The African American Heart Study – FAQ’s

 

Unlike other lipid risk factors, such as blood cholesterol levels, that can be influenced by lifestyle factors like diet and exercise, Lp(a) levels are predominantly inherited and are stable from childhood.

Lp(a) concentrations are measured in mass units (mg/dL) or molar units (nmol/L). International medical organizations generally recommend that medical laboratories measure Lp(a) with an assay that reports in nanomoles per liter (nmol/l). When you review your Lp(a) test results with your healthcare provider, you should note which measurement method is used.

Increasing levels of Lp(a) are associated with increased risk for cardiovascular events such as heart attack and stroke. There is a concern if your Lp(a) level is greater than 50 mg/dL or 100 to 125 nmol/L.

The cholesterol contained in Lp(a) particles cannot be separated from that in LDL particles and is therefore collectively reported as LDL-C (“bad cholesterol”) concentration.

Lp(a) is a presumed independent risk factor for cardiovascular disease. Lp(a) can infiltrate and enhance the atherosclerotic process in the body’s arteries, including the heart, brain, kidneys, and legs. The apo(a) protein that is part of the Lp(a) particle may also drive additional inflammation and blood clotting effects.

The amount of Lp(a) your body produces is determined by genes you received at birth from your parents. Lp(a) reaches its adult level by around age 5 and remains stable — except during acute illness and menopause (with declining estrogen levels), which can both cause Lp(a) to increase. As noted above, Lp(a) level is not associated with lifestyle factors

High Lp(a) occurs in all races or ethnicities, but it seems more common in Black individuals than in White, Hispanic, or East Asian individuals. More research and improved testing methods are needed to better understand the influence of race and ethnicity on Lp(a).

While 1 in 5 people, or 1.5 billion globally, are estimated to have high Lp(a), it is not part of the standard lipid panel; it is measured by a specific assay and is ordered separately.

Your doctor may suspect the presence of high Lp(a) if:
You have a family history of early cardiovascular disease (age 55 years for a male or 65 years for a female)– heart attack, stroke, poor circulation in your legs.
You’ve had a heart attack or stroke with no other known risk factors (such as high LDL, smoking, diabetes, or obesity).
People with familial hypercholesterolemia (FH) also may have high Lp(a). Therefore, anyone with FH should get an Lp(a) test

An Lp(a) test measures your Lp(a) level in your blood through a simple blood test. It is not a routinely ordered test as part of a standard lipid panel, so your clinician will need to order it directly if they suspect you may have high Lp(a).

Generally, results over 50 mg/dL or 100 to 125 nmol/L are considered high and could increase an individual’s risk for heart attacks and stroke.

As a genetic condition, high Lp(a) runs in families. When one person is diagnosed with high Lp(a), it’s time to test other family members, including parents, siblings, and children. Also referred to as “cascade screening,” it is a mechanism for identifying people at risk for a genetic condition through systematic family tracing.

Currently, no medicine is available to treat high Lp(a). Scientists are still studying why people with high Lp(a) levels are more likely to have heart attacks and strokes. They are also exploring how to treat high Lp(a) levels, including new medicines to lower them.

Ask your healthcare practitioner to test your Lp(a) level. If it’s elevated, your first-degree relatives should also be screened, and you should work to reduce all cardiovascular risk factors within your control — especially your LDL cholesterol.