Acetylsalicylic acid (ASA) currently remains the main drug for antiplatelet therapy in patients with coronary heart disease (CHD), but a significant number of patients receiving ASA don’t have suppression of platelet aggregation. Laboratory methods for determining the aggregation aspirin resistance (AAR) are not standardized and not available in each laboratory. The aim of the study was to identify clinical and biochemical predictors of AAR in hospital stage in patients with CHD. Material and methods. The study included 100 patients with various forms of CHD without acute myocardial infarction who are receiving ASA in dose 100 mg per day. In addition to routine laboratory tests in patients was determined in the blood concentration of natriuretic peptide B-type, D-dimer, the activity of the MB fraction of creatine kinase, the protein concentration in the urine and platelet aggregation by Born and O’Brien’s method with medium and high doses of the inducer of aggregation ADP. The presence phase of the release on aggregation curve in patients receiving ASA was considered as the presence of AAR. Results. Initially AAR was diagnosed in 14% of patients. A number of laboratory and clinical parameters in patients with initial AAR and without initial AAR had statistically significant differences. Patients with AAD had statistically significant higher concentration of protein in the urine. Of the 86 patients without initial AAR in 43% AAR developed during hospital stage, 57% didn’t have identified AAP in-hospital stage. Patients with hospital AAR had statistically significantly more frequently headache, pain in the heart area in the chest, fatigue, shortness of breath on exertion, weakness. Thus there was not any statistically significant differences in the biochemical parameters. Factor analysis for statistically significant factors in the development of AAR showed the highest value of the indicator «pain in the heart area in the chest». Conclusion. The results of this study demonstrate the possibility of early prediction of AAR based on clinical data without laboratory testing of platelet aggregation. It will allow to begin early correction of antiplatelet therapy.