Non-alcoholic fatty liver disease (NAFLD) progressing to non-alcoholic steatohepatitis (NASH), cirrhosis, end-stage liver disease (ESRD), and hepatocellular carcinoma (HCC) is emerging as a global epidemic. Obesity, diabetes, and metabolic syndrome are some of the leading risk factors for NAFLD. The most prevalent treatment to stop the progression is aimed at dietary modification and lifestyle changes. Bariatric surgery is indicated for patients with morbid obesity with NAFLD. The progression of NAFLD to NASH and HCC can be arrested at various stages of pathogenesis by the already prevalent drugs and the emerging newer molecular and genetic targets. This review article analyzed various preclinical animal trials and clinical trials and has summarized various groups of drugs that can be life-altering in patients diagnosed with NAFLD. This study also discusses the obstacles in taking these clinical trials to bedside treatment.

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Introduction: Surgical aortic valve replacement (SAVR) is recommended in symptomatic severe aortic regurgitation (AR) or asymptomatic severe AR with reduced left ventricular (LV) ejection fraction (LVEF). Although most patients have improvement in LV dimensions and LVEF early (< 6 months) after SAVR, severe baseline LV enlargement and reduced LVEF, along with persistent LV dilation after SAVR, carries a worse prognosis. We present a case in which a patient with these features had complete recovery of LVEF late (> 9 months) after SAVR for severe AR. Case Description: A healthy 62-year-old male presented with dyspnea and chest pain. Cardiac workup was significant for ECG showing left bundle branch block; both transthoracic and trans-esophageal echocardiograms showed bicuspid aortic valve with severe AR (Eccentric jet, pressure half time (PHT): 221 msec, jet width > 60% of LV outflow tract diameter), severely reduced LVEF 20-25%, and severe LV dilation (LVESD of 75 mm), and cardiac catheterization showed mild coronary disease. SAVR was performed without complications and heart failure therapy initiated. Patient declined cardiac resynchronization therapy. The LVEF and LVESD were persistently abnormal in TTE at 5 and 9 months. The TTE at 21 months showed normalization, with LVEF of 55% and LVESD of 46 mm, despite no prior improvement (Figure). Discussion: In severe AR following SAVR, volume overload reduction results in LV size reduction and improved LVEF, usually within a few months and in those with smaller baseline LV dimensions. Some studies suggest a specific LV dimension to perform SAVR. This report indicates that SAVR should not be excluded based on severe LV dilation alone. Conclusion: The incidence and mechanisms of delayed reverse cardiac remodeling in severe AR after SAVR and optimal timing of decision about device placement needs further investigation.