Endocrine–Cardiovascular Interactions in Metabolic Syndrome: Mechanisms of Cardiac Remodeling and Vascular Dysfunction

Abstract

Metabolic syndrome is a multifactorial condition characterized by metabolic and hormonal disturbances that substantially increase cardiovascular risk. Endocrine–cardiovascular interactions play a pivotal role in the development of cardiac remodeling and vascular dysfunction in this setting. Key mechanisms include insulin resistance, adipokine imbalance, activation of the renin–angiotensin–aldosterone system, and alterations in sex hormones, which collectively promote endothelial dysfunction, chronic inflammation, oxidative stress, and myocardial fibrosis. This study aims to summarize current evidence on the pathophysiological mechanisms linking endocrine dysregulation with structural and functional cardiovascular changes in metabolic syndrome. Available data indicate that these processes contribute to left ventricular hypertrophy, diastolic dysfunction, and increased arterial stiffness, even at early stages of the disease. A better understanding of these interactions is essential for early risk stratification and the development of targeted therapeutic strategies to prevent cardiovascular complications in patients with metabolic syndrome.