What is Lp(a)?

Let me tell you about Laura.

Laura is a slender, active 43-year old mother of two. Laura was concerned about her risk for heart disease, given her Dad's heart attack and bypass surgery at age 48, her brother's heart attack and two stents at age 42.

Laura has never smoked, has normal blood pressure (106/72), normal blood sugar, exercises regularly, and feels fine.

Is Laura at risk for heart disease?

Laura underwent a CT heart scan (NOT a CT coronary angiogram! CT heart scans are low-radiation screening tests for coronary plaque) that revealed a "score" of 443 - extremely high for a young female. In fact, this is the highest score for coronary atherosclerotic plaque I have ever seen in a young pre-menopausal woman. So, yes, Laura shared the risk of her brother and Dad and was heading rapidly towards a similar fate of heart attack, stents, bypass.

How about Kim? At age 45, Kim, like Laura, is a healthy-appearing, mother of a teenager. But Kim had severe carotid disease sufficient to undergo a carotid endarterectomy to reduce her risk for stroke - at age 45!

Both healthy-appearing women shared a genetic pattern called lipoprotein(a), or Lp(a) for short. Lp(a) is an aggressive risk factor for atherosclerotic plaque, whether in the coronary arteries (heart attack) or carotid arteries (stroke).

I call Lp(a) "the most aggressive risk factor for heart disease that nobody's ever heard of."  Why would that be? Why would the most aggressive known cause for heart and vascular disease be virtually unknown among the general public while cholesterol is a daily topic of conversation, the topic of countless TV commercials?

Easy: There's no profitable treatment for it. That does not mean there is no treatment for Lp(a). There's no profitable treatment for it. It shouldn't be that way, but that's the way the revenue-driven American medical system works.

What is Lp(a)?

11% of the population share a genetic pattern that causes the liver to produce a protein called apoprotein(a). When apoprotein(a) encounters an LDL cholesterol particle, it binds to it and forms the combination molecule, Lp(a). The added apoprotein(a) component confers much more aggressive behavior to the LDL particle.

The apoprotein(a) particle is subject to great variation in size, length, and weight, which can be responsible for variation in risk. Shorter, smaller apoprotein(a) molecules, for instance, confer much higher risk. There are even occasional people with Lp(a) who are at low-risk. (Presently, we are unable to characterize Lp(a) in clinical practice.) The only practical way to gauge the heart disease-causing potential of someone's Lp(a) is to look at family history or a measure of atherosclerosis, such as Laura's heart scan or Kim's carotid ultrasound.

Lp(a) has many unique features. For one, unlike LDL cholesterol, it is highly susceptible to hormonal shifts. Thus, estrogen (in females) and testosterone (in males), and DHEA (an adrenal gland hormone) in both men and women, have large effects on Lp(a); these three hormones can be used to treat Lp(a). Likewise, thyroid hormones have an outsized effect on Lp(a), especially the often-neglected T3 hormone (the one not contained in the commonly-prescribed levothyroxine).