Nonrheumatic Atrial Fibrillation Research Articles

Holter monitoring in the diagnosis of stroke mechanism.

Atrial fibrillation (AF), an important and treatable cause of ischaemic stroke, can occur as a sustained or a paroxysmal arrhythmia. Continuous cardiac rhythm monitoring (Holter monitoring) is often performed in stroke patients to identify paroxysmal AF, which is an indication for warfarin anti-coagulation in this patient population. The aim of this study was to assess the clinical utility of Holter monitoring in detecting occult AF in patients with possible cardioembolic stroke. The medical records of ischaemic stroke patients consecutively hospitalized at a single academic centre during a one-year period were reviewed. Data regarding patient demographics, stroke characteristics, electrocardiography and echocardiography results and duration and findings of Holter monitoring were abstracted. The primary outcome was yield of newly diagnosed AF on Holter monitoring. Of 465 consecutive patients admitted with a diagnosis of new ischaemic stroke, 210 underwent Holter monitoring. The mean duration of monitoring was 22.8 +/- 4.0 h. Previously undiscovered AF was -identified in five cases (2.4%), all of which represented non-rheumatic AF. In three cases, the Holter test was negative despite AF documented on an admission electro-cardiogram. Holter monitoring can identify occult paroxysmal AF, assisting targeted secondary prevention in patients with new ischaemic stroke. However, the standard 24-h duration of monitoring probably under-estimates the prevalence of paroxysmal AF in this population. Prospective studies are indicated to evaluate the value of longer monitoring periods in stroke populations.

Near Patient Monitoring of Anticoagulant Therapy in General Practice

Background and aims: New systems for monitoring anticoagulation in routine clinical practice should be evaluated to inform future service development. The aim of this study was to investigate the workload, patient characteristics and bleeding complications in a nurse run, near patient monitoring service serving a population of 23,368. Methods: Retrospective review of coagulometer and general practice case records. Results: Between 1995 and 2000 workload increased from 154 to 269 consultations per month. Three hundred and forty four patients were followed up during a cumulative period of 664.8 years. The 8 week period prevalence of anticoagulation was 8.6 per thousand patients at the close of the study. The median age at enrolment was 71 years. Eighteen per cent of treatment episodes were started when patients were 80 years or older. The most common indication was non rheumatic atrial fibrillation (NRAF) in 51% of treatment episodes. During the study 49.6% [95% confidence interval (CI) 47.8%–50.6%] of international normalised ratio (INR) tests were within target range and INR was estimated to be within the target range 62% (95% CI 61.8%–62.2%) of the time. INR control varied markedly between individual patients. There were 4 fatal bleeding events (0.6 per hundred patient years) and 14 major bleeding events (2.1/hundred patient years). Conclusion: Demand for anticoagulant therapy with warfarin has increased substantially. Service development is required to ensure that appropriately selected patients have access to adequately resourced monitoring which promotes optimum INR control and a minimum of bleeding complications.

Anticoagulants for preventing stroke in patients with nonrheumatic atrial fibrillation and a history of stroke or transient ischaemic attack.

People with nonrheumatic atrial fibrillation (NRAF) who have had a transient ischaemic attack (TIA) or a minor ischaemic stroke are at high risk of recurrent stroke. The objective of this review was to assess the effect of anticoagulants for secondary prevention, after a stroke or TIA, in patients with NRAF. We searched the Cochrane Stroke Group trials register (9 June 2003) and contacted trialists. Randomised trials comparing oral anticoagulants with control (no therapy) or placebo in people with NRAF and a previous TIA or minor ischaemic stroke. Control groups on aspirin did not meet the selection criteria. Both reviewers assessed trial quality and extracted data. Two trials involving 485 people were included. Follow-up time was 1.7 years in one trial and 2.3 years in the other. Anticoagulants reduced the odds of recurrent stroke by two-thirds (odds ratio (OR) 0.36, 95% confidence interval (CI) 0.22 to 0.58). The odds of all vascular events was shown to be almost halved by treatment (OR 0.55, 95% CI 0.37 to 0.82). The odds of major extracranial haemorrhage was increased (OR 4.32, 95% CI 1.55 to 12.10). No intracranial bleeds were reported among people given anticoagulants. The evidence suggests that anticoagulants are beneficial, without serious adverse effects, for people with NRAF and recent cerebral ischaemia.

Thromboembolic prophylaxis in nonrheumatic atrial fibrillation: utilization patterns, efficacy, and complications in a long-term follow-up of community patients

Objectives: To define the incidence, contemporary utilization patterns, efficacy, and complications of thromboembolic prophylactic treatment in patients with chronic (CAF) and paroxysmal atrial fibrillation (PAF). Background: Although recent randomized trials with antithrombotic therapy in nonrheumatic atrial fibrillation (AF) patients emphasized the benefits of warfarin in preventing stroke, warfarin treatment is still far from optimal. Methods: A retrospective analysis of the medical records of 506 patients with nonrheumatic PAF or CAF from 23 clinics in the north of Israel, including an interview with the patients' family physician. Results: (1) The most effective treatment for preventing thromboembolic events (a reduction of 75.9%) was warfarin at an international normalized ratio (INR) intensity of 2–3. (2) After diagnosis, 26.9% of the patients were treated with warfarin. (3) During the follow-up period (not following a thromboembolic event), an additional 26.9% of the patients began treatment with warfarin. (4) Elderly patients ( p<0.001), patients with limited activity of daily living (ADL) ( p<0.012) or instrumental activity of daily living (IADL) ( p<0.001), and patients with PAF ( p<0.0001) were less likely to be treated with warfarin. (5) Three new risk factors found for thromboembolic event were limited ADL ( p<0.001), limited IADL ( p<0.002), and extended duration of AF ( p<0.006). Conclusions: Less than optimal utilization patterns of thromboembolic prophylactic treatment with anticoagulants were found, especially regarding elderly patients, patients with limited ADL and IADL, and patients with PAF, despite the fact that their thromboembolic risk is as high or higher than that of other patients with AF.

Mortality and rate of stroke or embolism in atrial fibrillation during long-term follow-up in the embolism in left atrial thrombi (ELAT) study.

Patients with atrial fibrillation (AF) have a higher mortality and risk of stroke/embolism than patients with sinus rhythm. The aim of the study was to assess the association of clinical and echocardiographic characteristics with mortality and stroke/embolism and the use of antithrombotic medication in the year 2000 in patients who participated 1990-1995 in the Embolism in Left Atrial Thrombi (ELAT) study. The study included 409 outpatients with nonrheumatic AF (62 +/- 12 years, 36% women, 39% intermittent AF). Patients with thrombi received anticoagulation, patients without thrombi aspirin until follow-up in 1995; thereafter, anticoagulation according to clinical risk factors was recommended. Primary events were death and secondary events were stroke/embolism. All patients were contacted during the year 2000. Mean follow-up was 102 months. Mortality was 4%/year; the cause of death was cardiac (n = 84), fatal stroke (n = 26), malignancy (n = 23), sepsis (n = 5), and unknown (n = 24). Multivariate analysis identified age (p < 0.0001), heart failure (p = 0.0013), and reduced left ventricular systolic function (p = 0.0353) as predictors of mortality. Stroke/embolism occurred in 83 patients, with a rate of 3%/year. Multivariate analysis identified age (p = 0.0006) and previous stroke (p = 0.0454) as predictors of stroke/embolism. In the year 2000, 51 (21%) of the 247 surviving patients received no antithrombotic medication, 88 received (36%) oral anticoagulants, 102 (41%) acetylsalicylic acid, and 6 (2%) low-molecular heparin. Therapy for heart failure and oral anticoagulation in AF should be seriously considered, especially in elderly patients and in those with previous stroke.

Effects of sinus rhythm restoration in patients with persistent atrial fibrillation: a clinical, echocardiographic and hormonal study

The hemodynamic consequences of atrial fibrillation (AF) may lead to impairment of the left ventricular function and a reduction in exercise capacity. Studies on mechanical and neurohormonal remodelling in patients with AF are becoming increasingly important. The results could possibly enhance treatment strategies of these patients. The aim of this study was to assess changes in exercise capacity, echocardiographic findings and plasma atrial natriuretic peptide (ANP) concentrations in patients with non-rheumatic persistent AF, before and 30 days after successful cardioversion. Methods: We attempted cardioversion in 42 consecutive patients, aged 58±8 years, with persistent non-valvular AF of duration 7.1±7.1 months. They underwent echocardiography examination and submaximal exercise testing 24 h before and 30 days after cardioversion. Exercise capacity was determined during symptom-limited exercise testing, according to a modified Bruce protocol with peak VO 2 analysis. Plasma samples of ANP were obtained at rest: before, the day after, and 30 days after cardioversion therapy, and were prepared by refrigerated centrifugation and stored until radioimmunoassay. The control study group, without AF, comprised of 11 subjects. Results: Cardioversion was successful in 35 patients. However, in six of the 35 patients, AF reappeared within 1 month. There were no statistical differences before cardioversion in exercise tolerance and ejection fraction of left ventricle between the group with successful cardioversion and the group with unsuccessful cardioversion or with recurrence of AF. On the 30th day after cardioversion we recorded a significant increase in exercise tolerance: duration of exercise 13.7±3.2 versus 9.5±3.4 min, ( P<0.05); peak oxygen consumption 32.2±3.6 versus 19.85±3.5 ml/min per kg, ( P<0.05); and ejection fraction of left ventricle 58.6±9.4 versus 52.7±10.2% ( P<0.05); in the sinus rhythm group. There was no significant improvement observed in the AF group. The mean baseline ANP level was 58.5±15.7 pg/ml in the study group and 34.3±10.2 pg/ml in the control group ( P<0.01). The successful therapy reduced significantly the pretreatment mean plasma ANP concentration from 58.5±15.7 to 31.4±15.0 pg/ml, ( P<0.01); the day after cardioversion, in the group of 35 patients. It remained stable for the next 30 days (36.9±15.2 pg/ml) in the group of 29 patients who remained in sinus rhythm, and increased to 53.4±16.4 pg/ml in the group of six patients who had recurrence of AF. Plasma ANP did not change in the group of seven patients with unsuccessful cardioversion. Conclusions: The restoration of sinus rhythm in patients with persistent AF was associated with a significant improvement in cardiac performance and exercise tolerance 1 month after cardioversion. Such improvement was not observed in the group with unsuccessful cardioversion or with AF recurrence. The plasma ANP concentration in patients with AF was significantly reduced after successful cardioversion and remained stable for a period of 30 days.

Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation.

A prothrombotic or hypercoagulable state has been described in AF, which could increase the risk of thromboembolism. As inflammation has been related to thrombogenesis and endothelial activation, we hypothesised that the prothrombotic state in AF (as assessed by an index of thrombogenesis, prothrombin fragment 1+2 [F1+2]) and endothelial activation (soluble E-selectin (sEsel)) could be related to an index of inflammation (interleukin-6 (IL-6)). We studied 191 consecutive patients (98 male; mean age 72.3+/-9.2 years) with chronic non-rheumatic AF who were not on anticoagulant therapy. Plasma IL-6, sEsel and F1+2 were measured by ELISA. Research indices were compared to 74 controls in sinus rhythm matched for age and sex. In 43 patients with AF, the effects of introducing anticoagulation (INR 2.0-3.0) were also studied. Patients with AF had elevated levels of F1+2 (p<0.001) and IL-6 (p=0.045), but not sEsel. There was no significant correlation between F1+2 and IL-6. In multivariate analysis, only F1+2 levels were independently associated with the presence of AF (p=0.001). After oral anticoagulation, plasma levels of F1+2 and sEsel were significantly decreased (both p<0.01). High levels of IL-6 in AF suggest an inflammatory state, which appears to be more related to clinical variables of the patients, rather than to the presence of AF per se. There was no association of inflammation with endothelial activation (sEsel) or the presence of abnormal thrombogenesis (high F1+2 levels) in AF. Moreover, no changes in IL-6 levels were found despite the reduction of the other markers by oral anticoagulant therapy.

Ineffective anticoagulation prior to elective electric cardioversion for atrial fibrillation. Results of transesophageal echocardiography

Anticoagulation (AC) should be given for 3 to 4 weeks before elective electrical cardioversion to reduce thromboembolic events. During this period ineffective AC is a common problem. The aim of our study was to investigate the influence of the duration of ineffective AC on the incidence of left atrial thrombi (LAT) or spontaneous echocontrast (SEC) induced by hemostasis detected by transesophageal echocardiography (TEE). 56 consecutive patients (39 men) at the age of 64 +/- 9 years with non-rheumatic atrial fibrillation who were scheduled for electrical cardioversion after 3 to 4 weeks of AC and a documented ineffective AC underwent TEE. Cardioversion was performed after exclusion of a LAT by TEE or in patients with LAT after 4 more weeks of AC and repeated TEE. All patients received AC and were observed for at least 4 weeks after cardioversion. Echocardiographic, demographic and clinical parameters and available values of AC were recorded. In 5/56 (9 %) patients a LAT, in 10 (18 %) patients SEC was detected. No patient had both. In patients with LAT the duration of ineffective AC was 15 +/- 10 days (range 5 - 28) and did not differ significantly from patients without LAT (17 +/- 8 days; range 0 - 28) or to the group with SEC (23 +/- 6 days; range 12 - 28). There was no significant difference of demographic, echocardiographic and clinical parameters between these groups. There was no embolic event during follow-up. Neither the duration of ineffective AC nor clinical, epidemiologic or echocardiographic parameters could differentiate patients with or without LAT in our observed groups with small numbers of patients. In case of an ineffective AC patients who are to undergo electrical cardioversion should have TEE. In our study patients with SEC were not at a higher thromboembolic risk.

Left atrial size and function after spontaneous cardioversion of atrial fibrillation and their relation to n-terminal atrial natriuretic peptide

L atrial (LA) stunning after cardioversion of atrial fibrillation (AF) has been reported during spontaneous conversion to sinus rhythm.1 This observation suggest that atrial stunning is a function of underlying arrhythmia and not of the mode of cardioversion. It is known that AF causes atrial dilation, and progressive LA enlargement occurs when AF becomes chronic.2 Recently, it has been shown that multiple factors contribute to LA enlargement, including the presence and persistence of arrhythmia.3 Many reports suggest that if sinus rhythm is restored then dilation may regress.4 The Framingham Study showed a relation between LA size and the risk of stroke in men and the risk of death in both genders.5–7 Previous studies have suggested that N-terminal atrial natriuretic peptide (NANP) levels are elevated in patients with AF.8,9 It is unclear whether AF rather than LA dilation,10 hemodynamic impairment,11 or another hormonal alteration, can result in the elevation of N-ANP levels.8 The present report evaluates the changes in LA size and function after spontaneous cardioversion of AF and their relation to N-ANP. • • • Hemodynamically stable patients referred for cardioversion for nonrheumatic AF between September 1997 and March 2000 were considered for inclusion in this investigation. The initial study group included 202 consecutive patients; 98 patients spontaneously recovered sinus rhythm within 48 hours from the onset of arrhythmia and were selected for the study (Group A). The study population included 57 men and 41 women of mean age 60 16 years; patients were compared with 98 ageand gender-matched control subjects (mean age 61 16 years) who underwent pharmacologic cardioversion within 48 hours from the onset of arrhythmia (Group B). Patients received intravenous propafenone 2 mg/kg of body weight; the drug was dissolved in 100 ml of 5% glucose and infused over 30 minutes. Exclusion criteria were: atrial flutter, valvular stenosis, valvular prosthesis, significant valvular insufficiency, atrial and/or left ventricular thrombosis, spontaneous echo contrast, patent foramen ovale or an atrial septal aneurysm, or decreased LV function (ejection fraction 45%). No patients received long-term therapy with antiarrhythmic drugs. Demographic and clinical characteristics of the patients are listed in Table 1. Clinical records included age, gender, time and circumstances of the onset of symptoms related to AF, and the duration of AF estimated from the initial onset of symptoms until the time of the in-hospital conversion. The protocol was approved by the Ethical Committee of our university and all patients signed an informed consent form. The initial Doppler echocardiographic study was performed during AF and after cardioversion (mean 3 1.5 hours). A complete monoand 2-dimensional color Doppler echocardiogram was performed in each patient using a commercial Hewlett-Packard echocardiograph (Andover, Massachusetts) with a 2.5-MHz probe. LA function was assessed using these parameters: (1) transmitral pulsed Doppler recorded from the apical 4-chamber view with the sample volume positioned between the tips of the mitral leaflets; peak early filling (E) and atrial filling (A) velocities; and From the Departments of Cardiology and Biomedics, University of Modena and Reggio Emilia, Modena, Italy. Dr. Mattioli’s address is: Department of Cardiology, University of Modena, Via del pozzo, 71, 41100 Modena, Italy. E-mail: mattioli.annavittoria@ unimo.it. Manuscript received December 17, 2002; revised manuscript received and accepted March 3, 2003. TABLE 1 Demographics and Clinical Characteristics

Fibrillatory wave amplitude as a marker of left atrial and left atrial appendage function, and a predictor of thromboembolic risk in patients with rheumatic mitral stenosis

Background: Patients with mitral stenosis, especially those with atrial fibrillation, are at increased risk for thromboembolic complications. Size of the left atrium, left atrial appendage dysfunction and severity of mitral stenosis are known risk factors for thromboembolism in patients with mitral stenosis. It has been postulated that F-wave amplitude on surface ECG is correlated with left atrial size, left atrial appendage function, and risk of thromboembolism in patients with nonrheumatic atrial fibrillation. The aims of this study were as follows: (1) to examine the relationship between surface ECG F-wave amplitude and left atrial appendage function, and (2) to assess the clinical significance of F-wave amplitude as it relates to risk of thromboembolism in a group of patients with rheumatic mitral stenosis. Material and Methods: One hundred patients with rheumatic mitral stenosis and permanent atrial fibrillation but without moderate to severe mitral insufficiency were investigated by transthoracic and transesophageal echocardiography. Two groups were formed according to the presence of a coarse (Group 1; n=60; F-wave in lead V 1≥1 mm) or fine (Group 2; n=40; F-wave in lead V 1<1 mm) F-wave on surface ECG. Results: Comparison showed that Group 1 had significantly smaller mitral valve area (1.44±0.6 versus 1.7±0.74 cm 2, respectively; P<0.05), lower peak left atrial appendage flow velocity (18.8±2.1 versus 25.6±1.9 cm/s, respectively; P<0.005), higher-grade spontaneous echo contrast (2.05±1.44 versus 0.98±1.14, respectively; P<0.0001), and higher prevalence of thromboembolism (35% versus 12.5%, respectively; P<0.012). Multiple logistic regression analysis revealed that mitral valve area, left atrial appendage peak velocity, and coarse F-wave were independent clinical risk factors for thromboembolism in this patient group. Conclusion: The data suggest that presence of a coarse F-wave on surface ECG is associated with left atrial appendage dysfunction, and indicates higher thromboembolic risk in patients with predominant rheumatic mitral stenosis.

Embolism from the heart in the young patient: a short review

Embolism from the heart causes about one-fifth of ischemic strokes and transient ischemic attacks. Although a potential embolic source may be found in up to one-third of cases, which are actually caused by other mechanisms, in the young patient more than one source of embolism is less likely. The most-important embolic sources are non-rheumatic and rheumatic atrial fibrillation (AF), infective endocarditis, prosthetic heart valves, recent myocardial infarction, dilated cardiomyopathy, intracardiac tumors, and rheumatic mitral stenosis. Uncomplicated mitral valve prolapse should no longer be considered a cause of embolism from the heart to the brain; an additional disorder (i.e., gross mitral regurgitation, AF, infective endocarditis) must be present to suggest a cardioembolic origin of the stroke.

Is thrombogenesis in atrial fibrillation related to matrix metalloproteinase-1 and its inhibitor, TIMP-1?

Decreased matrix metalloproteinase-1 (MMP-1) and increased levels of its inhibitor, tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), reflect impaired matrix degradation with an increase in fibrosis. A prothrombotic state has been described in atrial fibrillation (AF), increasing the risk of stroke and thromboembolism. Because structural abnormalities and remodeling of atria have been observed in AF, we hypothesized that the prothrombotic state in AF may be related to abnormal indexes of matrix degradation. We studied 48 consecutive patients (30 men; age, 70.5+/-9.0 years) with chronic nonrheumatic AF who were not on anticoagulation. Plasma levels of MMP-1, TIMP-1, and prothrombin fragment 1+2 (F1+2, an index of thrombogenesis) were measured by enzyme-linked immunosorbent assay. M-mode, 2-dimensional, and Doppler echocardiographic studies were performed in all patients. Research indexes were compared with data from 32 control subjects in sinus rhythm who were of similar age and sex. Patients with AF had lower levels of MMP-1 (P=0.011) but increased levels of TIMP-1 (P=0.033) and F1+2 (P<0.001) and a higher ratio of TIMP-1 to MMP-1 (P=0.009) compared with control subjects. After adjustment for sex, age, hypertension, and diabetes, TIMP-1 levels and the ratio of TIMP-1 to MMP-1 correlated with F1+2 levels (r=0.24, P=0.038; and r=0.26, P=0.023, respectively). In multivariate analysis, there was no independent relationship between MMP-1, TIMP-1, or ratio of TIMP-1 to MMP-1 and the presence of AF. Patients with AF have evidence of impaired matrix degradation, but this was not independently associated with the presence of AF on multivariate analysis. However, an independent relationship was found between the MMP/TIMP system and prothrombotic state (assessed by F1+2 levels).

Plasma von Willebrand factor, soluble thrombomodulin, and fibrin D-dimer levels in acute-onset nonrheumatic atrial fibrillation

Plasma von Willebrand factor, soluble thrombomodulin, and fibrin D-dimer levels in acute-onset nonrheumatic atrial fibrillation

Factor V Leiden mutation and its relation to left atrial thrombus in chronic nonrheumatic atrial fibrillation.

The genetic defect of coagulation factor V, known as factor V Leiden, produces a resistance to degradation by activated protein C and increased venous thrombosis. However, the role of factor V Leiden in the formation of left atrial thrombus with nonrheumatic atrial fibrillation has not been studied. We investigated whether factor V Leiden is a risk factor for left atrial thrombus in patients with nonrheumatic atrial fibrillation. We analyzed clinical, echocardiographic, and biochemical data in 105 consecutive patients with nonrheumatic atrial fibrillation. These patients were divided into two groups: group A (n = 37) with left atrial thrombus and group B (n = 68) without left atrial thrombus. The study also included 42 control subjects. Left atrial thrombus was investigated by using both transthoracic echocardiography and transesophageal echocardiography. Blood samples from the patients and controls were analyzed for the factor V Leiden mutation by DNA analysis, using the polymerase chain reaction. There was no significant difference in the prevalence of factor V Leiden between the patients and control subjects. The prevalence of factor V Leiden mutation was 8.1% (3/37) in patients with left atrial thrombus, and 8.8% (6/68) in patients without left atrial thrombus. The prevalence of factor V Leiden was 7.1% (3/42) in control subjects. The prevalance of factor V Leiden was 10% (2/20) in patients with spontaneous echo contrast and 8% (7/85) in patients without spontaneous echo contrast. Multivariate analyses showed that left ventricular ejection fraction was an independent predictor of left atrial thrombus. Factor V Leiden mutation is not a risk factor for left atrial thrombus formation and spontaneous echo contrast in patients with nonrheumatic atrial fibrillation.

Anticoagulation or antiplatelet therapy for non-rheumatic atrial fibrillation and flutter

[Ann Emerg Med. 2003;41:141-143.]

Prevention of thromboembolism in patients with mitral stenosis and associated atrial fibrillation: effectiveness of low intensity (INR target 2) oral anticoagulant treatment

Mitral stenosis (MS) in association with atrial fibrillation (AF) is a clinical condition at high risk for systemic thromboembolism. Although oral anticoagulants greatly reduce the incidence of thromboembolism in these patients, the optimal intensity of treatment has never been tested in specific clinical trials, and current recommendations are derived from studies of nonrheumatic AF. In this study we tested the effectiveness of two different intensities. The study design was carried out as an open randomized prospective study in an anticoagulation clinic. We randomized 103 patients with MS and AF to a low (target INR = 2) or moderate (target INR = 3) anticoagulation regimen. The primary end points were systemic thromboembolism, major bleeding and vascular death. During a mean follow-up of 4.5 years, 1 systemic embolism occurred in the low intensity group (0.41 per 100 pt/yrs, CI 0.01-2.3), and 1 minor stroke occurred in the moderate intensity group (0.40 per 100 pt/yrs, CI 0.01-2.3; p = ns). Major bleeding occurred in 8 patients, with 3 in the low intensity (1.25 per 100 pt/yrs) and 5 in the moderate intensity group (2.0 per 100 pt/yrs, Incidence Rate Ratio 0.6, CI 0.1-3.1; p = ns). Total events (systemic embolism, major bleeding and vascular death) occurred in 7 low intensity patients and 8 moderate intensity patients. As expected, minor bleeding was more frequent in the moderate intensity group of patients, who actually had more intense treatment and required closer monitoring of oral anticoagulant treatment. These data suggest that low intensity anticoagulation, as performed in an anticoagulation clinic, is effective and safe in high risk patients with MS and AF.

Deciding on Anticoagulating the Oldest Old with Atrial Fibrillation: Insights from Cost‐Effectiveness Analysis

To better understand the tradeoffs between the efficacy of anticoagulation with warfarin and its side effects in the oldest old with nonrheumatic atrial fibrillation (AF). Cost-effectiveness analysis. Published literature, including meta-analyses when available, and web-based sources. Those aged 65 to 100 with AF. Anticoagulation with warfarin. Quality-adjusted life expectancy and cost. Anticoagulation is not effective in persons with AF who do not have other risk factors, even in the oldest old. The best argument for its use (prolongation of life at an acceptable cost) can be made in those at major risk for stroke because of previous stroke or transient ischemic attack, diabetes mellitus, and hypertension, but poor quality of life before anticoagulation and comorbidities that carry their own risks of dying diminish benefits. The decision to anticoagulate the oldest old with AF must take into consideration the risk of hemorrhagic stroke and of death from hemorrhagic stroke that existed before anticoagulation, the increased risk of hemorrhagic stroke and of death from hemorrhagic stroke while anticoagulated, and the efficacy of anticoagulation. Cost-effectiveness is also influenced by the cost of warfarin, the risk of major extracranial bleeding, the risk (natural and anticoagulated) of death from hemorrhagic stroke, the rate of ischemic stroke, the cost of major extracranial bleeding and hemorrhagic strokes, the cost of nursing home care, and the fraction of patients with stroke who need nursing home care. There is no compelling evidence to date that anticoagulation prolongs quality-adjusted life expectancy in the oldest old with nonrheumatic AF. More studies that better estimate the risk of intracranial bleeding with and without anticoagulation in the oldest old are needed before recommendations can be made. The oldest old who are most likely to benefit are those who have a high risk of stroke secondary to risk factors other than age alone, although quality of life and life expectancy related to these risk factors limit obtained benefit. Recommendations that all older persons with AF should be anticoagulated are premature.

Aortic Spontaneous Echocardiographic Contrast and Hemostatic Markers in Patients With Nonrheumatic Atrial Fibrillation

To determine the relationship between spontaneous echocardiographic contrast (SEC) in the descending thoracic aorta and plasma levels of hemostatic markers in patients with nonrheumatic atrial fibrillation (AF). A cross-sectional study at a university hospital. In 91 consecutive patients (mean +/- SE age, 70 +/- 1 years; 68 men) with nonrheumatic AF who underwent transesophageal echocardiography, plasma levels of markers for platelet activity (platelet factor 4 [PF4] and beta-thromboglobulin [beta-TG]), thrombotic status (thrombin-antithrombin III complex [TAT]), and fibrinolytic status (D-dimer and plasmin-alpha(2)-plasmin inhibitor complex [PIC]) were determined. Forty-three patients who had aortic SEC (AoSEC) were older (72 years vs 68 years; p < 0.05) and had a higher prevalence of chronic AF (88% vs 52%; p < 0.05) than 48 patients without AoSEC. TAT, PIC, and D-dimer levels were significantly higher in patients with AoSEC than in those without AoSEC, whereas PF4 and beta-TG levels were not different between the two groups. Although the prevalence of cerebral embolism did not differ between the two groups (23% vs 29%), the prevalence of peripheral embolism was higher in patients with AoSEC than in those without AoSEC (10% vs 0%; p < 0.05). Multivariate analysis revealed mitral regurgitation (odds ratio, 7.53; p < 0.02), SEC in the left atrium (odds ratio, 2.14; p < 0.02), and aortic atherosclerosis (odds ratio, 1.87; p < 0.04) emerged as independent predictors of AoSEC. Patients with nonrheumatic AF who have AoSEC appear to have enhanced coagulation activity but not platelet activity. Intensive anticoagulation treatment might be required for these patients.

A simple scheme to initiate oral anticoagulant treatment in outpatients with nonrheumatic atrial fibrillation

A simple scheme to initiate oral anticoagulant treatment in outpatients with nonrheumatic atrial fibrillation

Clinical trends in atrial fibrillation at the turn of the millenium

Clinical trends in atrial fibrillation at the turn of the millenium