New Research Yields Insight into Stroke Mechanism for Atrial Fibrillation Patients
Atrial fibrosis, not atrial fibrillation type, linked to afib stroke
February 24, 2011 — New research showing a link between atrial fibrosis (hardened tissue in the atrium) and stroke was just published in the Journal of the American College of Cardiology. Doctors at the Comprehensive Arrhythmia Research and Management Center (CARMA) in Utah have been studying the relationship between atrial fibrillation, atrial fibrosis, and catheter ablation outcomes for many years. Now, they’ve applied their knowledge of quantifying atrial fibrosis to stroke risk assessment.
Atrial Fibrosis and Remodeling
If left untreated, atrial fibrillation can lead to atrial fibrosis, which is called “remodeling” or “substrate modification.” Once the atrial substrate has been modified, it becomes increasingly difficult to treat atrial fibrillation. In the past, it was thought that only persistent forms of atrial fibrillation caused substrate modification. However, doctors at CARMA have shown that even patients with paroxysmal afib can have extensive remodeling. Dr. Nassir Marrouche, Executive Director of CARMA, presented research on this and how atrial fibrosis can affect catheter ablation outcomes at Heart Rhythm Society 2010.
Atrial Fibrosis and Stroke
Researchers at CARMA evaluated the atrial fibrosis of 387 patients using delayed enhancement magnetic resonance imaging (DE-MRI). Patients were categorized into four groups depending on the level of fibrosis. Stage I patients had the lowest amount of atrial fibrosis, at less than 8.5% of the left atrium. Stage IV patients had the highest, at more than 21.1% of the left atrium.
Analysis showed that extensive substrate modification was independently associated with stroke. Stage IV patients were four times more likely to have a stroke than patients with a low level of atrial fibrosis. (The odds ratio for having a stroke was 3.91 for Stage IV patients compared to only 0.07 for Stage I patients.)
The researchers compared the level of remodeling with patients’ CHADS2 risk scores. Of note, 16.5% of patients with a CHADS2 score of 0 (low risk) and 18.5% of patients with a CHADS2 score of 1 (intermediate risk) had Stage IV atrial fibrosis.
The study had two other important findings. First, the type of atrial fibrillation, paroxysmal or persistent, did not have an impact on the likelihood of stroke rate. Second, gender did. Women were three times more likely to have a stroke than men. Because men tend to get treatment for atrial fibrillation sooner than women, the researchers hypothesized that women in the study had more extensive remodeling than men, which led to a higher stroke rate.
Although doctors at CARMA don’t believe that atrial fibrosis evaluation should replace CHADS2, they think their staging system could help determine which patients should be placed on anticoagulation. For instance, a patient may be deemed to have low stroke risk based on a CHADS2 score of zero, but if that patient has extensive atrial fibrosis, that patient may be at high risk for stroke and need to be placed on anticoagulation medication.
Comment: Many afib patients are placed on rate control medication, which helps alleviate the symptoms of atrial fibrillation but doesn’t put the heart back into normal sinus rhythm. Thus, atrial fibrillation can continue and lead to substrate modification, which allows more afib to occur (“Afib begets afib”). This new research from CARMA shows that this also increases the risk of stroke. If this applies to you, this new finding may be a subject for discussion with your doctor.
See related information:
- Atrial Fibrillation as an Independent Risk Factor for Stroke: the Framingham Study
- Detection and Quantification of Left Atrial Structural Remodeling
- Stroke Risks from Afib
- Stroke Risk Factors
- Stroke Warning Signs
Disclaimer: Patients come first at StopAfib.org, and we do not compromise on that. For transparency, we note that Dr. Nassir Marrouche is on the StopAfib.org medical advisory board. However, he did not contribute to, or review, this article prior to publication.