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ESC Congress 2003: Inflammatory genes: "bad genes" for atrial fibrillation?

August 31, 2003

IMPORTANT: This press release accompanies a poster or oral session given at the ESC Congress 2003. Written by the investigator himself/herself, this press release does not necessarily reflect the opinion of the European Society of Cardiology

Atrial fibrillation is characterized by rapid and irregular activation of the atrium. Data from the international literature indicate that atrial fibrillation is the most common arrhythmia affecting from about 0.4% and up to 2% in the general population and from 7% to 14% in the elderly. Atrial fibrillation is associated with a 6-fold increase in the risk of stroke and thromboembolism and it represents a considerable financial burden for the health-care system.

Atrial fibrillation, in fact, results in stasis of blood flow in the left atrium, leading to a high risk of thrombus formation and cerebral and peripheral embolism, with consequent increase in mortality and physical disability.

A number of risk factors are frequently associated with increased risk of atrial fibrillation namely diabetes, hypertension, heart failure, rheumatic and non rheumatic valve diseases and myocardial infarction, but we do not completely know the exact mechanisms by which atrial fibrillation occurs. 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. However, little data are available on the possible role of genetic defects as risk factors for the development of atrial fibrillation.

On this purpose, we evaluated 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.

Our study was carried out in the Department of Medical and Surgical Critical Care of the University of Florence, Italy. It was funded by a grant from the Italian Government.

We studied 150 patients 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, and 150 healthy subjects, recruited from blood donors and staff of our hospital, age and sex-matched.   

In all subjects the DNA analysis was performed by using an innovative microarray technology and the genetic defects into the inflammatory genes (interleukin-1beta, interleukin-6 and C Reactive protein) were investigated.

Our results showed that the frequencies of the mutated alleles of the C-Reactive Protein 1059G/C and Interleukin 6 -174G/C polymorphisms in atrial fibrillation patients did not differ from those observed in the healthy subjects without atrial fibrillation. As to Interleukin-1 beta (IL-1Beta) -511C/T polymorphism, the mutated allele IL-1Beta -511 T is present in a higher percentage in atrial fibrillation patients in comparison to control subjects.

Our preliminary findings need to be confirmed in a larger number of atrial fibrillation patients. 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 provide new insights into the role of inflammation in atrial fibrillation and may form a basis for new, well tolerated pharmacological approaches to the control of thromboembolic risk in atrial fibrillation.

Professor Gian Franco Gensini
Department of Surgical and Critical Care Medicine, University of Florence; Careggi Hospital, Azienda Ospedaliera Careggi, Florence, Italy

European Society of Cardiology (ESC)