Author information
1 Liver Unit/ Division of Integrative Systems Medicine and Digestive Disease, Department of Surgery and Cancer, St Mary's Hospital Campus, Imperial College London, London, UK.
2 Department of Surgery and Cancer, Centre for Computational and System Medicine, Imperial College London, London, UK.
3 Department of Computer Engineering, School of Applied Technology, Technological Educational Institute of Epirus, Arta, Greece.
4 Department of Endocrinology, St Mary's Hospital, Imperial College Healthcare NHS Trust, London, UK.
5 National Heart and Lung Institute, Hammersmith Hospital, Imperial College London, London, UK.
6 Department of Cellular Pathology, St Mary's Hospital, Imperial College Healthcare NHS Trust, London, UK.
Abstract
BACKGROUND:
Atherosclerotic cardiovascular disease is a key cause of morbidity in non-alcoholic fatty liver disease (NAFLD) but appropriate means to predict major acute cardiovascular events (MACE) are lacking.
AIM:
To design a bespoke cardiovascular risk score in NAFLD.
METHODS:
A retrospective derivation (2008-2016, 356 patients) and a prospective validation (2016- 2017, 111 patients) NAFLD cohort study was performed. Clinical and biochemical data were recorded at enrolment and mean platelet volume (MPV), Qrisk2 and Framingham scores were recorded one year prior to MACE (Cardiovascular death, acute coronary syndrome, stroke and transient ischaemic attack).
RESULTS:
The derivation and validation cohorts were well-matched, with MACE prevalence 12.6% and 12%, respectively. On univariate analysis, age, diabetes, advanced fibrosis, collagen proportionate area >5%, MPV and liver stiffness were associated with MACE. After multivariate analysis, age, diabetes and MPV remained independently predictive of MACE. The "NAFLD CV-risk score" was generated using binary logistic regression: 0.06*(Age) + 0.963*(MPV) + 0.26*(DM1 ) - 16.44; 1 Diabetes mellitus: 1: present; 2: absent. (AUROC 0.84). A cut-off of -3.98 gave a sensitivity 97%, specificity 27%, PPV 16%, and NPV 99%. An MPV alone of >10.05 gave a sensitivity 97%, specificity 59%, PPV 24% and NPV 97% (AUROC 0.83). Validation cohort AUROCs were comparable at 0.77 (NAFLD CV-risk) and 0.72 (MPV). In the full cohort, the NAFLD CV-risk score and MPV outperformed both Qrisk2 and Framingham scores.
CONCLUSIONS:
The NAFLD CV risk score and MPV accurately predict 1-year risk of MACE, thereby allowing better identification of patients that require optimisation of their cardiovascular risk profile.