Statin Therapy for Vascular Failure

Abstract

There is increasing evidence that statins reduce cardiovascular events such as coronary artery disease or stroke in hypercholesterolemic patients in both primary and secondary prevention. The striking benefit achieved with statin treatments in patients with a wide range of cholesterol levels cannot be attributed to their cholesterol lowering effect alone. Substantial data has recently accumulated showing that statins exert various effects on multiple targets, namely pleiotropic effects, especially targeting the concept of 'vascular failure', including the improvement of vascular endothelial function, inhibition of vascular smooth muscle cell proliferation and migration, anti-inflammatory actions, anti-oxidative effects or stabilization of vulnerable plaques. These effects have potential in the treatments of coronary artery disease in various settings, such as prevention of its onset as well as its progression, or plaque rupture. Statin therapy should be more extensively applied even in normolipidemic patients if there are additional risk factors such as hypertension, diabetes mellitus, or others. Furthermore, statins may be used to intervene in earlier stage risk conditions such as postprandial hyperlipidemia or hyperglycemia, insulin resistant state, masked hypertension, or metabolic syndrome to further reduce mortality or morbidity of coronary artery disease and heart failure.

Effects of Statins and Xuezhikang on the Expression of Secretory Phospholipase A2, Group IIA in Rat Vascular Smooth Muscle Cells

“…[42][43][44] In addition to their pleiotropic effects (anti-oxidation, anti-inflammation and anti-thrombosis), statins can also inhibit proliferation and migration of VSMC by regulating the activities of different pathways. [45][46][47][48] In vitro and in animal models, the inhibition of Rho with statins was related to the reduction of calcium storage in VSMCs. 49) It was also reported that statins prevented VSMC proliferation via inhibition of the Rho/Rho-kinase pathway.…”

Do antilipidemic agents reduce blood pressure?

“…The effect of statin therapy on SBP and DBP was -4.0 mmHg and -1.2 mmHg in patients whose basal SBP and DBP was >130 mmHg and >80 mmHg, respectively, compared with -0.9 mmHg on DBP in control subjects 26) . Statins has been well known to exert pleiotropic effects on vascular cells, including eNOS activation in endothelial cells, inhibition of proliferation and migration of vascular smooth muscle cells, anti-inflammatory actions, downregulation of angiotensin II receptors, and antioxidant actions, resulting in improved endothelial function and reduction of BP in vivo 27,28) . Because statins may interact with the RAAS, statins may lower arterial BP when administered alone or together with antihypertensive drugs acting via the RAAS 29) .…”

Ginsenoside-Rd potentiates apoptosis induced by hydrogen peroxide in basilar artery smooth muscle cells through the mitochondrial pathway

“…While the precise mechanisms of cerebrovascular remodeling are not fully understood, it is generally accepted that the imbalance between cell proliferation and apoptosis leads to a significant increase in cell number and thus contributes to hypertrophic artery remodeling [3]. The perspective is also supported by recent reports that some agents, including statins, angiotensin II receptors blockers, and angiotensin converting enzyme inhibitors can improve vascular remodeling through preventing cells proliferation and increasing cell apoptosis in smooth muscle cells in hypertensive animal models [4,5].…”