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Non-alcoholic fatty liver disease (NAFLD) has emerged as an imperative public health problem worldwide. NAFLD is now the most common chronic liver disease in high-income countries, and is estimated to affect at least 25%–30% of the general population.1
NAFLD typically exists in a ‘milieu’ of altered metabolism, including abdominal obesity, insulin resistance, dysglycaemia and atherogenic dyslipidaemia.1 Cumulatively, these aetiological factors increase the risk for cardiovascular disease (CVD), and so it is, perhaps, not surprising that CVD is the leading cause of mortality in patients with NAFLD.
The challenge over the past decade has been to tease apart the complex inter-relationships between NAFLD and these aetiological factors, to establish whether NAFLD per se increases the risk of developing CVD. The validation of NAFLD as an independent risk factor would have direct relevance for primary preventative strategies against CVD.
A prior narrative review published in 2010 by Ghouri et al2 concluded that a diagnosis of NAFLD was not sufficient to consider patients as being at high risk for CVD, and that the evidence base for CVD risk screening based on the presence of NAFLD was weak.
However, over the years increasing evidence supports the existence of a strong association between NAFLD and increased CVD risk. Several cross-sectional studies have consistently demonstrated that NAFLD was associated with both clinically manifest CVD and various markers of subclinical atherosclerosis (including also increased coronary artery calcium (CAC) score).3 All these associations were independent of conventional CVD risk factors across a wide range of patient populations. Moreover, NAFLD was also associated with an increased prevalence of …