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Review
. 2023 Oct;24(5):901-919.
doi: 10.1007/s11154-023-09813-5. Epub 2023 Jun 26.

Obesity phenotypes and cardiovascular risk: From pathophysiology to clinical management

Affiliations
Review

Obesity phenotypes and cardiovascular risk: From pathophysiology to clinical management

Alberto Preda et al. Rev Endocr Metab Disord. 2023 Oct.

Abstract

Obesity epidemic reached the dimensions of a real global health crisis with more than one billion people worldwide living with obesity. Multiple obesity-related mechanisms cause structural, functional, humoral, and hemodynamic alterations with cardiovascular (CV) deleterious effects. A correct assessment of the cardiovascular risk in people with obesity is critical for reducing mortality and preserving quality of life. The correct identification of the obesity status remains difficult as recent evidence suggest that different phenotypes of obesity exist, each one associated with different degrees of CV risk. Diagnosis of obesity cannot depend only on anthropometric parameters but should include a precise assessment of the metabolic status. Recently, the World Heart Federation and World Obesity Federation provided an action plan for management of obesity-related CV risk and mortality, stressing for the instauration of comprehensive structured programs encompassing multidisciplinary teams. In this review we aim at providing an updated summary regarding the different obesity phenotypes, their specific effects on CV risk and differences in clinical management.

Keywords: Adipose tissue; Cardiovascular risk; Fat; Inflammation; Insulin resistance; Obesity.

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Conflict of interest statement

All other authors report no conflict of interest.

Figures

Fig. 1
Fig. 1
Cardiac fibrosis in dysmetabolic subjects. Patients with dysmetabolism are at higher risk of developing cardiac fibrosis. The long-term exposure to inflammatory, oxidative, and hyper-insulinemic environment causes the secretion of several molecules that concur in causing cardiac fibrosis. Microscopically, this process causes cells deaths, microvascular damages, and deposition of excessive extracellular matrix. Consequently, patients frequently experience heart failure, especially HFpEF, eventually arrhythmias, and even sudden death. HFpEF, heart failure with preserved ejection fraction; TGF-β, transforming growth factor beta; TSP-1, tronbospondin-1
Fig. 2
Fig. 2
Obesity phenotypes and cardiovascular risk. This figure summarizes the close relationship between the different obesity phenotypes and the CV risk. AF, atrial fibrillation; CV, cardiovascular; EAT, epicardial adipose tissue; HF, heart failure; LVH, left ventricular hypertrophy; MetS, metabolic syndrome; MHO, metabolically healthy obese; MI, myocardial infarction; MUNW, metabolically unhealthy normal weight; MUO, metabolically unhealthy obese; ROS, reactive oxygen species; SO, sarcopenic obese

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