8^th Global Cardiologists and Echocardiography Annual Meeting

Biography

Biography: Ersel Onrat

Abstract

Atrial fibrillation (AF) is the most common dysrhythmia and its incidence rises with aging. The cost of AF treatment per person ascends and it will ascends in the future, because of extending life span. AF impairs quality of life and increases mortality due to complications like thromboembolic events and heart failure. New treatments for AF are being developed every 5-10 years and also much more money is spent for these treatments. For all that an innovative method isn’t invented in AF treatment. The current treatment methods are not suitable for all patients. The new oral anticoagulants cannot be used instead of all warfarin indication, atrial appendix closure devices cannot be used for all patients and left atrial ablations cannot be performed in all patients. In fact, if we know the pathophysiology of AF, AF treatment is able to achieve greater success. Figure 1: Kourliouros et al. Am. Heart J 2009; 157: 243-252. There are 3 different parts in AF pathophysiology. These are structural remodeling, electrical remodeling and inflammation. Each of them associated with the others. One of these factors triggers AF, then the others penetrate the AF pathophysiology. Structural Remodelling: Atrial dilatation is the initiation factor in patients with mitral valve disease and AF. Atrial dilatation firstly occurs, then interstitial fibrosis and subsequent heterogeneity of conduction are formed. Structural changes like fibrosis, cellular hypertrophy and degeneration have been shown in patients with operated mitral valve and AF. Also these structural remodeling happened in experimental model AF (induced by atrial pacing). In experimental model and valvular disease with AF, there are some increased biomarker like collagen types, matrix metalloproteinase types, tumour growth factor beta-1 (TGFBeta-1), fibrillin, YKL 40, periostin, fibronectin, etc.,. There are two ways in atrial fibrosis, Angiotensin II and TGFBeta-1. It was shown that, pharmacologic treatment with some drugs have been decreased atrial fibrosis and altered atrial remodeling. These drugs are pioglitazone, candesartan, enalapril, spironolactone diacylglycerol kinase zeta, tetramethylpyrazine, pirfenidone or tranilast effect especially Angiotensin II and TGFBeat-1 pathways. Tranilast, pirfenidone, tetramethylpyrazine and diacylglycerol kinase zeta affects TGF Beta-1 pathway. Candesartan, enalapril and spironolactone fixes Angiotensin II pathway. It seems that these drugs can be new theraphy to reduce atrial fibrosis and to prevent atrial fibrillation formation by antifibrotic drugs and renin angiotensin system blockers. Atrial fibrosis is not only pathology in the formation of AF, but also the amount of atrial fibrosis detects the success of AF ablation. In the future, AF treatment with these drugs can be investigated. Imflammation: The inflammatory biomarkers level was higher in the patients with AF indicates that inflammation is also an important risk factor for AF. Especially after cardiac surgery, AF occurs in some patients due to imflammation. Corticosteroids, nonsteroid antiimflammatory drugs and colchicine prevent atrial fibrillation formation in postoperative period after cardiac surgery. These findings support postoperative AF is associated with imflammation. In population based cohort study, it was shown that high CRP levels were independently associated with future AF development in 6.5 years. Also CRP levels can predict successful cardioversion rate in patients with AF. The other imflamatuar biomarkers are C3, C4 and interleukin-6 which are asoociated with AF. All of these imflamatuar factors are associated with the amount of epicardial adipose tissue which is not only risk factor for AF but also as a prognostic factor for the determining the success of AF ablation. Up to now some cytokines secreted from adipose tissue were high level in patients with AF. These cytokines are Activin A, Resistin, Adiponectin and YKL 40. Conclusion: In the future, it seems that AF treatment model may be associated with the pathophysiological part (antifibrotic drugs, adipokines derivatives or blockers) of AF.