Coronary heart disease (CHD) causes atrial fibrillation (AF) in 20% of cases. Antithrombotic therapy is an essential component of AF treatment. Current guidelines do not provide an exact answer on the question of optimal antithrombotic therapy scheme in patients with CHD and AF. It is well known that the main link in CHD pathogenesis is lipid metabolism changes. Fatty acids (FA) are the basic building block of all lipids and the main energy source for cardiomyocytes. Effects of warfarin, new oral anticoagulants and antiplatelet combination therapy on atherosclerotic processes, especially FA metabolism, are still uninvestigated. Different antithrombotic therapy schemes have diversity impact on lipid and mineral metabolism, that can have pro- or antiarrhythmic properties. More detailed analysis and comparison of FA changes during the usage of different antitrombotic therapy schemes should be conducted to select the optimal scheme of antithrombotic therapy for CHD patients with AF.