Years For Atrial Fibrillation Research Articles

Carga de enfermedad atribuible a fibrilación auricular en Colombia (2000-2009)

ObjectiveTo estimate the disease burden of atrial fibrillation and describe its impact on the health of the Colombian population. MethodsThe number of healthy life years lost or of disability adjusted life years for atrial fibrillation, resulting from the sum of loss of health due to premature death and disability was calculated. For the calculation of life years lost the death registration on the National Department of Statistics for the period 2000-2009, as well as the abridged life tables for the years lived with disability, the individual records of service 2009-2010, bibliography and a map of weighted disability in the global study of the burden of disease were consulted. For data processing a template developed in Microsoft Excel 2007 was used, based on the methodology described by the World Health Organization in October 2001, taking into account the parameters and formulas that have been described by Murray and Lopez (1996) and Mathers et al. (2001). ResultsIn 2000, 2004 and 2009, 12,138, 13,188 and 15,327 years of healthy life were lost due to atrial fibrillation in the Colombian population, with a ratio of 0.30, 0.31 and 0.34 years of healthy life lost per thousand inhabitants respectively. The major relative weight of the lost years was given by the disability component (91.46%); males contributed on average to 58% of the healthy life years lost, and the most affected age was of 70-79 years. ConclusionThe number of healthy life years lost shows that atrial fibrillation is a highly disabling condition for the Colombian population during the study period, given the predominance of the component of years lived with disability.

Does Digoxin Increase the Risk of Ischemic Stroke and Mortality in Atrial Fibrillation? A Nationwide Population-Based Cohort Study

BackgroundDigoxin and related cardiac glycosides have been used for almost 100 years in atrial fibrillation (AF). However, 2 recent analyses of the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) trial showed inconsistent results regarding the risk of mortality associated with digoxin use. The goal of the present study was to investigate the relationship between digoxin and the risk of ischemic stroke and mortality in Asians. MethodsThis study used the National Health Insurance Research Database (NHIRD) in Taiwan. A total of 4781 patients with AF who did not receive any antithrombotic therapy were selected as the study population. Among the study population, 829 participants (17.3%) received the digoxin treatment. The risk of ischemic stroke and mortality in patients who received digoxin and those who did not was compared. ResultsThe use of digoxin was associated with an increased risk of clinical events, with an adjusted hazard ratio of 1.41 (95% confidence interval [CI], 1.17-1.70) for ischemic stroke and 1.21 (95% CI, 1.01-1.44) for all-cause mortality. In the subgroup analysis based on coexistence with heart failure or not, digoxin was a risk factor for adverse events in patients without heart failure but not in those with heart failure (interaction P < 0.001 for either end point). Among patients with AF without heart failure, the use of β-blockers was associated with better survival, with an adjusted hazard ratio of 0.48 (95% CI, 0.34-0.68). ConclusionsDigoxin should be avoided for patients with AF without heart failure because it was associated with an increased risk of clinical events. β-Blockers may be a better choice for controlling ventricular rate in these patients.

The Potential Effects of Dicloxacillin on Warfarin Management

Objective: To illustrate the effect that dicloxacillin may have on the anticoagulant properties of warfarin. Case Summary: A 69-year-old white male presented to the emergency department following a motor vehicle accident. He had been receiving a stable dose of warfarin of approximately 35–37.5 mg/wk for more than 2 years for atrial fibrillation. Computed tomography and magnetic resonance imaging revealed a 1 × 1.3 cm lesion in the anterior aspect of the pancreatic body. During a subsequent hospital stay for a distal pancreatectomy and splenectomy, the patient began a 6-week course of dicloxacillin to treat osteomyelitis of the elbow. During the course of treatment, the patient's warfarin dose was increased by 114% to reach a therapeutic international normalized ratio (INR) approximately 11 days after the antibiotic was discontinued. Discussion: Compared with previously published cases documenting the interaction between dicloxacillin and warfarin, to our knowledge, this is the first case to comprehensively assess and document other factors that potentially influenced the patient's INR. At every clinic visit, the patient was assessed for several factors that could have contributed to fluctuations in INR, none of which proved to have a significant effect. Conclusions: The addition of dicloxacillin to our patient's stable warfarin regimen resulted in a significant interaction that placed the patient at risk for thromboembolic complications. Careful monitoring of INR from the start of dicloxacillin therapy until 2 weeks after its discontinuation should be considered in patients who are taking warfarin and require dicloxacillin therapy.

Impact of heart failure with normal ejection fraction on the occurrence of ischaemic stroke in patients with atrial fibrillation

ObjectivesThe purpose of this study is to examine the risk of stroke in patients with heart failure with normal ejection fraction (HFNEF) and atrial fibrillation (AF).DesignClinical and echocardiographic data in...

A Case of Spontaneous Spinal Epidural Haematoma in the Emergency Department Associated with Warfarin Therapy

Spontaneous spinal epidural haematoma (SSEH) is a neurosurgical emergency that requires early diagnosis and treatment. An 88-year-old man presented to the emergency department with complaints of weakness in the legs, walking deficit, incontinence and back pain for the last two days. He had been on warfarin therapy for 5 years for atrial fibrillation. There was no antecedent trauma. The neurological examination revealed hypoesthesia below the T6 level, anaesthesia below the T10 level and complete paraplegia of both lower extremities. The INR level was 7.81 on admission. Magnetic resonance imaging revealed a posterolateral epidural haematoma extending from T2 to L5. He was given fresh frozen plasma and vitamin K in the emergency department. Emergency thoracic and lumbar laminectomy was performed by neurosurgeons. The probability of SSEH should be investigated in any patient under anticoagulation therapy who presents with signs of spinal compression in the emergency department.

Blindness from suprachoroidal haemorrhage in two patients with age‐related macular degeneration on systemic anticoagulation therapy or an antiplatelet agent

Clinical record Patient 1 A 90-year-old man with bilateral neovascular age-related macular degeneration (AMD) presented with sudden onset of painful visual loss in his left eye. Visual acuity in his right eye was 1/60 due to scarring associated with AMD, and visual acuity in his left eye had deteriorated to hand movements; it had previously been 6/120. He had been taking warfarin for about 2 years for atrial fibrillation and a transient ischaemic attack. The international normalised ratio (INR) had previously been measured almost weekly, but as it had been stable at 2.5–2.9 (target INR, 2.0–3.0), it had not been measured for 6 weeks. B-mode ultrasonography and dilated fundus examination revealed massive suprachoroidal haemorrhage (Figures A and B). The INR was 6.0, which was reversed with intravenous administration of two units of fresh frozen plasma and 1 mg of vitamin K. Visual acuity in the patient’s left eye deteriorated to light perception. As there were no signs of spontaneous improvement and this had been his better eye, surgery was performed to drain the haemorrhage. After surgery, the haemorrhage decreased in size but his vision did not improve.

Hundred years of atrial fibrillation: Current knowledge and perspectives

Atrial fibrillation (AF) is the most common sustained arrhythmia in general population. AF in humans was first described in 1903. Gradually, it has been well appreciated that AF is notjust an acceptable alternative for normal rhythm but rather a serious threat, related to increased mortality and cardiovascular morbidity. AF can precipitate or worsen pre-existing heart failure, may cause the development of tachycardiomyopathy and is an independent risk factor for thromboembolic events, most frequently stroke. It has long been believed that rhythm control is the best therapy for AF. Nowadays there is a clear scientific proof that rhythm control offers no benefit over frequency control, at least for older patients, even with advanced left ventricular dysfunction. However, optimal treatment for younger, highly symptomatic, otherwise healthy AF patients has not been designed. Available antiarrhythmics have considerable proarrhythmic potential or organ toxicity, and new safer drugs are under investigation. Nonpharmacological approaches, namely RF-catheter ablation, are rapidly developing. Prevention of thromboembolism is imperative, and new safer oral anticoagulants have been intensively investigated. Recent randomized studies (PIAF, RACE, STAF, AFFIRM, HOT-CAFE) did not solve the issue of optimal arrhythmia treatment, but they emphasized the prevention of thromboembolism based on risk factors, and not on AF type, mainly because asymptomatic episodes of AF may not be clinically recognised.

Changing Trends of Hospital Utilization in Patients After Their First Episode of Atrial Fibrillation

A marked increase in hospitalization for patients with atrial fibrillation (AF) has previously been noted. Whether this increase is related to a change in the prevalence of AF or a change in the pattern of practice with respect to the management of AF remains unclear. To determine the trends in hospital utilization after first AF in a community-based setting (Olmsted County, Minnesota), residents diagnosed with first AF from 1980 to 2000 were identified and followed until 2004. The primary outcome of interest was hospital admission for cardiovascular reasons. Of a total of 4,498 subjects (73 +/- 14 years old, 51% men), 2,503 (56%) were admitted to the hospital for cardiovascular causes >or=1 time during a mean follow-up of 5.5 +/- 5.0 years. Risk of first hospitalization was greatest during the first year of AF (cumulative incidence 31%, 95% confidence interval [CI] 30 to 32). First hospitalization was strongly related to age (p <0.0001) but not to sex (p = 0.38). From 1980 to 2000, the age-and sex-adjusted rate of first hospitalization increased, on average, by 2.5% a year (95% CI 1.8 to 3.2, p <0.0001), even after multivariable adjustment for co-morbidities. When we excluded all hospital admissions for the purposes of AF management, the increase in hospitalization was only 0.8% per year (95% CI 0.05 to 1.6, p = 0.04), which was no longer significant after multivariable adjustment for co-morbidities (p = 0.25). In conclusion, the marked increase in hospitalization after first AF diagnosis from 1980 to 2000 appeared to be largely driven by the changing practice pattern in AF management.

The History of Atrial Fibrillation: The Last 100 Years

Atrial fibrillation (AF) has had a rich history that has touched the careers of many of the great clinicians and investigators of the 20th century. More recently, there has been an explosion of research into various aspects of the mechanisms and therapy for AF, as evidenced by over 8,000 publications on AF from 2000 to 2007. A century of research and clinical observations, coupled with modern investigative technologies, has enabled modern investigators to have their own "fantastic voyage" as they travel beyond the cell borders into the ionic mechanisms responsible for AF and its many atrial perturbations. One can only imagine the satisfaction of Wenckebach, MacKenzie, and Lewis if they could see how their seeds of wisdom have grown into such sturdy ideas, or how delighted Scherf would be to learn that his ectopic focus theory for AF has been given new life. This paper on 100 years of AF was initially prepared for presentation as the Plenary Lecture at the AFib Summit for Heart Rhythm 2007 in Denver, Colorado. I have tried to provide the reader with some of the most important observations on AF, realizing that it would be impossible to include all or even most of the major research done during this time frame. I apologize to my many colleagues whose research has helped us to understand better the clinical and basic aspects of AF, yet who could not be cited for lack of space.

Potential Glucosamine‐Warfarin Interaction Resulting in Increased International Normalized Ratio: Case Report and Review of the Literature and MedWatch Database

We describe a 71-year-old man who had received warfarin 7.5 mg/day for 5 years for atrial fibrillation, which had maintained his international normalized ratio (INR) within a narrow range of 2.5-3.2. During this 5-year period, he had also been treating himself with the supplement glucosamine hydrochloride 500 mg-chondroitin sulfate 400 mg twice/day for arthritis. The patient then increased his dosage of glucosamine to 1500 mg and chondroitin to 1200 mg twice/day; his INR previous to this change was 2.3. Approximately 3 weeks later, his INR increased to 3.9. His supplement dosage was reduced to glucosamine 750 mg-chondroitin 600 mg/day; a repeat INR done 16 days later was 4.7. The supplement was then stopped, and his warfarin schedule was changed to 7.5 mg every other day alternating with 3.75 mg every other day. Sixteen days later, his INR was 2.6. This case report suggests that a potential interaction exists between warfarin and glucosamine that is associated with an increase in the INR. We therefore performed a pharmacovigilance survey of spontaneously reported adverse events in warfarin-treated patients concomitantly exposed to glucosamine, glucosamine-chondroitin sulfate, or chondroitin sulfate and present a literature review of this apparent drug-drug interaction. Using the United States Food and Drug Administration (FDA) MedWatch database, 20 reports of glucosamine or glucosamine-chondroitin sulfate use with warfarin associated with altered coagulation (manifested by increased INR, or increased bleeding or bruising) were identified. In some cases, a decrease in the supplement dosage was followed by a return of the INR to the previous therapeutic range. Similarly, a decrease in warfarin dosage was followed by a decrease in INR in one patient who received long-term warfarin therapy. One report described an intraventricular bleed and subdural hematoma, which resulted in a persistent vegetative state. The World Health Organization (WHO) adverse drug reactions database documented 21 spontaneous reports of increased INR associated with glucosamine use, 17 of which resolved when glucosamine was stopped. We located one published case report of concomitant use of glucosamine-chondroitin sulfate potentiating the effect of warfarin. In aggregate, the reports from the FDA and WHO, the published case report, and our case report suggest that the use of warfarin and glucosamine may lead to an increased INR. Patients should be advised that the use of the two products may cause an increase in INR, and they should inform their health care provider if they consume glucosamine. More information is necessary to define this interaction.

Abstract 3234: Patterns of Treatment of Patients with Atrial Fibrillation

Background: Atrial fibrillation (AF) is increasingly common, and a number of treatment options are available. Since trials such as AFFIRM show no mortality difference between rate or rhythm control strategies, we hypothesized that rate control would become more common with increased duration of AF. Methods: We evaluated history of treatment modalities in 1052 patients with AF referred to a dedicated AF center. 472 had AF for ≥ 5 years and 200 for ≥ 10 years. We recorded AF symptom burden, calculated as the product of frequency and duration of episodes, and treatment history from first AF episode using a database modeled on AHA-recommended key data elements. Results: The median (25th, 75th percentiles) AF duration was 4.5 (2, 9) years. The median symptom burden was 28% in the first year after symptoms started, and fluctuated from 10 to 15% thereafter. 37% had a CHADS2 score 0, 43% had score 1, and 20% had score ≥ 2. Anti-thrombotic use was near 40%. The Figure shows the spectrum of drug use. In the first year, rate control drugs (blue bars) were used 2.5 fold more commonly than AAD. Surprisingly, the use of anti-arrhythmic drugs (AAD) increased with duration of AF and after five years, they were nearly equal. 20% of patients had cardioversion in the first year, 3% in the second, and 1% or less for year 5 and after. 60% of all cardioversions were performed in the first year of symptoms. Conclusion: Cardioversion is more common during the first year of AF. In subsequent years, symptom burden falls and is relatively stable. AAD usage increases while rate control use remains constant. This suggests that physicians may continue to use AAD drugs to help control symptoms.

Atrial Fibrillation as a Cause of Left Ventricular Dysfunction After Cardiac Transplantation

We report 3 cases of late-onset atrial fibrillation several years after cardiac transplantation, each involving left ventricular systolic dysfunction in the absence of cardiac rejection or cardiac allograft vasculopathy. Although the etiology of late-onset atrial fibrillation in cardiac transplant recipients is not clear, its presence in the absence of cardiac rejection or coronary allograft vasculopathy can result in left ventricular systolic dysfunction, and therefore should be considered in the differential diagnosis of cardiac allograft failure. The onset of atrial fibrillation years after a heart transplant is not necessarily an indication of rejection. Aggressive rate control and restoration of normal sinus rhythm may improve allograft function in such cases.

One hundred years of atrial fibrillation

One hundred years of atrial fibrillation