Atrial Fibrillation - Science topic

Atrial fibrillation (AF)is the commonest dysrhythmia in adult cattle and can occur associated with various diseases including abomasal disorders. The presentation is generally paroxysmal (eg it reverts spontaneously to sinusal rythm within a week when adressing the primary presentation problem). The exact pathophysiology is not precisely known in cattle but the large atria size may increase the risk of ectopic foci of depolarisation especially when homeostasia is perturbed (eg electrolic imbalance observed in abomasal diseases but also with inflammatory diseases). Interaction with sympathetic/parasympathetic tone has also been mentioned. From my experience, I would not say it is commonly associated with abomasal displacement (I would say max 5-10% from my best guess so not "often" as mentioned in your post). Japanese researchers also reported that up to 2.5% dairy cows have AF (285 dairy cows followed 18months, Machida et al., 1993) which was more idiopathic (ie no specific disease associated with it but only hypothesizing that increased sympathetic tone could be associated with this form of AF). A small proportion of cattle also display persistent AF and in this case it has been associated with the presence of small fibrotic lesions within the atrial wall which may perturb the normal eletric conduction and increased the risk of ectopic depolarization foci (Machida et al., 2001).

A good overview of AF pathophysiology is available from general cardiology textbooks and it has to be remembered that this is generally considered as a relatively benign condition in cattle vs small animals where AF generally occurs associated with enlarged atrial size due to advanced stage of cardiac disease.

Machida N, Nakamura T, Kiryu K, Kagota K. Electrocardiographic features and incidence of atrial fibrillation in apparently healthy dairy cows. Zentralbl Veterinarmed A. 1993 Apr;40(3):233-9. doi: 10.1111/j.1439-0442.1993.tb00622.x. PMID: 8328231.

Machida N, Kiryu K. Cardiac lesions in dairy cows with idiopathic atrial fibrillation. J Vet Med Sci. 2001 Aug;63(8):873-8. doi: 10.1292/jvms.63.873. PMID: 11558542.

There is NO one best choice. It's all based on patient characteriistics, enabling us to tailor a treatment to the individual. What you need is a copy of the guidelines and I'll attach it. It's not a black-and-white world out there.

I am struck by the broad nature of some of the questions found on Research Gate. Many can be answered by Google. I think Research Gate is designed more for answers to esoteric research questions. Some of these questions actually sound as if someone is repeating a test question that they are trying to get an answer to.

I think the short answer is that inflammatory conditions contribute to but do not likely cause AF. There is insufficient data clarifying the actual role of inflammation and we know of no therapies specifically aimed at reducing inflammation that would/could reduce AF burden. [Ironically, I developed transient ulcerative colitis as the result of using ibuprofen regularly]

Sepsis and other systemic infections are obvious standouts, but like all other disorders, including non-inflammatory conditions, keeping the diseases under control as best you can is just what the doctor ordered.

Rheumatoid arthritis is a disorder that has a known and significant association with AF, but more so in regards to coagulopathy. However, there is no data to support an increase in the CHADSVaSc score based on its presence. Most patients with RA get a CRP every 3 months and to know it is consistently under 10 is definitely reassuring, especially if their CHADSVasc score is on the fence. I attached a very nice review on the topic.

As we know that Oral anticoagulant ( Warfarin) is still considered as DOC for Valvular AF. But use of warfarin in nonvalvular AF is underused because of interaction issue , compliance and PT-INR monitoring . Other DOAC ( Direct acting oral anticoagulant) are available having unique properties of shirt onset time and stop it immediately before any major Surgery

A very compelling example, albeit perhaps very unusual, I once observed at a clinic in Colorado Springs at Pikes Peak Cardiovascular if I recall correctly, an echocardiogram of a patient. The patient had a clot in the left atria about the size of a golf ball. The clot was spinning with each heart beat.

When blood stops moving, it sometimes clots. When blood pools from ineffective pumping as in atrial fib. and although not due to atrial fibrillation in the case of LVADS, a s similar problem can be observed, the blood clots. Eventually pieces of the clot can break off and go elsewhere, like the brain, and there then a devastating thrombosis event.

When blood isn't moving, it can get sticky so to speak, and patients at risk for devastating events.

Saw another presentation once at Columbia Presbyterian in NYC, LVAD conference over St Patricks Day weekend in March 2016. A presentation was given on how much is not enough with respect to anti-coagulation therapy. The point of the presentation was there clearly a place at which when anti-coagulation levels dropped below a certain level, thrombus events occurred with much greater frequency. Also presented was a significant confounding variable was patient compliance with medication. When patients forgot to take there anticoagulation meds, and their levels dropped, there a big increase in thrombi adverse events in LVADs.

I suspect the same could be true in atrial fibrillation, perhaps not to the same degree, but important to consider. When patients are economically challenged, or challenged due to other things related to current times, even post pandemic, their abilities to maintain compliance likely also impaired due to any number of reasons or challenges. Because of this, it would not be surprising if it were to be found that there in addition to any 'other' medical reasons that might contribute to increase in thrombus events for those with atrial fibrillation, patients compliance with medication dosing, will likely be an additional challenge.

Balancing bleeding events increased risk on anti-coagulation therapy vs reduction of thrombus events in atrial fibrillation should be a consideration. Genotypic response to anti-coagulation therapy could be considered in patients with atrial fibrillation. Genotype tests have come a long way in the last decade and can provide a cost effective guide to how each patient may need dosing in anticoagulation therapy, this also has been a lesson learned from LVADS that could translate over to Afib. There are things utilized like the Gage Algorithm that are utilized in dosing guidance in LVADS anti thrombolytic therapy. Point being, there might also be an opportunity to look at genotypic guided dosing in anticoagulation therapy in Afib. Perhaps not practical but also possible is Anti factor 10 activity. This studied in some hospitals and not in others with respect to what anticoagulant chosen. for example, one major hospital system in Houston does utilize this technology, while another larger hospital system, does not. Clinical approach is not always the same as what theoretic approach might tell or suggest.

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.

You can use MIT-BIH Arrhythmia Database even though it is not entirely similar but hope it helps.

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.

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.

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.

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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Good luck ...

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

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.

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.

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.

Try CurvFit app for Windows

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.

The mechanisms of AF are likely to vary between patients, depending on factors such as genetic determinants, cardiovascular risk factors, and concomitant heart disease.

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.

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.

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.

One of the suggested mechanisms is the vagotonic action of digoxin.

Please see in Desk Reference of Clinical Pharmacology, Second Edition

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.

Dear Dr. Rigopoulos,

Thanks for the comments, with  some of them I completely agree, like Myocardial Contrast Echo, which well accepted practice and should be used in all.  Most importantly it may delineate aberrant supply, which is a major concern.  I do use in all cases.

Your statement that AV block is transient is correct, but literature does not support and surgeons are claiming that their technique has much lower need for pacemaker implant. (Except a recent report from Australia where they found <5% need of pacers in less than 55 years patients, similar to surgery).

Selecting the branch with"milking effect", I am not sure if safety of this technique has been tested or reported.  Your statement suggests you have some definite information of the reports, please share with us.

In our modified technique,

At the moment we are using MCE and guidance with Milking of septal arteries but my assumption is that in future may mot require another machine in cath lab or another professional, thus simplifying the safe procedure.

Thanks.

Thank you dear Paul 

thank you @saleh alkarim and @biswajit majumder 

these links are helpful

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

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)

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).

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.

Attached is a fairly typical NHS checklist.

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

bisoprolol in the minimal dose does not significant changes in pulmonary function test for the AF patients without acute asthma. The higher dose can influence the LUFU and also Symptoms in pat with AF and AB.

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. 

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.

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. 

Thank you very much for your answer. 

Much obliged and best regards.

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.

 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.

Dear Dr. Auerbach. As you very well say : Please recognize this is a highly debated area of research.

Therefore, there is no clear and indisputable evidence. (however, your viewpoint seems good). Best regards

NOAC: as simple as that. Presumably Pradaxa 2x150 mg - superior anticoagulation profile with acceptable bleeding complications.

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. 

What about cholchicine? It is recommended both in acute and chronic pericarditis and af suppression postoperatively.

https://my.americanheart.org/idc/groups/ahamah-public/@wcm/@sop/@scon/documents/downloadable/ucm_433742.pdf 

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. 

I think Dr. Sachdeva has given a complete answer and patient need to be observed periodically.

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.

thank you

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 

My pleasure.

Good luck.

"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!

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?

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.

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.

We are doing work in this area and have found that radio frequency ablation (RFA) provides more consistent lesions and resulting electrical isolation.  There is, however, significant user variability.  Other techniques (e.g., cryoablation, lasers) show potential promise but the implementation of the technology is limited to date.  Our techniques have centered on improving the tools for applying RFA consistently and predictably.  The site http://www.ablacor.com/ has background information.

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. 

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.

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..)

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.

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.

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

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.

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.

This is very much what I suspected and thank you for the thorough reply!

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,

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..

Thank you, Dr. Waldman. I'll see what I can do to get in touch with him.

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...

We have to start anticoagulation for a new patient after a cardioembolic stroke associated with non vascular AF almost every week. We always offer both (coumadins and new anticoagulants) to our patients. We strongly believe in the efficacy of each medication when it is well indicated and well monitored. We do the follow up and monitor closely if a patient is treated with coumadin. But It´s very interesting the fact that many patients are choosing the new anticoagulants in order to avoid annoyng frequent blood test and frequent visit to the clinic. Taking into cosideration clinical characteristics of the patients, interactions with drugs, etc, we usually choose Dabigatran 150 mg twice a day for younger patients with less commorbidities. At the other hand, older patients with more risk of bleeding or more stroke risk factors we usually choose Rivaroxaban 20 mg once a day or Dabigatran 110 mg twice a day. We don´t have Apixaban yet. Our choise is based on the characteristics of the patients that participated in the trials of Dabigatran and Rivaroxaban. Kidney and liver function is very important to be verified before starting any of these drugs. We are just starting the new journey of cardioembolic stroke with these new drugs and a lot of new information will come!

The epicor System may be a good tool for Afib ablation during cardiac surgery. The system uses high intensity focused ultrasound (HIFU) energy.

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.