Letter: coronary atherosclerosis in patients with significant hepatic fibrosis in non‐alcoholic fatty liver disease—the role for non‐invasive testing

Abstract

EDITORS, With great interest we read the study by Dr Park and coauthors and would like to congratulate them on their findings linking liver stiffness in patient living with nonalcoholic fatty liver disease (NAFLD) to coronary artery calcification (CAC). NAFLD is a highly prevalent disease with a high economic burden.1 Excess mortality in these patients has been linked to advanced fibrosis stages defined as F3 and higher according to the NASH CRN classification.2 The current study3 utilises magnetic resonance elastography (MRE) to asses liver stiffness. While limited with regards to availability outside of clinical trials, MRE exhibits a high area under the receiver operated curve for the detection of hepatic fibrosis. The advanced disease stages— defined histologically as F3 and F4— are best detected using a cutoff of 3.64 kPa.4 The current study utilises the lower cut-\xadoff\xad ≥2.97\xad kPa,\xad thus\xad includes\xad also\xad significant\xad fibrosis\xad defined\xad as stage F2 and higher. In this groups of patients, a higher CAC score was detected compared to patients without increased liver stiffness.3 The value of MRE and its relevance over up to 5 years has recently been demonstrated in a study that linked liver stiffness to the risk of developing cirrhosis, hepatic decompensation and death.5 The current study evolves these previous findings by linking MREdefined hepatic disease stages to the extrahepatic manifestations that are seen in these patients.5 Coronary atherosclerosis and its sequelae are one of the major contributors to mortality in the western world. CAC is a specific feature of coronary atherosclerosis and can be quantified from noncontrast chest computed tomography (CT) examinations.6 Several largescale populationbased studies have linked the CAC score to future major adverse cardiac events in asymptomatic individuals.7,8 Hence, current international guidelines suggest CAC scoring as a supplementary tool for risk assessment to allow for guidelinebased management including preventive therapies.6 Additionally, CAC scoring has been demonstrated to be a costeffective decision tool that allows for risk stratification in patients eligible for statins according the American Heart Association.9 On the other hand, CAC scoring fails to identify noncalcified plaques and myocardial blood flow or perfusion reserve, which can only be assessed by contrast enhanced CT and MRI scans. The current study is remarkable for the following reasons. First, it links intermediate fibrosis to a clinically relevant cardiac phenotype. Second, noninvasive assessment of liver and heart disease will probably replace invasive procedures in the near future. Third, the close link between liver and heart disease is highlighted. These data expand the role of MRE beyond the estimation of hepatic fibrosis and provide evidence that individualised disease monitoring using noninvasive tools is feasible for risk assessment. Consequently, patients with NAFLD and at least F2 fibrosis should be evaluated to allow for guidelinebased risk estimation. It will only be through this type of association studies, that the broader medical community will recognise the high and currently unmet medical need to actively manage patients with NAFLD in the context of their metabolic multisystem disease, even before advanced stage of liver disease is reached.