Beneficial effects of statins on endothelial dysfunction and vascular stiffness.
Endothelial dysfunction and increased arterial stiffness are considered independent predictors of cardiovascular risk. Endothelial dysfunction primarily reflects decreased availability of nitric oxide, a critical endothelium-derived vasoactive factor with vasodilatory and anti-atherosclerotic properties. Techniques for assessing endothelial dysfunction include ultrasonographic measurement of flow-mediated vasodilatation of the brachial artery and plethysmographic measurement of forearm blood flow responses to vasoactive agents. Arterial stiffness can be assessed using pulse wave analysis to generate measures of pulse wave velocity, arterial compliance and wave reflection. It has been demonstrated that the preventive effect of statins on coronary events is not only attributed to cholesterol-lowering, but also to various effects on the vascular wall, which include improved endothelial function as well as antioxidant and anti-inflammatory activity. Previous studies have reported improvement of arterial stiffness by the antioxidant and anti-inflammatory effects of statin therapy in patients with or without hypercholesterolemia. The present review considers the pathophysiology underlying endothelial dysfunction and increased arterial stiffness associated with atherosclerotic disease and the beneficial effects of statins on these markers of atherosclerosis.
Dilaveris
Polychronis
P
Cardiology Department, School of Medicine, University of Athens, Hippokration Hospital, Athens, Greece. hrodil@yahoo.com
Giannopoulos
Georgios
G
Riga
Maria
M
Synetos
Andreas
A
Stefanadis
Christodoulos
C
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001158:Arteries / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D050197:Atherosclerosis / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D002318:Cardiovascular Diseases / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D004548:Elasticity; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D016896:Treatment Outcome
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors