Hypercholesterolemia and microvascular dysfunction: interventional strategies

Abstract

Hypercholesterolemia is defined as excessively high plasma cholesterol levels, and is a strong risk factor for many negative cardiovascular events. Total cholesterol levels above 200 mg/dl have repeatedly been correlated as an independent risk factor for development of peripheral vascular (PVD) and coronary artery disease (CAD), and considerable attention has been directed toward evaluating mechanisms by which hypercholesterolemia may impact vascular outcomes; these include both results of direct cholesterol lowering therapies and alternative interventions for improving vascular function. With specific relevance to the microcirculation, it has been clearly demonstrated that evolution of hypercholesterolemia is associated with endothelial cell dysfunction, a near-complete abrogation in vascular nitric oxide bioavailability, elevated oxidant stress, and the creation of a strongly pro-inflammatory condition; symptoms which can culminate in profound impairments/alterations to vascular reactivity. Effective interventional treatments can be challenging as certain genetic risk factors simply cannot be ignored. However, some hypercholesterolemia treatment options that have become widely used, including pharmaceutical therapies which can decrease circulating cholesterol by preventing either its formation in the liver or its absorption in the intestine, also have pleiotropic effects with can directly improve peripheral vascular outcomes. While physical activity is known to decrease PVD/CAD risk factors, including obesity, psychological stress, impaired glycemic control, and hypertension, this will also increase circulating levels of high density lipoprotein and improving both cardiac and vascular function. This review will provide an overview of the mechanistic consequences of the predominant pharmaceutical interventions and chronic exercise to treat hypercholesterolemia through their impacts on chronic sub-acute inflammation, oxidative stress, and microvascular structure/function relationships.

Taurine Attenuates Hepatic and Cardiac Damage and Apoptosis in Rabbits Fed a High-Fat Diet

“…Hypercholesterolemia induces oxidative stress and induce reactive oxygen species generation in different tissues such as liver, brain and kidney, which is known to cause damage of the cells (Park and Lee, 1998;Montilla et al, 2006;Prasad, 2008;Stapleton et al, 2010). The current study was designed to assess the possible protective role of taurine against hypercholesterolemia-induced hepatic and cardic changes by histological and immunohistochemical studies.…”

High blood pressure tends to increase carotid intima-media thickness in adult females

“…The optimal total cholesterol concentration is <200 mg/dL, that of LDL cholesterol <100 mg/dL, HDL cholesterol >40 mg/dL, and triglycerides <150 mg/dL. (6,7) The high LDL cholesterol concentration in the circulation and the decrease in the concentration of HDL cholesterol, which serves to transport cholesterol from the tissues to the liver, play a role in atherosclerosis. Subsequently LDL cholesterol adheres to the damaged endothelium and undergoes oxidative modification in the subendothelial space into oxidized LDL cholesterol (ox LDL), which has proinflammatory activity but may still be recognized by LDL receptors.…”

Effects of Unripened Cheese Supplements on Lipid and Antioxidant Status in Hypercholesterolemic SD Rats

“…대표적인 숙성치즈인 cheddar는 열량 423 kcal/100 g 단백질 함량 25.7%, 지방 33 4) ns: not significant. 5) Values in the same row that share a common superscript are significantly different at the p<0.05 level.…”