We owe fitness guru and TV host of The Biggest Loser series, Bob Harper, much gratitude for educating the public about his near-death experience in early 2017 from closure of his “widowmaker” heart artery while exercising. His efforts to highlight his missed warning signs, his recovery in cardiac rehabilitation classes, his ongoing emotional recovery with the support of his dog and fans, and the use of automatic defibrillators in gyms and other public settings to save lives has received much media attention and undoubtedly has done more to raise awareness of these issues than many prior efforts. Furthermore, Bob Harper pushed the envelope again by educating the public about a high level of a form of cholesterol he inherited that is neither rare nor benign. Harper indicated that his heart attack was due to an elevated level of Lipoprotein(a), a cholesterol particle related to but different than the better-known LDL-cholesterol. At my preventive cardiology clinic, I care for hundreds of patients with elevated Lipoprotein(a) and I want to share some of that experience with you.
1) What is Lipoprotein(a)?
Lipoprotein(a) is also known as Lp(a) or the “sticky cholesterol”. It is a particle in the blood that carries cholesterol, fats and proteins. Whether it is detectable in your blood depends on whether you inherited the ability to produce it from one or both parents. You can be thin, exercise, and eat a lot of kale and still have a very high level of Lp(a). The level of Lp (a) usually does not change much from childhood on. Diet, exercise, and statin medications like atorvastatin have little impact on lowering the level of Lp (a).
Lp (a) is a big molecule made in the liver separately from LDL-cholesterol that is a combination of fats, proteins and cholesterol. High levels in the blood increase the risk for of conditions that may alter cardiovascular health and fitness. It is the strongest inherited risk factor for heart disease in otherwise healthy persons. That means over 80 million people in the USA alone have elevated levels. It is more commonly inherited in African-Americans and those of Asian background.
All that is needed to check whether you have inherited Lp(a) from one or both parents is a simple blood test that is widely available and not expensive. Unfortunately, a measurement of Lp(a) is not included in standard cholesterol panels. Levels of Lp(a) are reported in different units, either mg/dL or nmol/L. A normal level is less than 30 mg/dL or less than 75 nmol/L. Some people I treat have Lp(a) levels of over 400 mg/dl!
2) When do you check Lp(a) levels?
Recently, the European Society of Atherosclerosis recommended widespread measurement of Lp(a) one time to determine if someone has a hidden risk for atherosclerosis. I agree with this recommendation but in the USA, the current advice is to have your Lp(a) blood level checked if:
3) What can be done about a high Lp(a)?
If an elevated Lp(a) is measure the most important steps are to follow a lifestyle known to reduce the overall risk of heart disease including:
Currently, there is no approved medication for those an elevated Lp(a). Unfortunately, statin cholesterol medication does not lower Lp(a) and often raises it. There are two injectable PCSK9 inhibitor medications that often lower both LDL-cholesterol and Lp(a) but they are only approved for lowering LDL-cholesterol and are expensive. Niacin or vitamin B3 lowers Lp(a) and also lowers LDL-cholesterol and triglycerides while raising HDL-cholesterol. There are no large and long-term studies using niacin in patients with Lp(a), however. In peri and post-menopausal women, a discussion about hormone replacement therapy (HRT) can lower Lp(a) levels. New injectable drugs used to lower cholesterol are now FDA approved and also lower Lp(a). New medications are in clinical trials to specifically lower Lp(a) but it will be several years before results are available. Finally, an advanced treatment called apheresis, similar to hemodialysis, cleanses the blood of Lp(a) through a filter. This is available and approved for use but is used infrequently due to the complexity and expense. At the Kahn Center we personalize the approach to Lp(a) and have been successful lowering it significantly in many patients while we participate with Novartis Pharmaceuticals in ongoing Lp(a) research.
Conclusion
Thank you Bob Harper, and others, who have worked to make Lp(a) a household word. At present, approximately 1% of physicians measure routine levels of Lp(a) but the word is getting out. If your goal is to maintain healthy arteries and a healthy life, asking for a measurement of your Lp(a) level may be an important at your next visit to your doctor.
