Science topic

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.
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How to manage anticoagulation in patient with hemorrhagic stroke and atrial fibrillation ?
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Actually It's very much rare association, commonly AF with Ischemic stroke,
but when hemorrhagic stroke with AF, we have to think about risk benefit ratio, considering HAS-BLED score & CHADVASc score. So far i know in that case anticoagulant must have STOP as because more chances of bleeding.
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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.
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You can use MIT-BIH Arrhythmia Database even though it is not entirely similar but hope it helps.
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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?
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Dear Muammer karakayali. Sorry, i need to correct a sentence :the rate of recurrence is inversely proportional to degee of scar tissue detectecd by MRI. Regards.
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Dear all,
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,
Silvia Hoirisch-Clapauch
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Dear Giuseppe, We assumed that anticoagulation improves placental angiogenesis and vasculogenesis, without correcting metabolic issues that could impair intrauterine neurogenesis. Also, nobody knows the effect of anticoagulants that cross the placenta on the fetal brain.
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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?
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Emphasis is on ruling out any coexisting possibly underlying condition (ASD with paradox embolism, Imflammation leading to plaque rupture in Carotid Artery, etc.)
At the moment there only exists consensus on VTE prevention by low molecular heparin. Which does not cover all possible events.
Given your experience and in case of ischemic stroke likely to be resulting from thrombembolism from the left atrial appendage due to persisting AFIB you should consider prescribing NOACs in the patients eligible due to CHADsVASc of one or higher, irrespective of COVID. I would also consider prescription right away since you do not know the onset of Afib in most cases. If sinus rhythm resumes after COVID and is well documented over a longer period of time, you can always stop the oral anticoagulation again.
If all other possible reasons for ischemic stroke are ruled out and you are confident to state that your patient had an ischemic stroke due to acute onset of AFIB due to COVID you should consider publishing this case report.
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Dear colleagues
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
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i think you have to analyze all data from the included studies not the association presented in each paper. and upon your meta-analysis you can conclude if there is association or not
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What is the mechanism linking “burnout” to “atrial fibrillation”?
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Share your views/reviws about significance of CMI
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to calculate how much percent of carbon sequest in soil under differ cultivation practies
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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?
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Good luck ...
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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
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This is tricky mainly because individuals are going to have 1) asymptomatic (Issue 1) or non-stroke like 'chameleonic' manifestations of focal ICH or cardioembolism (Issue 2). Moreover, if all participants are seen hyperacutely after symptoms, CT is less sensitive for hyperacute infarcts (Issue 3). This becomes a little bit more complicated that CTs can potentially miss focal infarcts in the brainstem(Issue 4) both in hyperacute or acute setting( Issues 4a and 4b)
If patients are likely to be seen less acutely ( or imaged only at follow up) a CT loses its ability to discriminate ischemic vs hemorrhagic lesions as days pass since event or symptoms (Issue 5)
Of course there is also a problem of hemorrhagic infarcts which can pose problems ascertaining the exact underlying problem
Hemorrhage smaller than infarct - easy (grade 1 and 2 HTI )
Hemorrhage as big as the infarct or bigger than the infarct often masquerades as a hematoma rather than a hemorrhagic infarct, thus misleading as to the exact mechanism (Issue 6). These limitations should be borne in mind. An MRI will resolve
Issues 1 and 2 ( if routine follow up MRIs are done at intervals)
Issues 3 and 4 (if MRI study triggered by presentation)
Issue 5 if GRE/SW sequences are undertaken
Issue 6 (I don't think even an MR can help here)
The reason history and examination are not being mentioned with emphasis(though very useful) is because of the difficulties they pose due to interpersonal variability in ascertaining or interpreting, individuals with pre-existing neurological signs (making new vs old virtually impossible to ascertain unless the clinician continuity is there - though that cant fix the problem entirely). There is then an argument of whether asymptomatic infarcts and bleeds classify as a stroke (but may classify as an adverse event happening whilst on anticoagulation)
Having MRI will help giving more clarity to the study you do but a CT could help in
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Is there any epidemiological data/ prevalence of left atrial remodelling (assessed mainly by left atrial volume) in patients with HFrEF AND AF
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Highly nsensitive parameter ti pick up /predict LA dysfunction is by speckled Echocardiography-called global longitudinal strain,for LA its LA strain.I extensive use this assesment in all those cobnditions esponsible for AF and HFrEF.Changes can be picked up well before change in LA volume.
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Does anybody knows a validated questionnaire (translated into German) to assess QoL in patients with paroxysmal atrial fibrillation?
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The Short Form 36 (SF 36) has been used in multiple studies but is not specific to AF. It is, however, a QoL questionnaire. The best questionnaire for AF specific symptoms is the modified EHRA score.
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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!
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This is a typical anomaly detection problem.
We've found great success in using Machine Learning tools such as Recurrent Neural Network (RNN) adopting the Long Short Term Memory(LSTM) algorithm. We've demonstrated its sensitivity and diversity on different kinds of heart diseases. We also found great application of the same methodology in other domain disciplines such as predicting and detecting anomaly in jet engines and oil rig machinery offline as well as real time.
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Anyone working on Atrial Fibrillation in Guinea Pig(or any other) Langendorff-perfused Heart? I need urgent help in protocol please replu
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Try CurvFit app for Windows
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  • 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,
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Thanks Enrico. It will be interesting to await the results of this study. However, given the open nature of the study and its small size, (50 patients per arm), it is highly unlikely that the study would support a regulatory submision (certainly in major agencies like the FDA and EMA) to expand the use of rivaroxaban in patients with mechanical prosthetic valves.
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The symptoms, some treatments and contributing factors are known. But what is going on at the cellular level to cause ectopic depolarization?
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The mechanisms of AF are likely to vary between patients, depending on factors such as genetic determinants, cardiovascular risk factors, and concomitant heart disease.
  • Ca2+-dependent triggered activity seems to underlie atrial ectopy in AF, and has complex underlying molecular mechanisms that increase both cellular Ca2+ load and the leakiness of the sarcoplasmic reticulum Ca2+-release channel (ryanodine receptor)
  • Molecular mechanisms promoting re‑entrant activity in patients with AF includeionic properties (such as larger left atrial inward-rectifier background current)and structural properties (such as atrial fibrosis)
Analysis of gene variants associated with AF can provide additional insights into basic mechanisms
(channel subunit mutations, usually accompanied by clear evidence of markedly accelerated repolarization in terms of short QT syndrome, have been described as the probable cause of AF; the involved genes and related K+-currents are KCNJ2, KCNE1, and KCNH2;
given that increased K+ current abbreviates refractoriness and promotes re-entry, while tending to reduce automaticity, these cases of AF are likely to be caused by re-entry).
Zhang et al. reported a family with a mutation in nuclear pore complex protein (nucleoporin) Nup155, which presented with AF and sudden death in early childhood. Ablation of Nup155 in mice resulted in abbreviated ERP and action potential duration, and spontaneous
development of AF probably mediated by re-entry. Several other reports suggest that abnormal automaticity can be central to the pathophysiology of AF. Kazemian et al. described a patient with catecholaminergic polymorphic ventricular tachycardia owing to a ryanodine receptor (RyR2) mutation, who presented with self-terminating AF paroxysms with exercise that were subsequently controlled by β-adrenergic blockade. A loss-of-function junctophilin mutation was identified in a patient with juvenile-onset AF, and found
to enhance RyR2 Ca2+ leak, DADs, and AF in a mouse model. Investigators in another study noted downregulation of the RyR2-targeting microRNA (miR)-106b-25 cluster in AF. Ablation of miR-106b-25 in mice increased RyR2 protein expression and Ca2+ leak, and caused atrial premature complexes and AF inducibility in vivo that were suppressed by an RyR2-stabilizing drug (K201, also known as JTV519)
The molecular determinants of re-entry susceptibility in patients with AF are less well studied than those of spontaneous ectopy. Indices of classical electrical remodelling, such as shortening of APD, are absent in right atrial tissue of patients with AF. In multicellular preparations of right atrial appendages, upstroke velocity, amplitude, duration at 20%, 50%, and 90% of repolarization of action potential, and resting membrane potential were similar in sinus rhythm and patients with AF, and were similarly unchanged in right atrial cardiomyocytes from patients with AF. Preliminary data point to increased small-conductance Ca2+-dependent K+ -current in patients with AF.
Read more link
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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?
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Hi,
After administration of one XL capsule, plasma flecainide concentrations gradually increase after a lag time of 2 to 3 hours to reach a peak between the 21st and 25th hour and remain at plateau levels until after the 30th hour.
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how can a patient be managed having Atrial Fibrillation with rapid ventricular response ?
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Controlling ventricular rate is critical in patients with mitral stenosis. Reduced diastolic filling period significantly increases LA pressure. Combination of beta blockers with Digoxin is required for rate control in many much patients, as has been rightly pointed out. Verapamil and Diltiazem for rate control should be avoided in MS patients with right ventricular systolic dysfunction.
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Digoxin a well known cardiac glycoside cause AV conduction delay responsible for its use in atrial fibrillation and frutter how does this drug achieve this ?
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One of the suggested mechanisms is the vagotonic action of digoxin.
Please see in Desk Reference of Clinical Pharmacology, Second Edition
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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.
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Hi Muhammad,
Thanks for your question, certainly a clinical conundrum encountered increasingly frequently and one for which direct evidence is limited. However, a nice review I read recently summarises this well, particularly the impact that NOAC profiles have on the risk:benefit decision you nicely present:
This article provides a very telling conclusion:
"The literature suggests that elderly adults with AF—even those with high bleeding risk—benefit from anticoagulation. The benefit of anticoagulation appears to be most marked in those with high stroke and bleeding risk, a category into which many elderly adults fall. By reducing the risk of ICH, the DOACs may tip this risk:benefit ratio even further toward anticoagulation."
Hope this helps.
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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.
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Dear Rajeev, I do not do septal ablation in adults but do so mainly in children. Alcohol ablation does not really apply to kids so I use radio frequency to obtain septal reduction - this has several advantages, including identification of the HIS to avoid heart block and sometimes selectively creating LBBB as this causes paradoxical septal motion and opens the LVOT thus reducing the gradient. We have also done it in adults and using CARTO Sound to map the area to be ablated thus reducing radiation. If the supply to the area of obstruction cannot be identified, the RF technique is a good and safe option. I hope this is helpful Jo DeGiovanni (Birmingham UK)
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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. 
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Thank you dear Paul 
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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?
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thank you @saleh alkarim and @biswajit majumder 
these links are helpful
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AF, Atrial cardiomyopathy, is it really histology proven cardiomyopathy 
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The working group proposes the following working definition of atrial cardiomyopathy: ‘Any complex of structural, architectural, contractile or electrophysiological changes affecting the atria with the potential to produce clinically-relevant manifestations’
Diseases like a hypertension, heart failure, valvular, genetic,diabetes,
myocarditis ... or conditions (like alone AF, smoking, isolated atrial amyloidosis,ageing, endocrine abnormalities...) are known to induce or contribute to an atrial cardiomyopathy
EHRAS classification of atrial cardiomyopathy ( class/ histological characterisation)
I  Morphological or molecular changes affecting ‘primarily’
the cardiomyocytes in terms of cell hypertrophy and
myocytolysis; no significant pathological tissue fibrosis
or other interstitial changes
II Predominantly fibrotic changes; cardiomyocytes show
normal appearance
III  Combination of cardiomyocyte changes (e.g. cell hypertrophy,
myocytolysis) and fibrotic changes Alteration of
interstitial matrix without prominent
IV Collagen fibre accumulation
Iva Accumulation of amyloid
IVf Fatty infiltration
IVi Inflammatory cells
IVo Other interstitial alterations
Read more: A. Goette et al. / Journal of Arrhythmia 32 (2016) 247–278
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Atrial fibrillation, ranolazine, rate and rhythm control. 
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Randomized controlled trials  (RCTs) on the use of ranolazine (RN) for prevention and cardioversion of atrial fibrillation (AF) have yielded  сontradictory results.
PubMed and EMBASE were searched until June 2016. Of 484 initially identified studies, 8 RCTs were finally analyzed. Meta-analysis suggests that RN may be effective in AF prevention, whereas it potentiates and accelerates the conversion effect of amiodarone of recent-onset AF. Larger RCTs with long-term follow-up in diverse clinical settings are needed to further clarify the impact of RN on AF therapy. (PMID: 27746384 DOI: 10.1016/j.hrthm.2016.10.008)
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Atrial fibrillation and genetics
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As new discoveries in the field of genetics, the group Idiopathic AF becomes every time ever less. Most often the genetic AF Is monogenic and autosomal dominant, affecting various potassium channels in phase 3. More rarely, AF may be autosomal recessive or sex-linked. In such cases, the channels of sodium are affected. There are also known forms of AF with mutations in many genes - family polygenic atrial fibrillation.
Genetic AF may be an independent nosological unit or accompany with such channel diseases as the syndrome of elongated or shortened Interval QT, Brugada's syndrome and catecholaminergic polymorphic ventricular tachycardia. In addition, AF may be associated with such structural genetic  cardiomyopathy, as family dilated cardiomyopathy, hypertrophic cardiomyopathy, idiopathic restrictive cardiomyopathy, arrhythmogenic dysplasia right ventricle as well as with other diseases (noncompact cardiomyopathy, fibroelastosis and mitochondrial diseases).
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Coronary bypass surgery.
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Tunica media of this vein resumbles  tunica media of an artery in that it contains lot of smooth muscle fibers. This is the logic behind it for its use in coronary bye pass surgery.
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PCI percutaneous coronary intervention
checklist of organizing work  pre, during and post intervention
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Attached is a fairly typical NHS checklist.
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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.
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Thomas is absolutely right, but your study poposal is different, because you want to see if there is any influence of training on LVEDP, and not to sepparate between normal and disturbed diastolic filling patterns. You are trying to sepparate lets say in otherwise healthy individuals between an LVEDP between 5 and 12 mmHg. In general TDI and conventional doppler may separate below and above 15 mmHg. Most important to me seems to have an absolutely sound study protocol. 1.) TDI and doppler parameters are age dependant (so you have to choose a quite narrow age margin (not more than 10 years, e.g. 15 to 25 years of age) 2.) perform all exams on the same machine and with the same technician (or by yourself) and the same condition (time of rest before exam), left shoulder recumbency etc....) 3.) if you suggest a LVEDP difference between the groups of 3 to 5 mmHg and you have an error of 3 mmHg (interobserver variability and day to day variance, and intraobserver variability and interindividual variability) you will need at least 50 probands per arm to detect a difference of 50% of LVEDP (e.g. 5 mmHG versus 7.5 mmHg), is the difference between training conditions less, you will need even more probands.
Best
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In patient with asthma and atrial fibrillation, does bisoprolol or any cardio-selective beta blocker changes pulmonary function test?
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It is assumed that beta-1-antagonists have less effect on the pulmonary system. This is an experimental research  claim. Nonetheless,in real life and humans all 'beta1-selective' beta-blockers affect the pulmonary system. This is especially true in asthma, because it is an inherent characteristic of this disease that beta-receptors are different from those of patients with normal pulmonary function. In asthma the 'selectivity' is partially lost. However, it is uncommon that the effect is large and really clinically significant.
It is a common experience that patients with asthma and overlap syndrome are treated with inhaled beta-agonists and also receive oral beta-blockers. This is a pharmacologic  wrong choice.
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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?
many thanks.
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Habib I am not familiar with the reliability of established LA tests- but my modeling research into LV function indicates the LA function can be conveniently assessed from the work it does on the LV during filling. Atrial filling work is the area beneath the LV's PV loop during the filling interval. Not sure if anyone has looked at it, yet I would not be surprised to see fruitful results from a filling work index. 
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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
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Drs. Karnik, Zuidema, and Alam have all great answers, but I would stress the importance of what Dr. Alam stated in that if neurosurgical intervention is crucially required then the surgical intervention must proceed without reversal due to time.  Also, keep in mind that if the neurotrauma patient suffered high energy blunt trauma the endemic anticoagulants from the neuro tissue is also released and therefore the amount of uncontrolled bleeding intracranially may not necessarily be only from the warfarin.
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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! 
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In post operative atrial fibrillation, the goal is rate control; not rhythm control.
Beata blockers are the first line treatment for achieving rate control in patients with post operative AF( whether established or new onset). If beta blockers are contra indicated or if pt hemodynamically unstable Intravenous Amiodarone infusion is indicated.  
When the pt becomes hemodynamically compromised due to fast ventricular rate and does not respond to drugs including digoxin, cardio version is indicated. After cardioversion Amiodarone should be continued and may be supplemented with beta blockers for achieving a acceptable rate control. 
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Since the point that the first one is more unafforfable in the real world.
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I prefer Dabigatran in AF treatment. 
1. There are two doses for potential usage. We can use 110 mg to decrease bleedng complication or 150 mg to increase the efficiacy.
2. Idarucizumab seems as a safe and effective agent to reverse bleeding side effects.
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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
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Thank you very much for your answer. 
Much obliged and best regards.
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Is it related to the results of a particular study? Why the 7 day cutoff?
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I think the 7-day cut-off was introduced without a specific rationale by a paper by Samuel Levy in 1995 (J Cardiovasc Electrophysiol, 6:69-74), see also
Eur Heart J. 1998 Sep;19(9):1294-320.
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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.
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 in this particular sceinario percutaneous tracheostmy will be right answer. this patient as somebody has already mentioned must be needing mechanical ventilation and will need it for pretty long time .You can always get benefits of right time tracheostomy in such cases.RE intercostal muscle weakness this patient will need tracheostomy for early weaning and preventing resp infections with good tracheal toilette.
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Why would this be a good strategy? What is the reasoning behind it? What is the evidence?
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Ablating the singularity point, which is the center of the reentrant arrhythmia (i.e., center of the tornado), may terminate the reentrant activity and thus atrial fibrillation. After circumferential ablation of the pulmonary veins and posterior wall of the atria, many EP labs employ dominant frequency mapping to localize the region of highest frequency activity,. Many argue this region is the driver of the arrhythmia. If this driver is a reentrant arrhythmia then ablating the singularity point has a high probability of terminating the arrhythmia. Please recognize this is a highly debated area of research.
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Which is the better, anticoagulant therapy only or combination of anticoagulant therapy and antiplatelet therapy?
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NOAC: as simple as that. Presumably Pradaxa 2x150 mg - superior anticoagulation profile with acceptable bleeding complications.
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Antiagregan therapy in non-valvular atrial fibrillation.
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This is a classical question . 
As it has been recognised, CHA2DS2-VASc is the best scheme to identify those patients at very low risk. These patients will not obtain benefit to be under oral anticoagulation. 
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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. 
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Dear Colleagues,
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.
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The protocol for evaluating neurocardiogenic syncope is not essentially different in patients with atrial fibrillation. It is 70 degree head up tilt for 45 min. As per American College of Cardiology consensus document, in patients with severe left ventricular outflow obstruction, critical mitral stenosis, known proximal coronary artery disease and known critical cerebrovascular stenoses, tilt table testing is relatively contraindicated. Nevertheless, it is always better to obtain go-ahead from a cardiologist, before carrying out HUTT for patients with AF. Also, it is necessary to have all necessary resuscitation facility nearby with the support of a clinician, in case of an eventuality. 
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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?
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I think Dr. Sachdeva has given a complete answer and patient need to be observed periodically.
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What about patients with less than 30 seconds episodes of AF?
A therapeutic difference is a should, may or must?
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The 30 seconds was determined by consensus to be a reasonable threshold by which most would consider calling that an episode of Afib.  However, it is still unclear how little is still significant.  We have pacemaker patient data saying that both several minutes of Afib per month is enough for increased events and that strokes occur in sinus rhythm in patents with a history of Afib (see ASSERT and IMPACT trials).  The 2014 AHA/ACC/HRS Atrial Fibrillation Guidelines took out the 30 sec comment and left it up to the reader to conclude how long of an episode should count.
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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
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thank you
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Atrial fibrosis mechanisms?
Chicken and egg paradox in AF?
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Hi Uğur, 
When you look at the risk factors for atrial fibrillation (age, hypertension, obesity, diabetes and Cv diseases) they will all contribute to fibrosis of ventricles and of atriae.  t can be simple. Rapid firing from the PV will irritate the atriae but will in most cases not bring the system out of balance and cause atrial fibrillation.  Let us phrase it as in the 2010 ESC guidelines: 
TRIGGER
Focal activity of pulmonary vein cells
Triggered activity and re-entry
This leads to extrasystoles and runs of extrasystoles. 
SUBSTRATE
Any kind of structural heart disease may trigger a slow but progressive process of structural remodeling in both the ventricles and the atria
WAVELETS
The impulse no longer progresses as a wavefront but as multiple small wavelets (> 350 pm) with micro-re-entry
On top of that atrial fibrillation and other expressions of cardiovascular diseases (infarction, heart failure, valvular heart disease) will exacerbate this fibrosis. 
So it is not a chicken and the egg story, it is rather an "AND" "AND" story.
This is how I look at this problem. What about you?
Best regards,
Thierry 
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Hi all,
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?
Thanks
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My pleasure.
Good luck.
Doug
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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?
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RF ablation creates a more transmural lesion than cryoballon ablation which will more effectively disconnect epicardial triggers. AV Node ablation post CRT implant is helpful for treating AF patients who are non adherent to their meds, who have drug refractory AF, 
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atrial remodelling in Atrial tachycardia or atrial flutter or Atrial Fibrillation
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"For non invasive modality such as ECG, ECHO, CT, MRI or PET, how could we differentiate that the atrial remodeling process already occur or not? Any atrial size enlargement was associated with atrial remodeling?"
It is possible to compare the volume of the atria, typically normalized by the body surface area, to various studies that have compared normal versus diseased populations.  However, you raise a significant point about how to differentiate between arrhythmia induced remodeling, and remodeling caused by other comorbidities, such as mitral valve regurgitation, hypertension, etc.  Because of the complex manner in which all of these factors intertwine, I don't think post-hoc attribution of causality is possible for any feature of atrial structural remodeling.  Fortunately, measurement of these features, e.g. fibrosis, or atrial volume, can help determine the best treatment options to pursue.
If you are looking for tools that can help you measure atrial volumes from image data, check out Seg3D.  It is a free image segmentation package that is quite stable and has releases for most major operating systems.  
"For CARTO 3, how could we differentiate between scarred tissue and true atrial remodeling?"
I am not certain what you are looking for here.  If a patient has an atrial arrhythmia (AF), and no prior ablation therapy, I would assume that any abnormal tissue is atrial remodeling.  If the patient has previously undergone an ablation procedure, then there may be a difference between scarred tissue, and remodeled tissues.  If you are interested in trying to classify these tissue types, I would look at work that has been done with voltage mapping.   Marchlinski et al. looked at the amplitude of intracardiac electrograms as a means of classifying different types of cardiac pathology.  Their work has largely focused on ventricular scarring, but I would start there anyway.
Good luck!
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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.   
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Hi Geraldine, I would not recommend left atrium catheterization for a single episode in a young patient. Firstly, I would monitor his cardiac rhythm to make sure he does not experience nocturnal paroxysms, may be anticoagulation could be indicated. Were you concerned about glutaminergic receptors hyperactivation for explaining AFib?
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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?
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I feel exactly the same as Dr Kautzner. In addition, I now almost exclusively perform all AF ablations with robotic assistance. We have exceeded 730 robotically assisted cases. It is unthinkable now for me to consider manual AF ablation. Current Robotic systems use conventional RF energy and are integrated with 3 D mapping. I remain concerned about radiation exposure with single shot technologies. Furthermore, the vast majority of patients with AF referred to me for ablation have persistent AF and require additional ablation over and above PV isolation.
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Could anyone point me to evidence for this please.
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Dear Sonia,
In haemodynamic stable patients AF after reperfusion from STEMI not a poor prognostic indicator. Atrial fibrillation and other supraventricular tachycardias may occur. Atrial fibrillation complicates 10-20% of AMI but other supraventricular tachycardias are rare and usually self-limited. Reperfusion arrhythmias (eg, ventricular ectopics, ventricular tachycardia or idio ventricular rhythm) which are usually benign and do not require therapy. Failure of reperfusion is less likely with the availability of primary percutaneous coronary intervention (PCI ). Reperfusion should reduce ST elevation to less than 50% within one hour. (Van de Werf F, Ardissino D, Betriu A, et al; Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003 Jan;24(1):28-66.)
Hope will satisfy your question.
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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!
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Two parameters that would be particularly useful are heart-rate variability and a-fib duration.  There are relatively simple algorithms that have been available for many years to capture and report these parameters.  If I can help further, please let me know. 
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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 
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Given the rarity of the condition, an off-label use of NOADs is possible.  However, the dosages of these drugs need to be calibrated such that they can be  safely and effectively used. There should be caution in the use of these agents that a specific antidote is not available.  Large clinical trials may be warranted to establish the evidence for the use of NOACs in cerebral vein thrombosis.
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Important factors to consider include: flexibility to obtain several outcome measures from the ECGs, ease of use and reasonable cost.
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There are several ECG digitizing software in the market as well as software to measure ECG intervals that can work along with the digitizing software. An examples for these software (which you can download free demo) are available at " http://www.amps-llc.com/website/index.php?option=com_rokdownloads&view=folder&Itemid=21". The time needed to scan the ECGs is not trivial, and the yield in terms of reading results is limited. So it is not that much practical for large volume of paper ECGs specially if the interest is to obtain several measures (i.e. ECG classification, intervals, etc..)
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For surgical intervention.
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Yes. As Dr. Dohmen has already stated it makes a lot of sense to perform an ablation in addition to replacing the valve and close the LAA.
A bioprosthetic valve leaves you with the option of performing TAVI in the future, a mechanical prosthesis does not.
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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?
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I join the opinion that we do not have yet valid proofs. One important issue is how successful AFib ablation is defined - real 100% long-term success can be prooved only by ILR, which is not used in everyday follow-up of such patients. One side-note - the inventor of the maze operation James Cox has reported an extremely low long-term embolic risk after this procedure that is attributed to the exclusion (by excision or closure) of the LA appendage from the blood flow. Exclusion of LAA cannot be done during AFib catheter ablation, so the eventual long-term stroke reduction (if any) would probably be of lower magnitude.
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In this economic situation there is a clear limitation about the use of new antithrombotic drugs. However, in my opinion there is a marked underuse of NOACs. Several reasons are underlying this situation. What is your opinion?
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Yes. I am agree.
But, we have several concern about safety (lack of antidot and variability of management) and analytical control (lack of specific assays) without practical answer
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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).
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For the ones who are interested in this topic you might also take a look at our article:
J Am Heart Assoc. 2012 Oct;1(5):e002212. doi: 10.1161/JAHA.112.002212. Epub 2012 Oct 25.
Swaans et al - Ablation for atrial fibrillation in combination with left atrial appendage closure: first results of a feasibility study.
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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?
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I agree with previous observations that patients with otherwise normal heart and at low CHADS2 score may have a high incidence of stroke. The reasons are multiple, including incomplete assessment of contributing factors.
I also agree that in some settings, additional information not covered by CHADS2 (or CHAS2DS2VASc) may be important. In hypertrophic cardiomyopathy, for example, both LV outflow gradient and AF presentation form (either paroxysmal or persistent) play key roles in risk stratification for stroke. Patients with carotid or ascending aorta plaques may be at increased risk for stroke as compared to those with plaques only in the abdominal aorta or the lower limbs territory. On the other hand, it is also a consensus that risk scores may simplify the stratification process.
Thus, development of tailored scores focusing on particular environments may represent an optimal approach and a trend to the future of risk stratification approach.
Peace and blessings.
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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?
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This is very much what I suspected and thank you for the thorough reply!
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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.
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Nice question, indeed! Congrats!
For me all of patients should be under OAC.
The most important factor in primary prevention is age. There is a nice paper by L Friberg in Circulation where the authors show the importance of age in the increased risk for stroke.
As Guidelines say we will improve the prognosis of our patients initiating OAC in most of the cases. So, I am not clear we should say "her only risk factors are..."
To the best of my knowledge, we should not calculate +1 or +2 points. CHA2DS2-VASc and HAS-BLED score were not proposed to add or subtract points.
Regarding echo findings, for my only LV systolic function is an established variable.
Best wishes,
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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)?
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dear colleagues: with a background in LAA occlusion I would like to take a different approach: in the AFIb ESC Guidelines 2011 you find on page 2382 a clear definition, namely "mitral stenosis or prosthetic heart valve". In these cases thrombi in AF come from the free atrial space, not the LAA. In all other cases (mitral regurg, aortic stenosis, aortic regurg etc.) 90% of thrombi come from the LAA. So either NOAC´s or LAA occluder should be considered. Admittetely, RE-LY and other studies excluded any patient with "severe heart failure" - so thats why those patients are excluded..
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"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?
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Thank you, Dr. Waldman. I'll see what I can do to get in touch with him.
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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?
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watchman has obviously more data backing its efficacy and safety..but with the ongoing ACP trial we will probably get some more details on amplatzer's device.. looking forward to the amulet by amplatzer as well as the WaveCrest device by Coherex...
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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?
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Dear Raul, you are right. There is nothing else to say. With my best personal greetings.
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Could you recommend the best device for A-fib surgery?
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The epicor System may be a good tool for Afib ablation during cardiac surgery. The system uses high intensity focused ultrasound (HIFU) energy.
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Medication adherence is a big problem in AF, especially warfarin - could it be that cognitive decline/deficits are partly responsible?
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Thanks Ken,
From my clinical experience, I have no doubt that anxiety plays a role and can drive sympathetic activity- certainly catecholamine release can explain tachycardias. I suspect that any change in blood flow to the cerebral blood vessels can't be a good thing but it would be interesting to see if there is co genitive decline over the years for those with chronic AF in the presence of hyptertension and in those who are normotensive.
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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?
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I have some experience with ivabradine in patients with advanced heart failure .
There is not a very large but a well defined group of patients with sinus tachycardia despite treatment who can benefit from adding ivabradine to ACE inhibiors and beta blocker. I have some positive experience with many patients. Certainly the cost is a limiting factor for the use of that drug. I do not think that ivabradine and digoxin can be used interchangeably in patients on sinus rhythm. I prefer to add ivabradin when the patient despite treatment has a tachycardia excceding 80 beats /min.