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has been cited by the following article:

• TITLE: Higher expression of connexin 40 in human atrial tissue of patients with type 2 diabetes who have undergone a coronary artery bypass graft surgery

  AUTHORS: Pascal Daleau, Geneviève Comeau, Dominique Fournier, Dany Patoine, Patrick Mathieu, Paul Poirier

  KEYWORDS: Diabetes; Gap Junctions; Atrial Tissue; Atrial Fibrillation

  JOURNAL NAME: Health, Vol.2 No.3, March 25, 2010

  ABSTRACT: Background: Although cardiac-related mortality rates are declining for the general population in the United States, this is not the case for patients with diabetes. Diabetes is a significant independent predictor of atrial fibrillation (AF), the most common cardiac rhythm disturbance responsible for substantial morbidity and mortality. Objectives: This research was designed to evaluate properties of the atrial tissue between patients with and without type 2 diabetes. Heart rate variability (HRV) indices were calculated and expression of Kv1.5, connexin 43 (Cx43), and 40 (Cx40) were compared. Methods: Patients undergoing a CABG were enrolled: 10 with type 2 diabetes and 8 without diabetes, paired for age, gender and co-morbidities such as hypertension and dyslipidemia. All patients showed normal ejection fraction. A sample of right auricular appendix was taken during CABG and Kv1.5, Cx40 and Cx43 protein contents were determined by western blotting and normalized to α-tubulin level. Results: No HRV difference was found between patients with and without diabetes. Cx43 and Kv1.5 levels were unaffected by diabetes (p=0.20 and 0.07, respectively) whe- reas Cx40 content was significantly increased by 55% (p=0.02). Levels of Cx43 phosphorylated and non-phosphorylated forms were non-significantly decreased in patients with diabetes. Conclusion: Patients with type 2 diabetes had higher expression of Cx40 in the right auricular appendix tissue. In light of other studies having demonstrated a link between AF and Cx40 expression, it is possible that higher prevalence of AF in patients with diabetes is explained, at least partially, by differential expression of gap-junction proteins.