Table 2.

Consensus statements on MAFLD and risk of CKD (using a Delphi procedure)

Domain and statements	Gradea
1. Epidemiology of MAFLD and risk of CVD
1.1 MAFLD is associated with an increased prevalence of CVD events compared with the non-MAFLD population	A
1.2 MAFLD is associated with an increased incidence of nonfatal CVD events compared with the non-MAFLD population	A
1.3 MAFLD is associated with an increased incidence of CVD mortality compared with the non-MAFLD population	A
1.4 The incidence of fatal and/or nonfatal CVD events in individuals with MAFLD is higher compared to that in the NAFLD population	B
1.5 MAFLD predicts better the risk of CVD events than NAFLD	B
1.6 Increasing severity of liver fibrosis is associated with higher CVD risk	A
1.7 Hepatic steatosis is associated with an increase in CVD risk	A
1.8 MAFLD is a risk factor for CVD events even after adjustment for traditional cardiovascular risk factors	A
2. Epidemiology of MAFLD and CVD outcomes
2.1 MAFLD is associated with greater carotid-artery intima-media thickness and increased risk of carotid atherosclerotic plaques	A
2.2 MAFLD is associated with atherosclerotic CVD events such as acute coronary syndromes	U
2.3 MAFLD is associated with increased risk of cardiac arrhythmias (mainly permanent atrial fibrillation)	A
2.4 MAFLD is associated with abnormal myocardial function and structure	A
3. Pathophysiological mechanisms linking MAFLD and CVD
3.1 MAFLD and CVD share multiple cardiometabolic risk factors, such as systemic low-grade inflammation, endothelial dysfunction, increased oxidative stress, insulin resistance and an atherogenic lipoprotein profile	A
3.2 Activation of the renin-angiotensin system is one of the mechanistic links between MAFLD and CVD risk	A
3.3 Some shared genetic polymorphisms (e.g., PNPLA3 I148M, and TM6SF2 E167K) may affect the risk of both MAFLD and CVD	A
3.4 Gut microbiota may play a role in both MAFLD and CVD	A
4. MAFLD and primary prevention of CVD
4.1 Carotid ultrasonography should be considered in most patients with MAFLD to improve CVD risk assessment	B
4.2 In CVD risk assessment, MAFLD may be considered a CVD risk factor	A
4.3 Screening for MAFLD should be considered in most patients with CVD	A
5. Managing MAFLD and the risk of CVD
5.1 Clinicians who manage patients with MAFLD should target cardiometabolic risk factors (overweight/obesity, diabetes, dyslipidemia and hypertension)	U
5.2 Lifestyle intervention (including a healthy dietary pattern, weight loss and regular physical exercise) is associated with improvement in both MAFLD and CVD	U
5.3 Alcohol avoidance of any type or amount is advisable in patients with MAFLD and CVD	A
5.4 Treatment with GLP-1RAs is beneficial in MAFLD patients with coexisting T2DM and may reduce CVD outcomes	U
5.5 Treatment with SGLT-2 inhibitors is beneficial in MAFLD patients with coexisting T2DM and may reduce CVD outcomes	U
5.6 Treatment with pioglitazone is beneficial in MAFLD patients and may reduce CVD outcomes, but potential adverse effects (e.g. weight gain, edema and worsening of pre-existing congestive heart failure) should be kept in mind	A
5.7 Statins (if required for the treatment of dyslipidemia or CVD risk reduction) should be prescribed for patients with MAFLD even with modestly elevated serum liver enzyme levels (< 3 ULN)	A
5.8 Bariatric surgery (if required in severely obese patients with MAFLD) improves liver histology features and reduces CVD risk	U

CVD cardiovascular disease; GLP-1RAs glucagon-like peptide-1 receptor agonists; MAFLD metabolic (dysfunction) associated fatty liver disease; PNPLA3 patatin-like phospholipase domain-containing protein 3; SGLT-2 sodium-glucose cotransporter-2; T2DM type 2 diabetes mellitus; TM6SF2 trans-membrane 6 superfamily 2; ULN upper limit of normal

^aGrade: U = unanimous (100%) agreement; A = 90–99% agreement; B = 78–89% agreement, and C = 67–77% agreement