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Aim: Guidelines for the clinical management of patients with atrial fibrillation suggest that treatment strategies for prescribing oral anticoagulant therapy should implicate change at age 60, 65 and 75 years. We examined if there is any threshold concerning risk of stroke by age., Methods: We identified 141,493 subjects, aged 40-89 years, with an incident hospital diagnosis of nonvalvular atrial fibrillation or flutter and no previous or concomitant diagnosis of stroke in the Danish National Registry of Patients from January 1, 1980, to December 31, 2002. The subjects were followed in the Danish National Registry of Patients for the occurrence of an incident diagnosis of stroke of any nature and in the Danish Civil Registration System for emigration and vital status. We examined the risk of stroke by age in men and women using Cox regression models, which included age categorized in intervals, linear splines of age with cut points at age 60 and 75 years, or at age 65 and 75 years. We also analyzed age as a continuous variable in linear and polynomial regression models., Results: During follow-up 15,964 incident strokes were reported to the Danish National Registry of Patients. The risk of stroke increased by increasing age at baseline. We did not find any evidence for a threshold concerning risk of stroke by age, and the best model fit was obtained in a third-order polynomial regression model., Conclusion: The risk of stroke increased gradually by increasing age, and we could not detect any threshold concerning risk of stroke by age., ((c) 2007 S. Karger AG, Basel.)

Background: In patients with atrial fibrillation (AF) information regarding exercise release of atrial natriuretic peptide (ANP) is sparse and data on plasma brain natriuretic peptide (BNP) response to exercise is lacking. The aim of this study was to investigate plasma ANP and BNP response to exercise in patients with permanent AF and to assess if the response was different from the response in healthy age- and sex-matched control subjects., Methods: Plasma venous concentrations of ANP and BNP were determined at rest, at peak exercise and 30 min from the end of exercise in 38 patients with permanent AF and in 43 age- and sex-matched healthy control subjects., Results: Plasma concentrations of ANP and BNP were significantly higher in AF patients compared with the healthy control group at rest, peak exercise and after 30 min of recovery (p<0.0001). ANP and BNP increased significantly during exercise in both patients with AF and in the healthy control subjects (p<0.05). The increase in plasma concentration of ANP and BNP during exercise was significantly higher in AF patients compared with healthy controls (p=0.0002 for ANP; p<0.0001 for BNP). In the recovery period plasma BNP decreased significantly (p<0.0001) where as the decrease in plasma ANP was insignificant (p=0.4)., Conclusions: Patients with permanent AF have elevated levels of ANP and BNP at rest and exhibit much higher exercise release compared to healthy control subjects. This enhanced secretion of potent vasodilating and natriuretic agents may represent an important compensatory mechanism to improve exercise capacity in patients with AF.

Background: Despite the efficacy of warfarin sodium therapy for stroke prevention in atrial fibrillation, many physicians hesitate to prescribe it to elderly patients because of the risk for bleeding complications and because of inconvenience for the patients., Methods: The Second Copenhagen Atrial Fibrillation, Aspirin, and Anticoagulation Study was a randomized, controlled trial examining the following therapies: warfarin sodium, 1.25 mg/d; warfarin sodium, 1.25 mg/d, plus aspirin, 300 mg/d; and aspirin, 300 mg/d. These were compared with adjusted-dose warfarin therapy (international normalized ratio of prothrombin time [INR], 2.0-3.0). Stroke or a systemic thromboembolic event was the primary outcome event. Transient ischemic attack, acute myocardial infarction, and death were secondary events. Data were handled as survival data, and risk factors were identified using the Cox proportional hazards model. The trial was scheduled for 6 years from May 1, 1993, but due to scientific evidence of inefficiency of low-intensity warfarin plus aspirin therapy from another study, our trial was prematurely terminated on October 2, 1996., Results: We included 677 patients (median age, 74 years). The cumulative primary event rate after 1 year was 5.8% in patients receiving minidose warfarin; 7.2%, warfarin plus aspirin; 3.6%, aspirin; and 2.8%, adjusted-dose warfarin (P = .67). After 3 years, no difference among the groups was seen. Major bleeding events were rare., Conclusions: Although the difference was insignificant, adjusted-dose warfarin seemed superior to minidose warfarin and to warfarin plus aspirin after 1 year of treatment. The results do not justify a change in the current recommendation of adjusted-dose warfarin (INR, 2.0-3.0) for stroke prevention in atrial fibrillation.

Chronic non-rheumatic atrial fibrillation is associated with a risk of thromboembolic complications of about 5% per year. Previous myocardial infarction seems to be a significant risk factor for development of thromboembolic complications in chronic atrial fibrillation, whereas paroxysmal atrial fibrillation and isolated atrial fibrillation in younger patients may be associated with a lower risk of emboli. Silent cerebral infarction occurs more often in chronic atrial fibrillation than among controls in sinus rhythm. Three prospective trials of patients with atrial fibrillation found effect of warfarin on the occurrence of thromboembolic complications. In one study aspirin 325 mg daily was effective in patients below 75 years of age, but not in patients above this age. The other trials revealed no effect of aspirin.

In a blinded controlled study, 58 consecutive patients with definite left atrial enlargement (M-mode dimension of at least 45 mm) were followed up after 1-2 years. The aim of the study was to examine the following: (a) the prospective risk of developing atrial fibrillation (AF); and (b) the effect of the heart rhythm on the left atrial size. Of 36 patients in sinus rhythm, one developed paroxysmal AF and one developed persistent AF during a median follow-up period of 20 months. Thus the incidence of new AF was 5% per year. Eighteen patients died before scheduled echocardiographic follow-up, but in the remaining subjects the left atrial dimension did not change significantly: the median increment was 1 mm in 20 patients who sustained sinus rhythm vs 2 mm in 16 patients with chronic AF (P greater than 0.05). Although left atrial dilatation may cause AF and vice versa, this study demonstrated that the incidence of new AF is low, despite the fact that the left atrial dimension is substantially increased. Similarly, AF per se does not appear to have any major impact on the left atrial dimension.

As previously reported, 1007 patients with chronic atrial fibrillation participated in the Copenhagen AFASAK study. Before inclusion to trial, they all had a physical examination, chest roentgenogram, and echocardiogram with determination of left atrial size. This study evaluated the importance of cardiovascular risk factors for development of thromboembolic complications. To exclude any treatment effects on occurrence of thromboembolic complications, we included only the 336 patients from the placebo group. Using Cox's regression model, previous myocardial infarction was a significant risk factor for development of thromboembolic complications. Age, gender, heart failure, chest pain, hypertensive heart disease, diabetes, systolic and diastolic blood pressure, smoking, relative heart volume, and left atrial size were all without statistical importance.

Atrial fibrillation (AF) is associated with an increased risk of stroke. In patients with chronic AF, without clinically known cerebrovascular disease, computed tomography (CT) has revealed a high frequency of abnormal low-density areas suggesting old asymptomatic infarcts. To investigate the frequency of such lesions in paroxysmal AF, 30 patients with paroxysmal AF and 30 controls matched in sinus rhythm, without history of cerebrovascular disease, were CT scanned. Four patients with paroxysmal AF (13%) and 3 controls (10%) had abnormal CT scans with areas of low density with sharp demarcation from surrounding tissue. The abnormal areas probably reflected small, clinically silent infarcts. There were no differences between paroxysmal AF and controls in number and size of abnormal areas with apparent tissue loss. In contrast to chronic AF, the risk of such lesions in paroxysmal AF does not seem to be increased compared with matched sinus rhythm controls. This is in agreement with the clinical experience of a low risk of stroke in paroxysmal AF.

The incidence of embolic complications among 426 patients with initial paroxysmal atrial fibrillation (PAF) was analysed. A distinct clustering of emboli was seen at the time of onset of PAF. After transition to chronic atrial fibrillation (CAF), which developed in 141 patients (33.1%), the incidence of emboli was seen to rise to a new level several times higher than the incidence level for patients with PAF. Also in this group a distinct clustering of emboli was seen during the first year after transition to CAF. On this background it is suggested that patients with PAF may benefit from treatment with anti-arrhythmic agents in order to prevent the development of CAF and that anticoagulants for stroke prevention seems especially desirable in atrial fibrillation (AF) of recent onset.

Four recent major studies concerning the prognosis in atrial fibrillation (AF) are reviewed. The one-year mortality ranged from 16.0 to 0.2%, highest in elderly, hospitalized patients with chronic AF and lowest in young individuals with paroxysmal AF without other heart disease. The recognized clinical impression that the prognosis in AF is determined by age, type of AF and clinical status is thus confirmed. In three studies, however, the prognosis in lone atrial fibrillation seemed to be poorer than previously thought. The overall rate of thromboembolic complications in AF was about 25% in several studies. The effectiveness of coumarin drugs in the prophylaxis of these complications is not proved, and the time has come to subject them to more careful clinical investigation.

From November, 1985, to June, 1988, 1007 outpatients with chronic non-rheumatic atrial fibrillation (AF) entered a randomised trial; 335 received anticoagulation with warfarin openly, and in a double-blind study 336 received aspirin 75 mg once daily and 336 placebo. Each patient was followed up for 2 years or until termination of the trial. The primary endpoint was a thromboembolic complication (stroke, transient cerebral ischaemic attack, or embolic complications to the viscera and extremities). The secondary endpoint was death. The incidence of thromboembolic complications and vascular mortality were significantly lower in the warfarin group than in the aspirin and placebo groups, which did not differ significantly. 5 patients on warfarin had thromboembolic complications compared with 20 patients on aspirin and 21 on placebo. 21 patients on warfarin were withdrawn because of non-fatal bleeding complications compared with 2 on aspirin and none on placebo. Thus, anticoagulation therapy with warfarin can be recommended to prevent thromboembolic complications in patients with chronic non-rheumatic AF.

Atrial fibrillation is associated with an increased risk of stroke. Different risk factors may be of importance regarding stroke incidence and mortality in atrial fibrillation. Retrospectively, we studied 786 patients with chronic atrial fibrillation, 229 with rheumatic heart disease and 557 without. In all, 127 patients had stroke (16%). Using Cox's proportional hazard model for failure-time data with age, gender, etiology, degree of heart failure and cardiac enlargement as explanatory (independent) variables, only etiology (rheumatic heart disease) was a significant risk factor for stroke (P less than 0.006). Significant risk factors for death in 653 patients without stroke were age (P = 0.000) and congestive heart failure at the onset of atrial fibrillation (P = 0.000). The need to identify other risk factors for stroke in patients with atrial fibrillation is emphasized, for selecting patients at high risk for prophylactic treatment with anticoagulants or aspirin.

Atrial fibrillation is a clinically important arrhythmia that carries important prognostic and therapeutic implications. Hypertension, ischemic heart disease, and rheumatic valvular disease are the commonest causes of atrial fibrillation. The presence of chronic or paroxysmal atrial fibrillation places the patient at increased risk for embolic stroke and/or death. When atrial fibrillation develops, there is loss of the atrial transport factor ("atrial kick"), with consequent decrease of cardiac output. Stroke output declines by 20-30% in normal individuals with loss of atrial kick; the decline in stroke output is considerably larger in patients with heart disease. Atrial fibrillation can be electrically or pharmacologically reverted to sinus rhythm. Even patients with refractory atrial fibrillation can be reverted to sinus rhythm with amiodarone.

Twenty-seven consecutive patients with suspected lone atrial fibrillation were studied by M-mode echocardiography. Echocardiography disclosed structural or functional cardiac abnormalities in only two (12%) of 17 patients without any sign of underlying heart disease by history or physical examination, whereas an accompanying or underlying cardiac disorder was found in 6 (60%) of 10 patients with ambiguous clinical findings. It is concluded that echocardiography is of minor value in patients with lone atrial fibrillation if symptoms and signs of other cardiac disorders are totally absent, but the presence of even minor or ambiguous clinical abnormalities seems to be a clear indication for echocardiography in these patients. It is, however, emphasized that echocardiography appears to guide the clinical management in less than 20% of patients with clinically suspected lone atrial fibrillation.