The Skeptical Cardiologist has promoted testing patients with premature atherosclerosis or strong family history of cardiovascular disease for lipoprotein(a), or Lp(a), as previously written about .
The National Lipid Association (NLA) published their last summer (summarized nicely ) and I've listed their key recommendations below.
1. For diagnosing high Lp(a), they chose a universal cutoff point of >100 nmol/L (approximately >50 mg/dL), which is at the 80th percentile among white Americans. This cutoff is not written in stone and may vary depending on risk, ethnicity, and comorbidities. Some labs report out Lp(a) in mg/dL, others in nmol/L. Pay attention to the units.
2. Lp(a) level is at least 80% genetically determined and reaches adult-like levels by approximately 5 years of age. Other than in acute inflammatory states, Lp(a) level remains stable regardless of lifestyle.
3. High-quality evidence supports a link between Lp(a) levels and a variety of cardiovascular-related outcomes. This table from the American College of Cardiology's on the NLA statement highlights that the risk of heart attack and aortic stenosis is elevated three- to four-fold.
4. The following populations should be considered for testing, again as summarized graphically by the American College of Cardiology commentary.
5. Neither diet nor lifestyle influences Lp(a) levels.
6. PCSK9 inhibitor drugs and niacin lower Lp(a) levels, but there are no data showing this changes clinical outcomes.
7. Similar to my approach, the NLA authors "recommend initiating a moderate- to high-intensity statin therapy in adults aged 40-75 years with a 10-year ASCVD risk of 7.5% to ≤20% with a Lp(a) ≥100 nmol/L. High-risk patients with LDL-C ≥70 mg/dL (non-HDL-C ≥100 mg/dL) and a Lp(a) ≥100 nmol/L on maximally tolerated statin should be considered for more intensive therapies (ezetimibe [Zetia] and PCSK9 inhibitors) to lower LDL-C."
8. Novel therapies being studied that selectively target Lp(a) include AKCEA apo(a)-LRx, an apo(a) antisense oligonucleotide that reduced Lp(a) up to 80% in phase II. An oxPL antibody against pro-osteogenic activity of Lp(a) has promising in vitro data.
The cost of the blood test for Lp(a) should be minimal. Medicare reimburses $14 for it. You can order it from Boston Heart Diagnostics for $11. Unfortunately, there is no telling what your local hospital lab will charge.
Since Lp(a) is inherited, patients with high levels should consider having first-degree relatives tested for Lp(a) to identify those who are going to be at high risk. This provides an early warning of who in the family is most at risk for cardiovascular complications early in life. Such patients should be considered for early screening for subclinical atherosclerosis. In addition, they should be additionally motivated to do everything possible to reduce their elevated risk by lifestyle changes.
In 2018, for the diagnosis of elevated Lp(a): one to help to identify asymptomatic patients with elevated Lp(a) (E78.41) and another for family history of elevated levels (Z83.430). Don't confuse Lp(a) with Apolipoprotein A1, which is the major protein component of particles in .
is a private practice noninvasive cardiologist and medical director of echocardiography at St. Luke's Hospital in St. Louis. He blogs on nutrition, cardiac testing, quackery, and other things worthy of skepticism at , where a version of this post first appeared.