Dyslipidemia is widely accepted as one of the major risk factors in cardiovascular disease mainly due
to its contribution in the pathogenesis of atherosclerosis in medium-sized and large arteries. However, it has become
increasingly accepted that high-cholesterol levels can also adversely affect the microvasculature prior to the
development of overt atherosclerosis. Moreover, hypercholesterolemia has shown, in preclinical animal models,
to exert detrimental effects beyond the vascular tree leading to larger infarcts and adverse cardiac remodeling
post-myocardial infarction. At a functional level, hypercholesterolemia has shown to impair endotheliumdependent
vasodilation because on defects on nitric oxide bioavailability. The pathogenic mechanisms underlying
microvascular dysfunction involve an enhanced arginase activity, enhanced production of free radicals and the
activation, recruitment and accumulation of leukocytes, primarily neutrophils, via their diffusion through postcapillary
venules. In turn, recruited inflammatory cells and certain inflammatory mediators enhance platelet adhesion,
overall inducing a proinflammatory and prothrombotic phenotype.
Within the present review, we aim to discuss the existing evidence regarding the presence of dyslipidemia - particularly
high low density lipoprotein-cholesterol levels - and the occurrence of microvascular dysfunction, the
mechanism by which high cholesterol levels induce functional alterations in the microvascular bed and, finally
comment on the impact of dislipidemia-induced microvascular dysfunction at the myocardial level.