Inflammation and atrial fibrillation
may have a genetic predisposition linked to expression of
pro-inflammatory proteins.
Researchers in Italy have discovered preliminary evidence that patients presenting at hospital with atrial fibrillation may have a genetic predisposition to the disease associated with the expression of high levels of pro-inflammatory proteins.
The team, led by Professor Gian Franco Gensini of the University of Florence and Careggi Hospital, reported their findings at the European Society of Cardiology congress in Vienna, Austria, which finishes today.
"Recently, the involvement of inflammation in atrial fibrillation has been documented, and high levels of pro-inflammatory proteins have been suggested to promote the persistence of atrial fibrillation by inducing structural and/or electrical remodeling of the atria," said the researchers. However, little data are available on the possible role of genetic defects as risk factors for the development of atrial fibrillation.
To examine this further, the scientists studied whether genetic defects in the sequence of the genes codifying for the inflammatory proteins could cause changes in the electrophysiological properties of the atria that, in turn, create a substrate for atrial fibrillation development.
The trial enrolled 150 patients who were admitted to the Electrophysiology Unit of the University of Florence for a pharmacological or electrical cardioversion, in order to restore the normal rhythm of the heart, as well as 150 healthy subjects, recruited from blood donors and staff at the hospital.
In all subjects, DNA analysis was performed using a microarray technology and the genetic defects into three inflammatory genes (coding for interleukin-1 beta, interleukin-6 and C reactive protein) were investigated.
The findings were mixed. There was no difference between the two groups in the frequency of mutations in the CRP allele (1059G/C) or that for IL-6 (6-174G/C). Intriguingly, however, a particular point mutation in the IL-1 beta gene - known as 511C/T - was present in a higher percentage of the atrial fibrillation patients than in controls.
"Our preliminary findings need to be confirmed in a larger number of atrial fibrillation patients,"said Prof Gensini. "Nevertheless, these data on the inflammatory gene polymorphisms, in addition to those regarding the increased inflammatory proteins found in circulating blood of atrial fibrillation patients … may form a basis for new, well tolerated pharmacological approaches to the control of thromboembolic risk in atrial fibrillation."
Atrial fibrillation affects up to 2 per cent of the general population - and 7 to 14 per cent of the elderly - and is associated with a six-fold increase in the risk of stroke and thromboembolism and a consequent increase in mortality and physical disability.
