Objective: To examine the hypothesis that major extracellular matrix (ECM) proteins are expressed differently in the left atrial tissue of patients in sinus rhythm (SR), lone atrial fibrillation (AF), and AF with underlying mitral valve disease (MVD). Design: Case-control study. Patients: 118 patients with lone AF, MVD+AF, and SR.

Atrial fibrillation is associated with an up-regulation of AT(1) in LA, but not in RA, and did not appear to influence the AT(2) expression in the atrium. Because we found an enhanced expression of AT(1)in the LA, we conclude that AT(1) might be involved in the pathogenesis of AF in the LA.

Objective: To test the hypothesis that atrial fibrillation (AF) is associated with changes in the expression of connexins 40 and 43 in the left atrium with more pronounced changes in mitral valve disease than in lone AF. Methods: Protein concentrations of connexin 40 and connexin 43 were analysed in left atrial tissue of patients undergoing cardiac surgery. One group of patients had lone AF (n = 41), one group had AF and mitral valve repair (n = 36), and one group in sinus rhythm served as controls (n = 15). Results: Western blot analysis of connexin 40 and connexin 43 expression showed an increase of both gap junctional proteins (connexin 43 . connexin 40) in patients with AF of all forms compared with patients in sinus rhythm (p = 0.01 and p = 0.011, respectively). Subgroup analysis showed increased concentrations of connexin 40 in lone AF and AF with mitral valve disease compared with sinus rhythm (p = 0.06 and p = 0.029, respectively), whereas the same analysis for connexin 43 reached significance only in the mitral valve disease group (p = 0.031). No differences in connexin 40 and connexin 43 expression were detectable between lone AF and AF with mitral valve disease. Within the groups connexin 40 and connexin 43 expression did not differ between patients with paroxysmal AF and patients with chronic AF.Conclusion: The present study shows for the first time that AF can induce changes in the left atrium with increased connexin expression. Furthermore, no systematic differences between patients with paroxysmal and chronic AF were detected.

Intensive endurance training is able to cause a distinct pattern of functional and structural changes of the cardiovascular system. In an unknown proportion of athletes a so called "athlete's heart" develops. There is an overlap between this type of physiologic cardiac hypertrophy and mild forms of hypertrophic cardiomyopathy (HCM), the most common genetic disorder of the cardiovascular system with a prevalence of 0.2%. HCM is caused by mutations in 14 genes coding for sarcomere proteins. In the literature up to 50% of cases of sudden cardiac death (SCD) in younger sportsmen were connected to hypertrophic cardiomyopathy. It is therefore the most common cause of SCD in highly trained young athletes. Because of this data a great interest in distinguishing these two diagnoses exists. Apart from clinical examination and some non-specific ECG-changes, Echocardiography is the method of choice. The athlete's heart shows an eccentric biventricular hypertrophy with wall thicknesses under 15 mm and a moderately dilated left ventricle (LVEDD up to 58 mm). HCM is commonly characterized by asymmetric left ventricular hypertrophy with a reduced LV-diameter. In up to 70% of cases left ventricular outflow tract obstruction is evident during stress echocardiography. Systolic function is normal in highly trained athletes and the majority of HCM patients as well. There are important differences regarding diastolic filling patterns. Physiological hypertrophy is consistent with a normal diastolic function with even increased early diastolic filling. In case of HCM diastolic dysfunction (mostly relaxation disturbances) occurs in the majority of patients and is therefore inconsistent with an athlete's heart. If the diagnosis could not be stated using echocardiography, methods like cardiac-MRI, metabolic exercise testing, histological studies of endomyocardial biopsies and genetic testing can provide further information. A correct diagnosis may on the one hand prevent some athletes from sudden cardiac death. On the other hand sportsmen with an athlete's heart are reassured and able to continue as competitors. New insights into electrophysiological changes during physiological hypertrophy could probably change this view.