Atrial Fibrillation - Science topic
Atrial Fibrillation is an abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.
Questions related to Atrial Fibrillation
Hello everyone, I am doing research on the detection of Atrial Fibrillation from the ECG signal. For my research purpose i need datasets that will contain Atrial Fibrillation data. I have learned about AF termination challenge dataset and MIT-BIH database but i need more data. So, please suggest datasets that can be used in MATLAB for detecting Atrial Fibrillation from ECG signals.
Atrial fibrillation (af) ablation and cardiac mri
What do you think about the evaluation of ablation lesions with postablation cardiac MRI, especially in patients with permenant atrial fibrillation who require multiple atrial fibrillation ablation?
We'll soon start to apply questionnaires analyzing the impact of anticoagulants during pregnancy on the offspring's behavior and learning skills. The inclusion criteria is either heparin use for at least the first seven months of pregnancy or warfarin use from 14 to 36 weeks of pregnancy (e.g. mothers with mechanical heart valves or with biological heart valves and atrial fibrillation). The kids must be 7 to 15 years old and controls will be matched by neighborhood.
Let me know if you want to join our team and I'll send you the rationale and the methodology. Thank you in advance,
All you have the same experience? Does any intervention needed for this? Have any complications related to this AF? May we conduct a research with this findings?
I am doing a systematic review on the occurence of stroke in atrial fibrillation. Many studies compare a healthy group with a patient group, suffering from atrial fibrillation.
Multiple logistic regression analysis is done to adjust for confounders like age, gender, LVEF and so on.
Let's say atrial fibrillation is still associated after adjusting for the confounders. Is it correct to conclude, that atrial fibrillation is associated with stroke independent of age, gender and LVEF?
Let's say the association for atrial fibrillation and stroke gets not significant after adjusting for the confounder age, gender and LVEF. Is it correct to conclude, that the null hypothese is probable and the data is rather coincidence? If not, what does it mean?
Thank you so much for your answers
What would be the best model/algorithm for Genetic Risk Score calculation (for risk prediction) based on genotype information of multiple SNPs.
For example, I have identified 10 SNPs that are reported to increase the risk of Atrial Fibrillation in several GWAS studies. I've curated data, like OR/Risk allele frequency, for these 10 SNPs. Now, if I get a random sample from a person, in whom all these 10 SNPs are genotyped simultaneously. I would like to calculate cumulative risk score of this person for atrial fibrillation using this genotype information from all 10 SNPs (like additive model). Would it be feasible to calculate such risk score? If yes, can any one suggest/share views/algorithms?
I am doing reserch that prospectively follow pt with atrial fibrillation on warfarin for incidence of stroke hemorrhagic due to SIde effect of warfarin or ischemic due to cardioembolism I WONDER if NONcontrast CT beside history and exam and coagulation profile is sufficient to diffrentiate ischemic from hemorrhagic
Does anybody knows a validated questionnaire (translated into German) to assess QoL in patients with paroxysmal atrial fibrillation?
A computer disc drive mfg. company had a problem similar to this irregular heart beat problem, 1985. The disc drive model consisted of 3 modified Lorentz functions. The model was tried on 200 drives; 199 drives agreed with a small standard deviation. But, the last drive showed a -major- defective drive. Thus solving a mfg. problem with a least-square curve fit. So, it can be done ... try it!
Research Proposal (Human) Heart Beat Math Model found with the CurvFit App ......
- NOACs are currently contraindicated in patients with metallic prosthetic valves. Furthermore, there is no evidence of their benefit in patients with significant valvular Atrial Fibrillation. Will this postion change in the future? Are there ongoing trials in patients with metallic prosthetic valves or high risk valvular AF patients that may drive the addition of these indications to the utility of NOACs,
The symptoms, some treatments and contributing factors are known. But what is going on at the cellular level to cause ectopic depolarization?
Is it after reaching the steady state concentration (3-5days) or it may take more days to reach the maximum effect for atrial fibrillation control?
Non-valvular atrial fibrillation (NVAF) is more common with increasing age. Doctors are increasingly asked about anticoagulation in such patients.
Is it appropriate to give anticoagulation in patients aged ≥ 90 years with NVAF who are:
a. Ambulatory and having preserved cognition.
b. Partially dependent with impaired cognition and brain CT evidence of lacunar infarcts.
c. On Nosogastric (NGT) or PEG tube feeding with associated Alzheimer's disease and bedridden status.
Any evidence-based answers will be appreciated.
I am performing septal ablation by avoiding empirical 1st septal artery ablation. The branches are selected with 3S(Systolic squueze of Septal artery), supplying the hypertrophied septum responsible for the obstruction. I small series transient A-V block was seen in less than 10%( No requirement of Permanent pacing). The limitation is the bias because of small sample size. Clinical improvement is significant with no recurrence in 5+years follow up.
We want to know the most common polymorphism of β adrenergic receptor gene associated with bisoprolol therapy in heart failure studies. We want replicate in our population.
which cell line would best to study atrial fibrillation (OR lncRNA role in atrial fibrillation) . and if we have to use mice/ rat model for invivo study, then which strain would be best? AND WHY most researchers prefer using C57BL/6 in AF mice model?
My project is to evaluate the LVEDP in trained vs untrained/deconditioned individuals. I don't want to cath the subjects. Is there an accurate way to measure the LV filling pressures? Thank you.
In patient with asthma and atrial fibrillation, does bisoprolol or any cardio-selective beta blocker changes pulmonary function test?
I want to like to ask experts in echocardiography and atrial function assessment about the following:
What is the current test and hypothetical research test that can be used to assess left atrial function in patients with atrial fibrillation?
Currently, I am working with individual segmental atrial strain, Strain rate, pulmonary vein assessment, TACT, and few other parameters. I am getting a little confused with too many emerging tests for atrial function and no clear validated test. Can someone explain to me the best few tests that can be used and potential research tests that would be able to give me a accurate assessment of left atrial function?
One day, an elderly patient with an isolated head injury has been admitted to your ED. The patient is known to use warfarin for atrial fibrillation and has an INR of 2.8. I really want to konw:1. what tool you will choose to evaluate the coagulation function of this patients? 2. Does the INR need to be revised? 3. What agents you will use to revise the INR and what is the target INR? I am looking for your answer.H
What can we do against postoperative atrial fibrillation after cardiac surgery? Is Perioperative β-blockade the only (real) answer for our big problem? Thanks for the attention!
Nattel S ; Department of Medicine and Research Centre, Montreal Heart Institute and Université de Montréal, 5000 Belanger Street East, Montreal, H1T1C8 QC, Canada
Yang B; Department of Pharmacology, Harbin Medical University, Harbin, Heilongjiang Province 150081, China
Patient has major stroke on the left middle cerebral artery, right side no sensation except the foot, with atrial fibrillation and polymyositis. Would the intercostal muscles be strong enough to allow breathing ? Patient is 79 year old female.
Why would this be a good strategy? What is the reasoning behind it? What is the evidence?
Which is the better, anticoagulant therapy only or combination of anticoagulant therapy and antiplatelet therapy?
Pericarditis is a risk factor for development of atrial fibrillation. If atrial fibrillation should arise in the presence of pericarditis, will it then be more difficult to treat (i.e. convert to sinus rhythm) with anti-arrhythmic agents compared to atrial fibrillation without underlying pericarditis?
I'm only interested in the topic from a phamacological point of view, I'm not interested in ablation.
Can anyone tell me if there is a validated method of testing cardiovagal and adrenergic autonomic function testing in patients with atrial fibrillation? With Tilt table testing - is this a validated method in AF?
Lastly, are there any modifications in tilt such as unsupported postural provocation - i.e. sitting, standing, lying (all unsupported)?
Thank you for any guidance.
Heart rate and AF association?
Do agents blocking AV node or SA node predipose patients to the AF?
Ivabradin use and AFare associated or not with each other?
Hi everybody, it is a great pleasure for me to let you know that the open Special Issue published in Biomedical Signal Processing and Control which is focused on Atrial Fibrillation is now available online. The access will be opened without the need of subscription for two months. To access the Special Issue check the link below
I am analysing atrial fibrillation in mouse models equipped with telemetry. Unfortunately from literature I cannot find a good example (picture) or reference to refer to.
How would you define an AF in mouse model? Lenght? Is it an erratic RR interval with loss of P wave and unstable baseline? Is it associated to bradycardias?
AV node or catheter ablation is generally performed for the treatment of atrial fibrillation. Radiosurgery cardiac ablation for atrial fibrillation is recently reported. What are some of the potential advantages of radiosurgery cardiac ablation over the other procedures?
Glutamine supplement used in fit and healthy person with no known cardiac history who presented wit AF rate 110bpm. All lab results normal. On no medication.
With the growing development of cryoablation and catheters like the nMARQ, do you think there will be room for the conventional radiofrequency for paroxysmal AF in the next few years or do you think its use will be reserved for persistent AF?
Greetings! I am an entrepreneur who is working with some colleagues to develop an application that allows AFIB patients to keep track of the occurrence of episodes and their length. The advantage of this application is that the information can be shared with their health care provider at the time of service to allow them to design treatment plans to improve the quality of care and reduce the cost of repeated care for their office.
We are interested in talking to health care providers and researchers involved with AFIB to hear what sort of information would be most valuable to them. We have an outline of the remote monitoring system and would like to get some feedback on features that would provide the greatest value to both health care provider and patient. If you have any thoughts that you could share with us in the body of this question or we would be able to discuss and share our current prototypes offline to get your feedback (please PM me for details).
Thanks very much for your help, we're looking forward to hearing from you!
Cerebral venous thrombosis is an uncommon condition with difficulties in diagnosis and treatment. There is limited study on the best treatment option. The mainstay of treatment remains systemic anticoagulation with a lengthy duration of oral anticoagulants, which has a troublesome unpredictable drug effect, various drug and food interactions, and increased risk of bleeding. Recent availability novel anticoagulants provides an alternative treatment option for other medical conditions, such a prevention in stroke for Non-valvular Atrial Fibrillation patients (ROCKET, RE-LY or ARISTOTLE i.e.) . Do you think that a multi-center design protocol for standard treatment vs according to best medical and scientific practice could be made on this scenario
Concerning the preliminary information regarding the reduction of stroke and thromboembolic events in patients undergoing catheter ablation of AF, what do you think? Do the available studies already suggest a benefit? or is it too soon and we should quitely wait for the results of prospective trials (CABANA) before getting over-enthusiastic?
Current evidence suggests that percutaneous occlusion of the left atrial appendage (LAA) is efficacious in reducing the risk of thromboembolic complications associated with non-valvular atrial fibrillation (AF).
Do you think this clinical risk factor-based approach will last or do you think that biomarkers and echocardiographic parameters will drastically change this field in the next few years?
Morphologically the cardiac structures seem to be very close in nature. I could find little literature on the goat heart-could ablation or BBB models that can be created with these?
CHA2DS2-VASc and HASBLED scores is recommended for anticoagulation therapy decision. I would be grateful if any reader would consider the four scenarios that indicate for limitations of the currently recommended scores for thrombotic/bleeding risk in patients with AF.
First, an 81 years normotensive old male with permanent AF. Otherwise, without any other risk factors. Echocardiographic examination revealed a marginal LVH, normal cardiac dimensions including the LA dimension of 38 mm.
Comments: it is enough to be older than 75 years of age to reach 2 points of thrombotic risk score (to be treated with anticoagulants). Meanwhile, the HASBLED score reaches 1 point. The net difference equals the (+) 1 point.
Second, an 81 years old hypertensive male with permanent AF. Otherwise, without other risk factors. Echocardiographic examination revealed a huge LVH due to the aortic stenosis, small cardiac dimensions, and a large LA dimension of 50 mm.
Comments: it is enough to be a hypertensive, older than 75 years of age with hypertension to reach 3 points of thrombotic risk score (to be treated with anticoagulants). Meanwhile, the HASBLED score reaches 2 points. The net difference equals the (+) 1 point.
Third, a 48 years old mild hypertensive female with persistent AF who suffered from diabetes. Echocardiographic examination showed normal cardiac dimensions including the LAD dimension of 33 mm.
Comments: her only risk factors are female gender and diabetes. It is enough to reach 2 points of the CHA2DS2-VASC score (to be treated with anticoagulants). Meanwhile, the HASBLED score reaches 0 point. The net difference equals the (+) 2 points.
Fourth, a 48 years old normotensive female with permanent AF suffered from non-ischemic congestive heart failure with enlarged (echocardiographically determined) cardiac dimensions (LVEDD of 70 mm, LAD of 52mm).
Comments: her only risk factors are female gender and CHF. It is enough to reach 2 points of the CHA2DS2-VASC score (to be treated with anticoagulants). Meanwhile, the HASBLED score reaches 0 point. The net difference equals the (+) 2 points.
Please provide the answer to the question: in whom of four subjects you are eager to prescribe oral anticoagulants (either warfarin or the newer oral alternatives)?, and what is considered as a main determinant for taking decision? Please consider only one: age, gender, diabetes, hypertension (systemic), cardiac dimension, LA dimension.
Is it atrial fibrillation other than in patients with rheumatic heart disease? Do you also exclude patients with hypertrophic cardiomyopathy and prosthetic heart valves? Do you consider moderate valvular disease (e.g. mitral and aortic regurgitation or stenosis)?
"The major mechanism underlying the early recurrence of atrial fibrillation after ablation is mainly reconnection of the isolated pulmonary vein" - Sotomi et al. (attached)
I assume this is primarily due to incomplete isolation that manifests in recurrent AF as the ablated tissue heals.
In patients with LA volume-enlarging conditions such as hypertension, valvular heart disease, etc., could there be another explanation for AF recurrence? I assume that the increasing volume in such diseases is at least partly due to cardiomyocyte proliferation. If such is the case, could the new cells form electrically-conductive bridges across the ablated tissue, allowing AF recurrence?
After the recent results of the PREVAIL trial, which will be the preferred device? The Watchman or the Amplatzer? Do you think that head-to-head trials are needed?
Despite the theoretical advantages in specific contexts, which agent to chose when the patient has no specific comorbidities, despite an indication for oral anticoagulation according to the CHADS2 and CHA2DS2-VASc scores?
Medication adherence is a big problem in AF, especially warfarin - could it be that cognitive decline/deficits are partly responsible?
The effect on symptoms is marginal; heart rate decreases statistically, but the clinical effect is minor. Ecocardiographic parameters do not improve much, NB-proBNP is almost unchanged. In the many patients with atrial fibrillation, the drug is considered ineffective. What are the drugs good for? What should they be used for?