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Cardiometabolic Insights into Metabolic Dysfunction: From Mechanisms to Therapeutic Strategies

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Dr. Alessandro Andreis

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1. Advanced Cardiovascular Echocardiography Unit, Cardiovascular and Thoracic Department, Città della Salute e della Scienza di Torino University Hospital, 10126 Turin, Italy
2. Division of Cardiology, Città della Salute e della Scienza di Torino University Hospital, 10126 Turin, Italy
3. Department of Medical Sciences, University of Torino, 10126 Turin, Italy
Interests: pericarditis; cardiovascular imaging; echocardiography; cardiac magnetic resonance; cardiovascular medicine; pericardial effusion
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Dr. Guglielmo Beccuti

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Division of Endocrinology, Diabetology and Metabolism, Department of Medical Sciences, University of Turin, 10126 Turin, Italy
Interests: endocrinology; diabetology; metabolism

Dr. Angelo Armandi

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1. Department of Medical Sciences, University of Turin, Corso Dogliotti 14, 10126 Turin, Italy
2. Metabolic Liver Disease Research Program, I. Department of Medicine, University Medical Center of the Johannes Gutenberg-University, Langenbeckstrasse 1, 55131 Mainz, Germany
Interests: liver diseases; non-alcoholic fatty liver disease; NASH; portal hypertension; liver fibrosis; hepatocellular carcinoma; liver cirrhosis; spleen stiffness; sarcopenia; nutrition in liver disease; insulin resistance
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Special Issue Information

Dear Colleagues,

Over the past decade, the parallel rise of obesity, type 2 diabetes, and metabolic dysfunction-associated steatotic liver disease has been mirrored by a sharp increase in cardiovascular complications. A growing body of experimental and clinical data suggests that these conditions converge on shared inflammatory, metabolic, and profibrotic circuits capable of undermining myocardial integrity long before overt heart disease appears.

This Special Issue seeks to clarify those converging pathways and to translate emerging knowledge into earlier diagnosis and more precise therapy. We welcome manuscripts that probe underlying mechanisms, introduce or validate novel imaging and biomarker platforms, or test interventional strategies—pharmacological, procedural, or lifestyle-based—designed to lessen cardiometabolic risk. Original investigations, robust methodological papers, and critical, up-to-date reviews that draw on the combined expertise of cardiology, endocrinology, and hepatology will all be considered.

Dr. Alessandro Andreis
Dr. Guglielmo Beccuti
Dr. Angelo Armandi
Guest Editors

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14 pages, 883 KB

Open AccessArticle

Liver Fibrosis as a Predictor of Cardiovascular Risk in Patients with Severe Obesity

by Alina N. Saidi, Willy B. Theel, Vivian D. de Jong, Stefanie R. van Mil, Aart-Jan van der Lely, Diederick E. Grobbee, Jan Apers, Ellen van der Zwan-van Beek and Manuel Castro Cabezas

J. Clin. Med. 2025, 14(23), 8532; https://doi.org/10.3390/jcm14238532 - 1 Dec 2025

Cited by 1 | Viewed by 1071

Abstract

Background: Obesity is a substantial global health issue associated with increased risk of cardiovascular disease (CVD) and metabolic dysfunction-associated steatotic liver disease (MASLD). Despite the known link between obesity, CVD and MASLD, it remains unknown which factors contribute to higher cardiovascular (CV) risk in patients with obesity-induced liver fibrosis. Liver fibrosis, assessed by the Fibrosis-4 (FIB-4) index, may help to identify patients with obesity at increased CV risk. Methods: Patients with severe obesity (Body Mass Index (BMI) ≥ 40 kg/m²) scheduled for bariatric surgery were subdivided into FIB-4 categories. Systemic leukocyte activation markers were measured by flow cytometry. Additionally, markers of vascular damage, namely the carotid intima media thickness (cIMT) and pulse wave velocity (PWV), were included. Results: The cohort predominantly consisted of women (74%) with an average age of 41 years and mean BMI of 42.7 kg/m². Patients with an elevated FIB-4 (≥1.3) had higher systolic (146 ± 16 vs. 139 ± 15, p = 0.002) and diastolic blood pressure (91 ± 13 vs. 83 ± 12, p = 0.002), increased cIMT (0.66 ± 0.11 vs. 0.55 ± 0.10, p < 0.001), and higher PWV (8.2 ± 0.9 vs. 6.8 ± 1.1, p < 0.001) compared to those with a low FIB-4 (<1.3). Additionally, patients with a high FIB-4 tended to show increased expression of CD66b on granulocytes. Conclusions: Patients with severe obesity who were at risk of liver fibrosis showed greater signs of vascular damage, insulin resistance, and systemic inflammation. This suggests that liver fibrosis can be a useful marker for identifying patients with obesity at high CV risk. Full article

(This article belongs to the Special Issue Cardiometabolic Insights into Metabolic Dysfunction: From Mechanisms to Therapeutic Strategies)

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