Related Experiment Video
Updated: Jan 24, 2026
05:12
Transesophageal Atrial Burst Pacing for Atrial Fibrillation Induction in Rats
Published on: February 14, 2022
3.8K
Anticoagulation Resumption After Stroke from Atrial Fibrillation
Brian Mac Grory1, Shane Flood2, Matthew Schrag3
1Department of Neurology, Warren Alpert Medical School of Brown University, Providence, RI, USA.
Current Atherosclerosis Reports
|May 22, 2019
Summary
Resuming anticoagulation after stroke from atrial fibrillation requires balancing recurrent stroke risk against hemorrhagic transformation. Current research limitations highlight the need for personalized treatment strategies based on individual patient factors.
Area of Science:
- Neurology
- Cardiology
- Pharmacology
Background:
- Atrial fibrillation increases stroke risk, necessitating anticoagulation.
- Ischemic stroke carries a risk of recurrent stroke and hemorrhagic transformation, especially in the early post-stroke period.
- Early anticoagulation resumption after stroke is complex due to competing risks.
Purpose of the Study:
- To review existing literature on anticoagulation resumption timing after stroke in atrial fibrillation patients.
- To identify challenges and limitations in current research regarding anticoagulation resumption protocols.
- To emphasize the need for personalized treatment decisions balancing risks.
Main Methods:
- Literature review of studies on anticoagulation resumption after ischemic stroke.
- Analysis of risks associated with recurrent stroke and hemorrhagic transformation.
- Examination of ongoing clinical trials comparing anticoagulant resumption protocols.
Main Results:
- Oral anticoagulants significantly reduce the relative risk of recurrent stroke.
- The early post-stroke period (2 weeks) presents elevated risks of both recurrent stroke and hemorrhagic transformation.
- Existing studies have limitations in accounting for crucial patient-specific factors like infarct size and bleeding diatheses.
Conclusions:
- The decision to resume anticoagulation requires a careful balance between preventing recurrent stroke and avoiding hemorrhagic transformation.
- Personalized treatment strategies are crucial, considering individual patient factors not fully addressed in current research.
- Ongoing trials aim to refine anticoagulant resumption protocols, particularly for non-vitamin K oral anticoagulant users.
Related Concept Videos
03:03Amyloid Fibrils
11.7K
Amyloid fibrils are aggregates of misfolded proteins. Under most circumstances, misfolded proteins are either refolded by chaperone proteins or degraded by the proteasome. However, in the case of a mutation or a disease, these proteins can accumulate to form large clusters and often further assemble to form elongated fibers, called fibrils.
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
Amyloid deposits were observed as early as 1639 in the liver and the spleen. In 1854, Rudolph Virchow performed iodine staining,...
11.7K
03:03Amyloid Fibrils
6.4K
6.4K
01:18Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
2.2K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
2.2K
01:11Fibril-associated Collagen
3.3K
Fibril-associated collagens are a type of collagens present in the extracellular matrix with interrupted triple helices or FACIT (Fibril-associated collagens interrupted triple-helices). FACIT help connect and attach the collagen fibrils with each other as well as with other proteins of the extracellular matrix.
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
For example, the type II collagen fibrils in cartilage have covalently bound type IX fibril-associated collagens at regular intervals. Other types of fibril-associated collagens are...
3.3K
01:30Anticoagulant Drugs: Low-Molecular-Weight Heparins
1.8K
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
1.8K
01:27Regulation of Stroke Volume
4.8K
The regulation of stroke volume, which is the amount of blood the heart pumps out during each heartbeat, is critical for maintaining a healthy circulatory system. Stroke volume is influenced by three main factors: preload, contractility, and afterload.
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
Preload refers to the degree of stretch on the heart before it contracts. It's analogous to the stretching of a rubber band; the more it's stretched, the more forcefully it snaps back. This concept is encapsulated in the Frank-Starling law of the...
4.8K