Controlling blood pressure and cholesterol help lower cardiovascular disease risk.
Some people with hypercholesterolemia, or high blood cholesterol, may also have hypertension, or high blood pressure. Together, they can lead to cardiovascular disease and increase your risk for heart attack and stroke. Cholesterol-rich low-density lipoproteins circulating in the blood can invade artery walls and lead to development of fatty plaques in a process called atherosclerosis. Hypertension can increase the accumulation of this вЂњbadвЂќ form of cholesterol in artery walls. Hypercholesterolemia and hypertension often work together to compromise normal artery function. Combination therapies that target several risk factors, such as hypercholesterolemia, hypertension and artery function, may more effectively treat cardiovascular disease than a therapy that targets a single risk factor.
Your artery walls must be flexible, or elastic, to accommodate changes in blood flow as your heart beats. Loss of artery flexibility and increased stiffness is a hallmark of atherosclerosis and hypertension. The artery wall is composed of several layers. More stiffness in the arteries involves structural changes in the artery wall, including thickening of connective tissue and muscle cell layers.
The innermost layer of the artery wall that is in direct contact with the blood is called the endothelium, or endothelial cell layer. The endothelium is only a single cell layer deep, but it has an important role in regulating artery elasticity. Reduced endothelial cell production of nitric oxide, a compound that helps to relax artery muscle tone, may compromise normal artery function and contribute to hypertension and cardiovascular disease.
Different classes of fat-protein complexes, called lipoproteins, carry cholesterol, triglycerides and phospholipids through your blood. Each lipoprotein class carries all 3 types of fats, although in different proportions. In the blood, triglyceride-rich very low-density lipoproteins are eventually converted into cholesterol-rich LDLs, some with an abnormally small size. Normal-sized and small LDLs that become trapped in the artery wall contribute to loss of artery elasticity. The presence of LDLs in artery walls triggers an inflammatory response involving free radical production, or oxidative stress, which causes oxidation of LDLs.
Oxidized LDLs inhibit endothelial nitric oxide production, which contributes to artery stiffening. Oxidized LDLs also inhibit the ability of high-density lipoproteins, a вЂњgoodвЂќ type of lipoprotein that protects against cardiovascular disease, to remove cholesterol from artery sites of LDL accumulation.
High blood cholesterol may also lead to high blood pressure through increased salt sensitivity. Cholesterol accumulation in kidney cells increases sodium retention. Sodium retention can increase blood volume, which increases blood pressure. Sodium retention also lowers endothelial cell nitric oxide production.
High salt intake in people with salt-sensitive hypertension causes a decrease in artery elasticity and raises blood pressure, according to a study published in the February 2001 issue of вЂњHypertension.вЂќ Increased blood pressure can, in turn, drive more LDLs into the artery wall, setting the stage for a vicious cycle that promotes atherosclerosis.
The statin class of cholesterol-lowering drugs can inhibit cholesterol production and effectively lower blood LDL cholesterol levels in many people. Statins may also help lower blood pressure, especially when used in combination with drugs that can decrease kidney sodium retention and relax muscle tone in artery walls.
In people with both hypertension and hypercholesterolemia, combined daily therapy with 40 mg simvastatin and 320 mg valsartan, a drug that helps relax artery walls, for 12 weeks lowered LDL cholesterol by 37 percent, and blood pressure was brought under control in 50 percent of the subjects. The study was published in the October 2008 issue of вЂњClinical Therapeutics.вЂќ