13.9 ± 1.9 (P 13.3 ± 1.1 (P τ fast (ms) 2.8 ± 0.1 3 ± 0.2 2 ± 0.2 (P 2.3 ± 0.2 5 ± 0.5 (P 3 ± 0.2 τ slow (ms) 22.4 ± 2.3 20 ± 1.7 11.5 ± 2.1 (P 17.9 ± 2.7 32.2 ± 3.9 18.1 ± 1.7 V1/2 activation (mV) –8 ± 1 –7 ± 1.6 — 9.1 ± 1.1 –16 ± 1.9 –14 ± 1.1 K activation (mV) 5.3 ± 0.3 5.6 ± 0.5 — 6.1 ± 0.4 5.8 ± 0.4 6.3 ± 0.4 V1/2 inactivation (mV) –79.9 ± 2.4 –74.9 ± 4 — –78.6 ± 2.1 –79.4 ± 4 –84.7 ± 1.4 K inactivation (mV) 11.7 ± 1.5 12 ± 2.1 — 13 ± 1 16.4 ± 1.8 14 ± 1.7

BACKGROUND: Physiologic changes of pregnancy can predispose women to cardiac arrhythmias. Atrial fibrillation is rare in pregnancy and usually occurs in women with underlying cardiac anomalies. CASE: A young woman at 22 weeks of gestation presented with new-onset atrial fibrillation with rapid ventricular response. Thorough evaluation revealed atrial fibrillation with no underlying cause and ultimately required treatment with electrical cardioversion. CONCLUSION: Lone atrial fibrillation in pregnancy requires exclusion of all possible etiologies before diagnosis. Cardioversion is the treatment of choice. Women with persistent atrial fibrillation require anticoagulation and rate control, as well as fetal growth surveillance and antenatal testing.

To the Editor: Endurance athletes may be at increased risk for lone atrial fibrillation.1–5 We describe a middle-aged physician athlete with paroxysmal lone atrial fibrillation in whom cardioversion consistently occurs with vigorous exercise. At 45 years of age, the patient had atrial fibrillation at an average ventricular rate of approximately 55 beats per minute. The results of physician examination, echocardiography, tests of thyroid function, and measurements of electrolytes were normal. After 24 hours of observation, external electrical cardioversion was attempted at progressive energy levels up to 400 J, without success. The patient was discharged home with instructions to take . . .

Left ventricular (LV) function was studied in 30 patients with lone atrial fibrillation (AF) (paroxysmal [n = 27] and persistent [n = 3]) before and after ablation of atrioventricular conduction. In all patients, drug treatment did not control ventricular rate during AF or prevent recurrences of the arrhythmia, or both. LV ejection fraction, and LV end-systolic and end-diastolic, and left atrial dimensions were measured by echocardiography before (mean 7 +/- 10 months, range1 to 37) and after (14 +/- 20 months,1 to 77) ablation. Before ablation, LV ejection fraction wasor = 50% in 12 patients (group I) and50% in 18 (group II). After ablation, LV ejection fraction increased significantly in group I from 43 +/- 8% to 54 +/- 7% (p0.0001). There were also significant decreases in LV-end systolic and end-diastolic, and left atrial dimensions. No changes in these parameters were observed in group II. Groups I and II had a significant difference in the duration of AF (group I: mean 11 years, range 8 to 28; and group II: 5 years, 2 to 14) (p0.05). No difference was present in age, sex, New York Heart Association functional class for dyspnea, or type of ablation procedure. Thus, some patients with lone AF may show deterioration of LV function, which appears to be related to the duration of the arrhythmia; in these cases, LV function may improve significantly after ventricular rate control is accomplished by ablation of atrioventricular conduction.

Assessment of risk of thromboembolism and potential benefit of prophylaxis with long-term anticoagulant therapy in lone atrial fibrillation is hampered by a lack of consensus regarding definition of lone atrial fibrillation. In general, patients less than 60 years of age with normal left ventricular function and left atrial size have a low risk of thromboembolic events and are unlikely to gain any significant benefit with anticoagulants; however, patients older than 60 years with impaired left ventricular function, enlarged left atrium, and/or associated conditions such as hypertension have an increased risk of thromboembolism and would benefit from long-term anticoagulant therapy. Decisions regarding anticoagulant usage would be simplified by using a scoring system containing clinical and investigational variables.

Randomised trials confirm that anticoagulants reduce the risk of emboli in atrial fibrillation. To apply this evidence to practice, we developed an expression relating all relevant factors. Trial-based estimates of the risks of emboli and haemorrhage, and of the effects of anticoagulants on these risks were used to derive the extent to which haemorrhage has to be seen to be more detrimental than emboli to justify not using anticoagulants. Information from other studies was used to assess the risks for the types of patients not included in the trials. Haemorrhage needs to be assessed as being at least six times more detrimental than emboli to warrant withholding anticoagulants from patients like those in the trials. Only in patients with lone atrial fibrillation and in those with features suggesting a bleeding risk six times higher than the trials' average would a perception of equal detriment risk justify not giving anticoagulation.

Lone atrial fibrillation (AF) is relatively uncommon in patients aged 1,2 In contrast, AF is relatively common in patients with the Wolff-Parkinson-White syndrome, even though most have no organic heart disease. 3 In the latter patients, AF occurs after an initial period of atrioventricular (AV) reciprocating tachycardia that may no longer be evident at the time of presentation. This mechanism of AF has also been postulated to occur in AV nodal reentrant tachycardia (Figure 1). 4 We postulated that younger patients with apparently lone AF may have underlying AV or AV nodal reentrant tachycardia as a precipitating factor for AF. This would be of clinical importance, because the latter arrhythmias can be managed expediently with radiofrequency ablation to prevent the supraventricular tachycardia that precipitates AF.

Treatment of a patient with new onset atrial fibrillation with intravenous adenosine was followed by transient but significant acceleration of the ventricular rate. This unexpected response to adenosine can be explained by a predominating increase in sympathetic discharge relative to the drug's direct atrial ventricular nodal-blocking action.

A 69-year-old male visited our clinic in 1973 because of atrial fibrillation noted during an annual check-up for the aged. Blood pressure, heart rate and CTR in chest X-ray films showed 110/80 mmHg, 150/min and 55%, respectively. There were no signs of valvular heart diseases, and a diagnosis of lone atrial fibrillation was convincing. Since then, repeated ECGs recorded twice or more a year had shown atrial fibrillation until 1988, when sinus rhythm with both first degree AV block and low P-wave amplitude appeared. The motion pattern of the anterior mitral leaflet on M mode echocardiography was abnormal with almost complete disappearance of the A-wave, whereas the motion pattern of the tricuspid valve was normal.

Atrial fibrillation (AF) is a common arrhythmia and is often difficult to manage. The classical risk factors for AF include hypertension, valvular disease, thyroid disease, cardiomyopathies, including ischaemic cardiomyopathies. When AF represents an electrophysiological phenomenon in structurally normal hearts it is termed lone AF. There are currently no studies to describe the clinical characteristics and outcomes of patients with lone AF in Africa. This study's purpose is to describe the clinical characteristics and outcomes of Lone AF patients attending Groote Schuur Hospital (GSH).

A retrospective analysis was performed on 23 subjects with lone atrial fibrillation who were followed for an average of 6.2 years (1.1-12.8 years). In all patients, underlying organic heart disease was excluded based on history, physical exam, electrocardiogram, echocardiogram, and Doppler ultrasound interrogation. All patients had at least two echocardiographic studies during the period of observation. Atrial fibrillation was chronic in 11 subjects and paroxysmal in 12. All echocardiographic measurements were obtained by averaging the measurements of two blinded investigators. Left atrial size increased an average of 5.6 mm which translates into a 14.7% increase over the baseline measurement. This increase in size was not associated with a change in left ventricular mass or fractional shortening as determined by echocardiography. Subjects with chronic atrial fibrillation had a larger percent increase than subjects with paroxysmal atrial fibrillation (18.9 vs. 10.8%), although this relative change in size failed to reach statistical significance. The only variable which significantly contributed to the change in left atrial size was the duration of follow-up. We conclude that atrial fibrillation occurring in patients with lone atrial fibrillation may cause a slow and progressive increase in left atrial size independent of changes in left ventricular size or function.

To the Editor: In the Japan Atrial Fibrillation Stroke Trial (JAST),1 aspirin at 150 to 200 mg per day does not seem to be either effective or safe for the prevention of stroke in patients with nonvalvular lone atrial fibrillation (AF). JAST is an important trial because many guidelines suggest that low risk patients with AF should be treated with aspirin, although the evidence, until recently, was limited. Previous studies already suggest that aspirin …