Because Lp(a) levels are established at a young age and often remain consistent, the risk for an Lp(a)-associated cardiovascular event is lifelong. This means Lp(a) test results can inform a lifetime of proactive cardiovascular care.^1,2 The National Lipids Association and the American College of Endocrinology suggested screening a broad range of patients for elevated Lp(a).^2,3

See the Consensus

There are currently no targeted treatments for elevated Lp(a).⁴ Lp(a)-reducing therapies, the first ever developed, are in advanced stages of clinical testing. An antisense oligonucleotide for apo(a) and an investigational small interfering ribonucleic acid (siRNA) molecule targeting apo(a) RNA are both currently being evaluated in phase 3 clinical trials to assess effects on ASCVD outcomes. In the meantime, there are other options available to help patients with elevated Lp(a) and their loved ones reduce their overall cardiovascular risk.⁵

See Other Options

Lp(a)-reducing therapies are being assessed in multiple clinical trials and at various phases of testing. Two therapies are at advanced (phase 3) stages of clinical testing to assess effects on ASCVD outcomes: an antisense oligonucleotide for apo(a) and an investigational small interfering RNA (siRNA) molecule targeting apo(a) RNA. In the meantime, it is important to help people with elevated Lp(a) reduce their overall cardiovascular risk.⁵

How to Help

• Drive conversations with patients about initiation of and adherence to treatments for other cardiovascular risk factors^1,4,6,7

• Enforce sustainable and heart-healthy lifestyle choices, even in the absence of other cardiovascular risk factors^6,8,9

• Test family members to identify others at risk of heart attack or stroke¹⁰

Find Out More 

Resources are available to support you and your patients with elevated Lp(a). These tools can help simplify conversations about what elevated Lp(a) is and what can be done to improve overall heart health.

Find Resources

A discussion guide is one of the many resources available to aid in conversations with patients who have elevated Lp(a) about what it is and what they can do to reduce their overall cardiovascular risk.

Download the Guide

Lp(a) levels are measured with a simple blood test that can be added to a standard lipid panel.⁴ ICD-10-CM and CPT codes for elevated Lp(a) screening are available.^11,12

How to Screen

Lp(a) levels are measured with a simple blood test that can be added to a routine blood work.⁴ Historically, Lp(a) levels have been measured in mg/dL, with some assays now providing results in nmol/L; either can be used to determine if a person is at risk.¹ ICD-10 and CPT codes for elevated Lp(a) screening are available.^11,12

How to Screen

Historically, Lp(a) levels have been measured in mg/dL, with some assays now providing results in nmol/L. While the latter is thought to be a more accurate measurement, either can be used to determine if a person is at risk.¹

Interpreting Results

Although out-of-pocket costs vary, elevated Lp(a) screening is generally inexpensive with cost ranging between $50 and $100. Lp(a) testing is readily available commercially and does not require fasting. Lp(a) testing is also covered by public insurance in many states.¹³

Risk thresholds for Lp(a) are as follows*^1,14,15:

• Elevated Lp(a) (increased cardiovascular risk): ≥50 mg/dL (≥125 nmol/L)

• Borderline cardiovascular risk: 30 mg/dL (75 nmol/L) to 50 mg/dL (125 nmol/L)

• Normal: <30 mg/dL (75 nmol/L)

• Lp(a) levels <3 mg/dL (7.5 nmol/L) to 5 mg/dL (12.5 nmol/L) are associated with an increased risk of incident type 2 diabetes mellitus

*Risk thresholds may be lower depending on the population (eg, postmenopausal women, patients with diabetes, people of certain ancestries).

Genetic, Mendelian randomization, and genome-wide association studies have established that elevated Lp(a) is an independent and causal cardiovascular risk factor in the general population.¹⁵ Elevated Lp(a) can increase the risk of heart disease by 2- to 4-fold, even in the absence of other risk factors^1,15-17; is considered one of the strongest single genetic risk factors for coronary artery disease; and is the only known single genetic risk factor for calcific aortic valve stenosis.¹⁵

See the Data