Are your blood cholesterol levels too high?
Increased total and LDL cholesterol levels boost the risk of coronary heart disease (CHD) by increasing the amount of cholesterol deposited within the walls of the arteries. The National Cholesterol Education Program guidelines recommend that total cholesterol levels be kept below 200 mg/dL to reduce risk.
The target for LDL cholesterol depends on how many of the following risk factors are present:
- cigarette smoking;
- high blood pressure (140/90 mm Hg or higher) or use of blood-pressure-lowering medication;
- HDL cholesterol level below 40 mg/dL;
- family history of a premature CHD event (under 55 years old in men, under 65 in women) in a first-degree relative; and
- older age (45 years or older in men, 55 or older in women).
For people with none or one of these risk factors, LDL cholesterol levels should be less than 160 mg/dL. In individuals who do not have known cardiovascular disease or diabetes but have two or more of these risk factors, LDL cholesterol levels should be kept below 130 mg/dL. In all people with known cardiovascular disease or diabetes, LDL cholesterol levels should be lowered to less than 100 mg/dL, with an optional goal of less than 70 mg/dL.
A low HDL cholesterol level (less than 40 mg/dL) is considered a risk factor for CHD. In fact, a total blood cholesterol level of 200 mg/dL or lower--the level considered desirable--may still be associated with an increased risk of CHD if HDL cholesterol levels are below 40 mg/dL, particularly in women. A high level of HDL cholesterol (60 mg/dL or higher), however, is considered protective against CHD and cancels out the effects of one other CHD risk factor (such as increased age) when determining one's total number of risk factors.
Triglyceride levels between 150 mg/dL and 199 mg/dL are considered borderline, and levels between 200 mg/dL and 500 m/dL are high. Levels greater than 500 mg/dL are very high. About 35 percent of men and 24 percent of women are thought to have triglyceride levels above 150 mg/dL. The CHD risk of elevated triglycerides is especially great when combined with low levels of HDL cholesterol and small, dense LDL particles. This pattern is common in people who are obese or have diabetes or pre-diabetes. Elevated triglycerides also impart high risk when associated with a high ratio of LDL to HDL cholesterol or when due to one of two inherited conditions--familial combined hyperlipidemia or dysbetalipoproteinemia. Both of these disorders cause high blood cholesterol and/or high blood triglyceride levels.
Size and density of LDL particles can also affect CHD risk. LDL particles vary in size and density to produce two patterns: A and B. People with pattern A have mostly large LDL particles, while people with pattern B have a predominance of small, dense particles. Pattern B patients have a higher risk of CHD than pattern A patients. The majority of people with triglyceride levels above 150 mg/dL have pattern B. Men are more likely than women to have pattern B, which may be genetic or develop as a result of elevated triglycerides or diabetes.
The reason for the increased risk of CHD with pattern B is that smaller LDL particles enter the arterial wall more easily and are more prone to oxidation than larger LDL particles. However, the presence of mostly small LDL particles is often linked to higher triglyceride and lower HDL cholesterol levels, as well as to a greater number of LDL particles, and this combination may have a more important effect on CHD risk than particle size alone.
High levels of lipoprotein(a), also known as Lp(a), are another risk factor for CHD. The structure of Lp(a) is similar to LDL, except that it contains another protein called apo(a), which resembles the blood protein plasminogen. Plasminogen is converted into the enzyme plasmin, which plays a role in eliminating arterial blockage by breaking down fibrin, a major component of blood clots.
Two explanations have been proposed for why Lp(a) increases the risk of CHD. First, because of the similarity of apo(a) to plasminogen, Lp(a) might interfere with the conversion of plasminogen to plasmin, thus promoting the persistence of blood clots by reducing the beneficial action of plasmin. Second, like LDL, Lp(a) can deposit in arterial walls and contribute to plaque formation.
