Background and aims: Use of direct acting antivirals (DAAs) has allowed to clear HCV in almost all patients even in the presence of advanced cirrhosis. Although it has been suggested that cirrhotic portal hypertension may regress after SVR, the ultimate effect of HCV clearance on the development and progression of oesophagogastric varices (OV) is still unexplored. We assessed in a prospective cohort of patients with cirrhosis the evolution of endoscopic features of portal hypertension induced by SVR obtained with DAAs.Method: 321 consecutive patients (mean age: 65.1 ± 10.5, males: 58%) with HCV Child-Pugh A cirrhosis treated with DAAs were enrolled between January 2015 and May 2016. All patients underwent esophagogastroscopy (EGS), liver ultrasound (US), liver stiffness measurement (LSM) by Transient Elastography and laboratory tests before the starting DAAs and after achieving SVR. LS * spleen diameter/platelet ratio (LSPS) was calculated as previously described .Results: Forty-one patients were excluded from the analysis, 32(10%) since they had F2/F3 OV at baseline, and 9(2.8%) since they did not achieve SVR. Overall, 280 SVR patients were analysed. At baseline, 100 patients (35.7%) did not have OV and 180(64.3%) had small OV. None received beta-blockers. After a median time of 24.6 months EGS showed de novo development of OV in 24/100(24%) patients and progression from F1 to F2/F3 OV in 30/180 patients (16.7%), p = 0.68 by Kaplan–Meier. By Cox regression analysis, LSPS as continuum variable (HR: 1.06, CI95%: 1.01–1.11, p = 0.025) or at a cut off ≥ 3(HR: 3.16, CI95%: 1.64–6.09, p = 0.001) was associated with OV progression. Age (p = 0.15), gender (p = 0.93) and BMI (p = 0.07) did not correlate with progression of OV.Conclusion: Progression of clinically significant portal hypertension, as assessed by the evolution of oesophagogastric varices, is not uncommon among patients with HCV cirrhosis after HCV clearance. Non-invasive evaluation using combined data of LS, spleen diameter, and platelet count can assist in identifying patients in whom portal hypertension is likely to progress notwithstanding SVR.