Metabolic dysfunction associated steatotic liver disease and the heart

Author:

Driessen Stan1,Francque Sven M.2,Anker Stefan D.34,Castro Cabezas Manuel567,Grobbee Diederick E.58,Tushuizen Maarten E.9,Holleboom Adriaan G.1

Affiliation:

1. Department of Vascular Medicine, Amsterdam University Medical Center, Amsterdam, The Netherlands

2. Department of Gastroenterology and Hepatology, University Hospital Antwerp, Antwerp, Belgium

3. Department of Cardiology (CVK) of German Heart Center Charité; Institute of Health Center for Regenerative Therapies (BCRT), German Centre for Cardiovascular Research (DZHK) partner site Berlin, Charité Universitätsmedizin, Berlin, Germany

4. Institute of Heart Diseases, Wroclaw Medical University, Wroclaw, Poland

5. Julius Clinical, Zeist, The Netherlands

6. Department of Internal Medicine, Franciscus Gasthuis & Vlietland, Rotterdam, The Netherlands

7. Department of Internal Medicine and Endocrinology, Erasmus MC, Rotterdam, The Netherlands

8. Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, The Netherlands

9. Department of Gastroenterology and Hepatology, Leiden University Medical Centre, Leiden, The Netherlands

Abstract

The prevalence and severity of metabolic dysfunction associated steatotic liver disease (MASLD) are increasing. Physicians who treat patients with MASLD may acknowledge the strong coincidence with cardiometabolic disease including atherosclerotic cardiovascular disease (asCVD). This raises questions on co-occurrence, causality and the need for screening and multidisciplinary care for MASLD in patients with asCVD, and vice versa. Here we review the interrelations of MASLD and heart disease and formulate answers to these matters. Epidemiological studies scoring proxies for atherosclerosis and actual cardiovascular events indicate increased atherosclerosis in patients with MASLD, yet no increased risk of asCVD mortality. MASLD and asCVD share common drivers: obesity, insulin resistance and type 2 diabetes mellitus (T2DM), smoking, hypertension and sleep apnea syndrome. In addition, Mendelian randomization studies support that MASLD may cause atherosclerosis through mixed hyperlipidemia, while such evidence is lacking for liver-derived pro-coagulant factors. In the more advanced fibrotic stages, MASLD may contribute to heart failure with preserved ejection fraction by reduced filling of the right ventricle, which may induce fatigue upon exertion often mentioned by patients with MASLD. Some evidence points to an association between MASLD and cardiac arrhythmias. Regarding treatment and given the strong co-occurrence of MASLD and asCVD, pharmacotherapy in development for advanced stages of MASLD would ideally also reduce cardiovascular events, as has been demonstrated for T2DM treatments. Given the common drivers, potential causal factors and especially given the increased rate of cardiovascular events, comprehensive cardiometabolic risk management is warranted in patients with MASLD, preferably in a multidisciplinary approach.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Hepatology

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