Non-Alcoholic Fatty Liver Disease as an Emerging Risk Factor for Heart Failure

Figures

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  Fig. 1. Forest plot and pooled estimates of the effect of NAFLD on the risk of new-onset heart failure in eleven eligible cohort studies, stratified by methodologies used for the diagnosis of NAFLD. Data are reproduced from Mantovani et al. [33•]

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  Fig. 2. Putative pathophysiological mechanisms underlying the association between NAFLD and risk of new-onset heart failure. In NAFLD, many alterations occur within the liver, resulting in an increased production of proinflammatory cytokines, worsening of insulin resistance, promotion of a more pronounced atherogenic lipid profile, exacerbation of oxidative stress, activation of the renin–angiotensin-aldosterone system (RAAS) and alteration of gut microbiota, accompanied by an increased production of bioactive microbial metabolites. All these factors, along with specific genetic polymorphisms, may lead microvascular dysfunction, myocardial remodeling and hypertrophy, as well as cardiac arrhythmias, thereby resulting in an increased long-term risk of new-onset heart failure

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  Fig. 3. (A) Forest plot and pooled estimates of the effect of GLP-1RAs on the absolute percentage of liver fat content as assessed by magnetic resonance-based techniques (n = 7 randomized controlled trials) when compared with placebo or reference therapy. Data are reproduced from Mantovani et al. [68]. (B) Forest plot and pooled estimates of the effect of SGLT-2 inhibitors on the absolute percentage of liver fat content as assessed by magnetic resonance-based techniques (n = 7 randomized controlled trials) when compared with placebo or reference therapy. Data are reproduced from Mantovani et al. [69].