Patty, a 42-year old, slender executive assistant, has already had one carotid surgery. At age 41, her doctor detected an abnormal sound (a "bruit") in the left carotid artery in her neck; ultrasound demonstrated a 99% blockage. Before she knew it, Patty had a 5-inch incision in the left side of her neck to surgically remove the blockage to prevent stroke.
At age 47, Karen had a perfect life: A part-time teacher and mother of 3 girls, she felt great. She exercised, ate healthy foods, and was socially involved, in addition to managing her family and career responsibilities. But Karen suffered a heart attack that necessitated emergency insertion of a stent in her left anterior descending coronary artery.
Prior to Patty's carotid surgery and Karen's heart attack and stent, both women had relatively ordinary cholesterol values. Because both women were pre-menopausal, their doctors felt they were both at low risk for atherosclerotic disease. Neither ever smoked, both were at or near ideal weight, neither had high blood pressure or diabetes.
So what caused two young women to have a disease that, in many cases, can cripple or kill people? Lipoprotein(a).
Lipo what, you say?
Lipoprotein(a), or Lp(a), is a relatively common genetic factor that can cause some of the most aggressive coronary and carotid disease around. In families that carry the gene, it is not uncommon to have men in their 40s, women in their 50s with heart attacks, stents, and bypass, or strokes at similar ages. Lp(a) affects approximately 11% of the U.S. population.
Lp(a) is among the most clear-cut among inherited patterns: If your Dad had it, there's a 50% likelihood that you have it. If you have it, there's a 50% likelihood that each of your children has it. Having the gene means that your liver produces a protein called apoprotein(a), a peculiar structure that aggressively binds to LDL cholesterol and increases its ability to both create atherosclerotic plaque and trigger blood clot formation.
How do you know you have Lp(a)? Easy: Ask your doctor to test for it. Testing is widely available, at least in most major testing laboratories.
In standard cholesterol panels, Lp(a) is lumped together indistinguishably with LDL cholesterol and therefore cannot reveal whether or not you have Lp(a). A Lp(a) test must be requested and tested specifically. While most physicians advise testing Lp(a) only in people from families demonstrating high-risk, or don't advise testing at all, my view is that Lp(a) should be tested in everyone at least once. Because it is a genetic pattern, if you don't have Lp(a), you will never get it. Repeat testing is therefore unnecessary.
Unfortunately, because Lp(a) is genetically transmitted, many doctors assume that it is hopeless, a risk factor that cannot be corrected or reduced. Completely untrue. There are a number of factors that have been shown to reduce Lp(a).
However, Lp(a) can be a tricky customer. Because of wide variation in the gene, the effects of Lp(a) can vary substantially from one individual or family to another. In some people, Lp(a) can account for a heart attack or stroke at age 40, while in others it may not cause these conditions until age 78. There are even some that don't' cause disease at all. Given our current lab testing technology, we are unable to distinguish the various forms of Lp(a) (except in research settings using methods not yet available clinically). Should you have Lp(a) detected at abnormal levels, the best way to gauge it's potential for causing heart or vascular disease is to examine your family's history: If there are people with coronary or carotid disease at, say, age 55, then you likely share a similar risk.