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Guidelines and Lp(a)
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Adult Guidelines

 

  • Use of Lipoprotein(a) in Clinical Practice: A Biomarker Whose Time Has Come. A Scientific Statement from the National Lipid Association 2019 see full statement slide deck here 


    Lp(a) and Primary Prevention:  Summary (Also includes pediatric statement)

  • The Importance of Shared Decision Making
    A decision to measure Lp(a) should be made after a thoughtful benefit-risk discussion between the patient and his/her healthcare provider. Shared decision-making should reflect an individual’s preferences and values. Decisions should also be based upon family history, the presence of comorbid conditions, race/ethnicity, and/or concern of future risk. In the absence of an acute illness, the level of Lp(a) is stable throughout an individual’s lifetime and unaffected by lifestyle. Therefore, a case could be made to measure Lp(a) in all individuals, at least once in a lifetime, based upon strong support for the association between elevated Lp(a) levels and increased risk, together with genetic findings that indicate elevated Lp(a) is causally related to premature ASCVD and VAS. However, there is no current evidence to substantiate the benefit of such an approach, and there is currently no targeted treatment(s) to lower Lp(a) levels that have been proven to affect ASCVD outcomes or progression of VAS. Therefore, although some panel members supported it, a recommendation for universal testing of Lp(a) was not made at this time. The Scientific Statement Committee acknowledges that there is likely little harm from a universal screening approach and that the cost of the test is relatively inexpensive compared to other cardiovascular disease screening tests. As more data become available in the future, the potential role of universal testing should be re-evaluated.

  • Lp(a) and Secondary Prevention: Summary

    • Be aware of Lp(a)-associated increased risk for recurrent events
    • Continue to follow Guideline based therapies, as most lipid-related risk is still attributable to LDL-C
    • Consider more aggressive LDL-C lowering for ASCVD patients with increased Lp(a)
    • Consider earlier use of PCSK9 inhibitors in ASCVD patients with elevated Lp(a)

 

AHA/ACC/AACVPR/AAPA/ABC
/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA 
Guideline on the Management of Blood Cholesterol 2018

  • States that elevated levels of Lp(a) are associated with an increased risk for premature ASCVD, and are largely genetically determined.

  • In adults 40 to 75 years of age without diabetes mellitus and 10-year risk of 5%-19.9%, risk-enhancing factors favor initiation of statin therapy. Risk-enhancing factors include family history of premature ASCVD; persistently elevated LDL-C levels ≥160 mg/dl (≥4.1 mmol/L); metabolic syndrome; chronic kidney disease; history of preeclampsia or premature menopause (age <40 years); chronic inflammatory disorders (e.g., rheumatoid arthritis, psoriasis, or chronic HIV); high-risk ethnic groups (e.g., South Asian); persistent elevations of triglycerides ≥175 mg/dl (≥1.97 mmol/L); and, if measured in selected individuals, apolipoprotein B ≥130 mg/dl or ≥2500 nmol/L, high-sensitivity C-reactive protein ≥2.0 mg/L (190 nmol/L), ABI <0.9, and lipoprotein (a) ≥50 mg/dl or 125 nmol/L, especially at higher values of lipoprotein (a).

    Expert Perspective: Other risk-enhancing factors include systemic lupus, and radiation therapy for left breast cancer and other radiation therapies where the left main, left anterior descending, and proximal right coronary artery is in the field.

2018 Cholesterol Clinical Practice Guidelines  - Adults here

 

Canadian Cardiovascular Society - Nov 2016

  • We suggest that Lp(a) might aid risk assessment in subjects with intermediate FRS or with a family history of premature coronary artery disease (Conditional Recommendation; Moderate-Quality Evidence). Values and preferences. Lp(a) is a marker of CVD risk. Particular attention should be given to individuals with Lp(a) levels > 30 mg/dL for whom CVD risk is increased by approximately twofold. Although no randomized clinical trials are available to support basing treatment decisions solely on the basis of an elevated Lp(a) level, identification of high levels of Lp(a) might be particularly useful for mutual decision-making in intermediate-risk subjects. Moreover, in younger patients who have a very strong family history of premature CVD suspected to be related to atherogenic dyslipidemia but who by virtue of young age, do not meet usual risk criteria for treatment, detection of high Lp(a) might help inform mutual decision-making regarding treatment. Lp(a) is not considered a treatment target and repeat measures are not indicated.

Canadian Cardiovascular Society Guidelines for the Management of Dyslipidemia for the Prevention of Cardiovascular Disease in the Adult here.

 

ESC/EAS - Aug 2016

 

  • Lipoprotein(a) is a low-density lipoprotein to which an additional protein called apolipoprotein(a) is attached.
  • High concentrations of Lp(a) are associated with increased risk of CAD and ischemic stroke and Mendelian randomization studies support a causal role in CVD for Lp(a).
  • At present there is no justification for screening the general population for Lp(a), but it may be considered in patients at moderate risk to refine risk evaluation or in subjects with a family history of early CVD.

 

Catapano, et al. European Heart Journal (2016) DOI: http://dx.doi.org/10.1093/eurheartj/ehw272 ehw272 First published online: 27 August 2016

 

 

Pediatric Guidelines Dec 2011 
 
2011 Dec;128 Suppl 5:S213-56. doi: 10.1542/peds.2009-2107C. Epub 2011 Nov 14.

  

Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: summary report.

   

In terms of other lipid measurements, (1) most but not all studies have found that measurement of apolipoprotein B and apolipoprotein A-1 for universal screening provides no additional advantage over measuring non-HDL cholesterol, LDL cholesterol, and HDL cholesterol levels, (2) measurement of lipoprotein(a) is useful in the assessment of children with both hemorrhagic and ischemic stroke, (3) in offspring of a parent with premature CVD and no other identifiable risk factors, elevations of apolipoprotein B, apolipoprotein A-1, and lipoprotein(a) have been noted, and (4) measurement of lipoprotein subclasses and their sizes by advanced lipoprotein testing has not been found to have sufficient clinical utility in children at this time (grade B).

 

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