Most patients with atrial fibrillation (AF) should receive long-term oral anticoagulation to decrease the risk of ischemic stroke and other embolic events.

Dear Dr. Faezeh Khodadadi

Please, read this information from a review (reference is indicated below, bold accentuation by me):

MECHANISMS OF THROMBOEMBOLISM IN ATRIAL FIBRILLATION

Left atrial thrombi are found in up to 14% of patients in whom AF lasts more than 2 days by transesophageal echocardiography (TEE); thrombi size ranges between 0.2 and 4.2 cm.

In addition, there is a small but significant chance of LA thrombus formation despite oral anticoagulation treatment in patients with AF. TEE revealed LA thrombus in 1.6% of patients treated with warfarin for at least 6 months. Most often, thromboembolism occurs during episodes of AF, or in the first 10 days after conversion to sinus rhythm. AF is characterized by disorganized electrical activity in the atria, resulting in ineffective irregular contraction and incomplete ejection of blood from the atria into the ventricles and stasis of blood, especially within the left atrial appendage (LAA), which is the main source of thrombus formation in patients with AF. The LAA is the main site of thrombus formation in AF, and more than 90% of the thrombi found in patients with nonvalvular AF and 57% found in valvular AF are formed in the LAA.

Beside blood stasis in the LAA, other components of the Virchow’s triad, such as structural heart disease with endocardial damage and hypercoagulable state (caused by abnormalities in platelet and hemostatic variables) play roles in thrombogenic tendency among patients with AF. AF results in increased platelet activation (detected by increasing platelet P-selectin) and thrombin generation (detected by increasing thrombin-antithrombin complex) especially in circulation and to a greater extent in LA. In addition, AF leads to endothelial dysfunction (detected by increasing asymmetric dimethylarginine) and inflammation (detected by increasing soluble cluster of differentiation 40 [CD40] ligand). Patients with AF have more than 2-fold higher circulating levels of CRP (a marker of systemic inflammation) compared with those without AF, and CRP level increase is more prominent in persistent AF compared with paroxysmal AF. Some small studies showed that systemic inflammation has a significant role in thromboembolism among patients with AF.

Therefore the patients with AF should take anticoagulants for prevention of thrombi formation.

https://www.cardiacep.theclinics.com/article/S1877-9182(19)30138-8/fulltext

to reduce the risk of thromboembolization

@Gennadiy Taradin

Dear.Dr. Taradin

Thank you for your response. The information, you sent was perfect.

@Jasim Al Hayali

Yes👍

Hello Gennady Taradin

Thank you for that extra information. Do you, or Faezeh Khodadadi or Jasim Al Hayali have any further advice regarding whether to use warfarin or the newer anti-coagulant medications (eg rivaroxaban, apixaban)?

Anticoagulation in AF patients required because of systemic embolization of clot lin the form CVA, Renal Ischemia , Peripheral vascular disease leads to fatal outcome . Most of the cause of AF is Cardiac origin

Stagnation of blood in atria leads to coagulation of blood that might lead to clot embolisation causing stroke and peripheral vascular disease . Anti cougulation therapy in patients suffering from AF is recommended.

Right told by A Mathur, Loss of atrial kick lead to stagnation of blood in atria , that get clotted lead to systemic embolization . Most of recommendation suggested the use of anticoagulant to prevent morbidity and mortility

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.

Nicely explained by Scott Corron .

thank you Alok Kumar Bharti

To reduce blood clots and reduce the risk of stroke, patients may take blood-thinning drugs, such as anticoagulants and antiplatelet agents.

There is increased risk of systemic thromboembolism if anticoagulant has not started.Some study recommend that even you can start prophylactic anticoagulant in patients having risk of atrial fibrillation in setting of valvular heart disease particularly Mitral stenosis in pregnancy until and unless contraindicated ( First Trimester)

Patients with atrial fibrillation are at high risk of thrombus formation and hence increased risk of cardioembolic stroke. Anticoagulants reduce this risk significantly.

As we all know that Patient with atrial Fibrillation having increased risk of thromboembolic event . So Prophylactic use of anticoagulant , reduces the risk of thromboembolic events. Anticoagulation required before cardioversion in such type of patients , otherwise thromboembolic event may occured during cardioversion