Inflammation and atrial fibrillation
LINKOPING, SWEDEN. It is well recognized that there is a significant association between the level of the inflammatory markers C-reactive protein (CRP), and interleukin-6 (IL-6) and atrial fibrillation (AF) in general. However, it is not clear whether inflammation causes AF or AF causes inflammation. There is also evidence that the observed relationship between inflammation and AF is due not to afib as such, but rather to the comorbid conditions (heart disease, hypertension) that generally accompany it. Swedish researchers now add the results of a small pilot study to the knowledge base regarding AF and inflammation.
Their study involved 28 patients scheduled for radiofrequency ablation. Ten had paroxysmal AF, while 8 had permanent AF. None had structural heart disease or inflammatory conditions. The control group consisted of 10 patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF. After catheterization, but before ablation all patients had blood samples drawn from the femoral vein, right atrium, coronary sinus, and the left and right pulmonary veins. The level of CRP, IL-6, and IL-8 (interleukin-8) were measured in the samples.
All study participants were found to have normal levels of CRP and IL-6, thus confirming that lone AF is not associated with an increased CRP or IL-6 level. The level of IL-8, however, was elevated in participants with permanent AF, specifically in the samples from the femoral vein, right atrium, and coronary sinus. Surprisingly, the IL-8 level was not elevated in the samples from the pulmonary veins. The researchers conclude that permanent AF is associated with a systemic inflammation, perhaps caused by vascular endothelial damage or dysfunction. They also speculate that IL-8 may somehow be consumed during passage through the lungs. Their final conclusion is that, "Taken together, these data seem to support the concept that the elevated levels of C-reactive protein and IL-6 in patients with AF reported in other studies were likely related to the presence of other co-morbid conditions that existed in these patient cohorts rather than to AF itself."
In an accompanying editorial two researchers point out that the increase in IL-8 may be related to endothelial activation, perhaps due to local perturbations in shear stress related to the irregular and fast heart rate experienced in permanent afib.
Liuba, I, et al. Source of inflammatory markers in patients with atrial fibrillation. Europace, Vol. 10, 2008, pp. 848-53
Melenovsky V and Lip, GYH. Interleukin-8 and atrial fibrillation. Europace, Vol. 10, 2008, pp. 784-85 (editorial)
Their study involved 28 patients scheduled for radiofrequency ablation. Ten had paroxysmal AF, while 8 had permanent AF. None had structural heart disease or inflammatory conditions. The control group consisted of 10 patients with Wolf-Parkinson-White (WPW) syndrome and no evidence of AF. After catheterization, but before ablation all patients had blood samples drawn from the femoral vein, right atrium, coronary sinus, and the left and right pulmonary veins. The level of CRP, IL-6, and IL-8 (interleukin-8) were measured in the samples.
All study participants were found to have normal levels of CRP and IL-6, thus confirming that lone AF is not associated with an increased CRP or IL-6 level. The level of IL-8, however, was elevated in participants with permanent AF, specifically in the samples from the femoral vein, right atrium, and coronary sinus. Surprisingly, the IL-8 level was not elevated in the samples from the pulmonary veins. The researchers conclude that permanent AF is associated with a systemic inflammation, perhaps caused by vascular endothelial damage or dysfunction. They also speculate that IL-8 may somehow be consumed during passage through the lungs. Their final conclusion is that, "Taken together, these data seem to support the concept that the elevated levels of C-reactive protein and IL-6 in patients with AF reported in other studies were likely related to the presence of other co-morbid conditions that existed in these patient cohorts rather than to AF itself."
In an accompanying editorial two researchers point out that the increase in IL-8 may be related to endothelial activation, perhaps due to local perturbations in shear stress related to the irregular and fast heart rate experienced in permanent afib.
Liuba, I, et al. Source of inflammatory markers in patients with atrial fibrillation. Europace, Vol. 10, 2008, pp. 848-53
Melenovsky V and Lip, GYH. Interleukin-8 and atrial fibrillation. Europace, Vol. 10, 2008, pp. 784-85 (editorial)
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A third donation method, beyond choosing either the Donate with PayPal or Donate with Credit/Debit card described elsewhere on this site, is for those who prefer to directly mail a check or money order to our business address at: The AFIB Report, A Non-Profit 501(c)(3) Corporation, C/O Shannon Dickson, P.O. Box 1016, Sedona, Arizona 86339. Any of the three donation options are fine with us based on each donor's preference, and with our sincere gratitude!
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