title: Metabolic syndrome and cardiovascular disease: challenges and opportunities.
abstract: Metabolic syndrome (MetS) has been defined in different ways. However, key components common to most definitions are a constellation of risk factors including abdominal adiposity, impaired fasting glucose, hypertension, and dyslipidemia. A major mediator of MetS appears to be insulin resistance, which relates to the development of the vascular and metabolic dysfunctions that precede overt cardiovascular disease and type 2 diabetes. Evidence suggests that the mechanisms underlying the elevated cardiovascular risk associated with MetS begin with subclinical organ damage. Therapy for MetS targets individual components of the syndrome and includes lifestyle interventions, lipid-modifying therapy, and antihypertensive agents, particularly those that inhibit the renin-angiotensin system. Results of trials of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have demonstrated reductions in new-onset diabetes and cardiovascular events in a wide range of patients. Clinical trials to investigate further the role of these drugs in the primary prevention of type 2 diabetes in patients with MetS are currently under way. The purpose of this paper is to review the MetS from the perspective of the cardiology workforce with the hope that a better understanding of the links between MetS and cardiovascular disease could lead to improved management of persons at risk.
authors.affiliation: Division of Cardiovascular Medicine, University of Florida College of Medicine, Gainesville, Florida 32610-0277, USA. dehofrm@medicine.ufl.edu
authors.forename: Rhonda M
authors.initials: RM
authors.lastname: Cooper-DeHoff
authors.forename: Carl J
authors.initials: CJ
authors.lastname: Pepine
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D002318:Cardiovascular Diseases / Q000188:drug therapy*; D006801:Humans; D007333:Insulin Resistance; D024821:Metabolic Syndrome / Q000188:drug therapy* / Q000503:physiopathology; D047492:Peroxisome Proliferator-Activated Receptors / Q000187:drug effects; D012084:Renin-Angiotensin System / Q000187:drug effects
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D047492:Peroxisome Proliferator-Activated Receptors