Heart of the matter: Coronary dysfunction in metabolic syndrome

Metabolic syndrome (MetS) is a collection of risk factors including obesity, dyslipidemia, insulin resistance/impaired glucose tolerance, and/or hypertension. The incidence of obesity has reached pandemic levels, as ~ 20–30% of adults in most developed countries can be classified as having MetS. This increased prevalence of MetS is critical as it is associated with a two-fold elevated risk for cardiovascular disease. Although the pathophysiology underlying this increase in disease has not been clearly defined, recent evidence indicates that alterations in the control of coronary blood flow could play an important role. The purpose of this review is to highlight current understanding of the effects of MetS on regulation of coronary blood flow and to outline the potential mechanisms involved. In particular, the role of neurohumoral modulation via sympathetic α-adrenoceptors and the renin–angiotensin–aldosterone system (RAAS) are explored. Alterations in the contribution of end-effector K+, Ca2+, and transient receptor potential (TRP) channels are also addressed. Finally, future perspectives and potential therapeutic targeting of the microcirculation in MetS are discussed. This article is part of a Special Issue entitled “Coronary Blood Flow”.

► Metabolic syndrome impairs the balance between myocardial oxygen supply and demand.
► Obesity impairs coronary response to exercise, ischemia, and vasodilator agonists.
► Increased neurohumoral and RAAS activation limits coronary blood flow.
► Alterations in functional expression of coronary ion channels are explored.