Abstract : Obesity is an excess of body fat and characterized by adipose tissue dysfunction causes an increase in proinflammatory adipocytokines, including C-Reactive Protein (CRP). Studies have shown the increasing of CRP levels in obese patients. C-reactive protein can cause left ventricular remodeling by myocyte biological remodeling, myocyte apoptosis and degradation of extracellular matrix which cause changes in myocardial mechanics and changes in left ventricular systolic function. This study aims to investigate the hs-CRP as a marker of subclinical left ventricle (LV) systolic dysfunction in young adults with obesity. This study was conducted in a single center with cross-sectional design to all young adults with obesity that worked in Hasan Sadikin General Hospital, Bandung, during August-November 2019. The inclusion was subject with normal ejection fraction (EF) > 50%. We excluded subject with poor echocardiography window, cardiac rhythm other than sinus rhythm, diabetes mellitus, hypertensive heart disease, history of coronary artery disease, congenital heart disease, valvular heart disease, dilated cardiomyopathy, restrictive cardiomyopathy, hypertrophic cardiomyopathy, pericardial disease, myocarditis, heart failure, infection, inflammatory disease , necrotic condition, malignancy, statin consumption, and dyslipidemia. Hs-CRP was measured by particle enhanced turbidimetric assay. Left ventricle function was measured by Global Longitudinal Strain (GLS) with speckle tracking echocardiography technique, performed by 2 independent examiners. The correlation between hs-CRP and GLS was analysed using Pearson correlation. A total of 29 patients (69.0% male, 30.55 + 5,38 years old) included in this study. The average of hs-CRP level was 8.8 (1.07 – 35.1) mg/L and the average of GLS was -19.18 ± 0.72%. After data log transformation of hs-CRP, there was a significant negative correlation (r= -0,542, p=0,001) between the hsCRP and GLS in young adults with obesity. Increasing hs-CRP level may predict subclinical LV systolic dysfunction in obese young adults with no other comorbidities