Pathophysiology and pharmacotherapy of cardiovascular complications in metabolic syndrome

Metabolic syndrome (MetS) symbolises a cluster of interrelated risk factors including central obesity, dyslipidemia, insulin resistance and hypertension, those significantly increase the risk of cardiovascular diseases (CVD). Individuals with a MetS have a two- to fourfold greater risk of coronary artery disease, stroke, myocardial infarction, and heart failure. The pathophysiology of cardiovascular complications in MetS is multifactorial, driven by visceral obesity, insulin resistance, atherogenic dyslipidemia, endothelial dysfunction, oxidative stress, low-grade chronic inflammation, and prothrombotic states. They accelerate the vascular stiffness, atherosclerotic and thrombotic cascades, eventually increasing CVD related morbidity and mortality. Emerging evidences also associates gut microbiota-derived metabolites, mitochondrial dysfunction, and epigenetic alterations as novel contributors. Pharmacotherapy in MetS mainly focuses to control the different components to prevent cardiovascular complications. Antihypertensives, including ACE inhibitors and angiotensin receptor blockers (ARBs) provide vascular protection with beneficial effects on other metabolic conditions. Calcium channel blockers have the protective effects on cardiovascular complications without any adverse action on other metabolic abnormalities. Newer antidiabetic agents such as GLP-1 receptor agonists and SGLT2 inhibitors demonstrate cardioprotective benefits independent of glycemic regulation. Statins, fibrates, ezetimibe, PCSK9 inhibitors, and omega-3 fatty acids are key in managing dyslipidemia. Antiplatelet agents, particularly aspirin and P2Y12 inhibitors, reduce thrombotic risk. Future perspectives highlight anti-inflammatory therapies, endothelin and mineralocorticoid receptor antagonists, dual RAS-neprilysin inhibitors, gut microbiota-targeted interventions, and personalized medicine approaches as promising strategies. Thus, an integrated understanding of pathogenesis and pharmacotherapy is vital to mitigate the growing global burden of MetS-related cardiovascular complications.