High Cardiovascular Risk is Associated with the Degree of Fibrosis in Nonalcoholic Liver Disease - European Medical Journal


High Cardiovascular Risk is Associated with the Degree of Fibrosis in Nonalcoholic Liver Disease

2 Mins
*David Niederseer,1 Adam Bakula,1 Christian Datz2

The authors have declared no conflicts of interest.


The authors gratefully acknowledge A. Stadlmayr, U. Huber-Schoenauer, D. Lederer, C.M. Schmied, M. Ploederl, E. Aigner, and W. Patsch for their contributions to this work.

EMJ Cardiol. ;6[1]:59-60. Abstract Review No. AR5. .

Each article is made available under the terms of the Creative Commons Attribution-Non Commercial 4.0 License.

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Cardiovascular diseases remain the leading cause of death worldwide.1 Nonalcoholic fatty liver disease (NAFLD), encompassing steatosis, nonalcoholic steatohepatitis, and cirrhosis, has a global prevalence of 25% and is associated with increased liver-specific and cardiovascular mortality.2,3 Both groups of diseases have been associated with risk factors from the metabolic syndrome spectrum.4

In our study, we analysed a cohort of 2,138 asymptomatic subjects from the SAKKOPI registry (Salzburg Colon Cancer Prevention Initiative). From this cohort, subjects with a non-invasive diagnosis of NAFLD were selected. Subsequently, the correlation between two scores of 10-year cardiovascular risk, the Framingham Risk Score (FRS) and European Society of Cardiology (ESC) HeartScore (HS), and two scores estimating the degree of fibrosis in NAFLD based on risk factors and laboratory parameters, the NAFLD Fibrosis Score (NFS) and Fibrosis 4 Score (Fib4), was assessed in this subgroup.

While an association between NAFLD and cardiovascular morbidity and mortality has been shown previously, this study not only showed an increased cardiovascular risk in subjects diagnosed with NAFLD (no NAFLD: FRS: 5.5±5.2%, HS: 2.9±3.8%; NAFLD: FRS: 8.8±6.5%, HS: 3.7±4.1%; p<0.001) but also pointed to a progressive increase in cardiovascular risk with higher degrees of estimated liver fibrosis.

The FRS was 8.0±6.1%, 11.5±5.2%, and 10.8±6.4% in patients with a NFS F0–F2, NFS F3–F4, and indifferent NFS, respectively. HS showed a similar pattern: NFS F0–F2: 3.0±3.4%, NFS F3–F4: 7.0±5.7%, and indifferent NFS: 5.4±4.5%. NFS correlated significantly with FRS (r=0.18; p<0.001) and HS (r=0.27; p<0.001). Also, the Fib4 estimation of the degree of fibrosis correlated with FRS (r=0.25; p<0.001); in patients with F0–F1 according to Fib4, the FRS was 7.3±5.8%, while the FRS was 11.1±6.9% and 11.1±6.7% in patients with F3–F4 (Fib4) and indifferent Fib4, respectively. However, there was no correlation between Fib4 and the HS (r=0.02; p=0.55); the HS values, assessing cardiovascular risk, were F0–F1 (Fib4): 3.2±3.6%, F3–F4 (Fib4): 2.9±3.9%, and indifferent Fib4: 3.3±3.8%.

These results show the need for a high clinical suspicion for cardiovascular disease and a multidisciplinary approach to patients with NAFLD, especially those with a high degree of fibrosis. Furthermore, routine cardiovascular screening in this cohort of cardiovascular asymptomatic NAFLD patients should be considered. Screening strategies, including assessment of coexisting risk factors, physical examination, laboratory testing, cardiovascular risk scoring, and ultrasound imaging of the carotid arteries or CT coronary artery calcium scoring, have been proposed.5 However, the impact of such an approach on hard endpoints, as well as cost-effectiveness, needs further investigation in prospective studies. The symmetrical increase in cardiovascular risk and estimated liver fibrosis could also illustrate the systemic interactions underlying both diseases, including the traditional risk factors as well as other metabolic, inflammatory, vasoactive, and thrombogenic processes.5 This raises the question of whether emerging pharmacological treatment strategies for NAFLD or nonalcoholic steatohepatitis, which include antifibrotic agents,6 could result in the reduction of the cardiovascular burden in this significant patient population.

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