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Are All Cardiovascular Risk Factors Created Equal: Can Lp (a) be a contributor to cardiovascular disease?

by Joyce Ross, MSN, ANP, CS, CRNP, Diplomat ACCL, Clinical Lipid Specialist, FNLA, FPCNA

by Joyce Ross, MSN, ANP, CS, CRNP, Diplomat ACCL, Clinical Lipid Specialist, FNLA, FPCNA

As providers we are all aware of that patient who presents with premature heart disease, or that patient who closes off a newly placed stent shortly after placement in spite of treatment with traditional medications of statins, anti-coagulants, along with Beta blockade or ACE or ARB inhibition. Today we are becoming increasingly aware of another prevalent but uncommonly recognized independent risk factor that may shine light on this problem. Lipoprotein (a), (or Lp little a) is a unique lipoprotein abnormality and causal agent in cardiovascular disease that is highly heritable. (Jacobson 2013) This genetically influenced abnormality is heterogenic in worldwide populations. Nordestgaard (2010) indicates that elevated Lp(a) affects one in five people and is found in 63 million Americans. Suspicion arises for presence of this risk factor among patients presenting with premature vascular disease and strong family history. Lp (a) is not identified by testing of a traditional lipid panel but requires a specific test which to date may show variations within assays. While diagnostic for inheritance, it is not always indicative of disease severity. On examination a lipoprotein is noted that is very similar to an LDL-C particle that is linked to a plasminogen molecule, and when elevated has a profound affect on clot formation, which provides some hint as to how this informs atherosclerosis. To date the absolute function of Lp (a) is unknown. Treatment includes mostly clinically based therapies such as dramatically lowering LDL-C with stain therapy, which is important since Lp (a) travels as a kringle with LDL-C. Lifestyle management has not been shown to have a positive effect on Lp (a). It is important to reinforce that lowering Lp (a) alone has not been shown to change vascular outcomes; further research is necessary in this arena. While we know that statin therapy has no independent influence on Lp (a) Niacin as well as estrogen therapy have been shown in clinical trials to lower Lp (a), however no evidence is reported that treatment of this independent factor changes outcome. The newest class of dyslipidemia medications PCSK9 inhibitors appear to hold promise in their effect to reduce Lp (a), we await outcomes of this work.

In the meantime this author feels that identification of this independent risk factors can have utility in prevention or halting the progression of cardiovascular disease. When elevated levels are found in the patient with known CVD or family history of CVD this knowledge may be helpful to inform the treatment plan. For those with known CVD, LDL-C thresholds can be lowered to < 70 mg/dL. In the case of primary prevention prevalence knowledge of this factor can inform the primary prevention plan by treating with fastidious lifestyle management and setting the threshold for all root atherogentic lipids, LDL-C, Non-HDL, TGs from those of a low/moderate to moderate/high risk for CVD. A foundation has been established which seeks to educate, enlighten and encourage acceptance of this independent and unique risk factor. Please go to the website for further information about Lp (a) www.lipoproteinafoundation.org

References:
Jacobson, T., MD Lipoprotein (a), Cardiovascular Disease, and Contemporary Management. Mayo Clic Proc. November 2013;88(11):1294-1311
Nordestgaard B et al: European Atherosclerosis Society Consensus Panel. Lipoprotein (a) as a cardiovascular risk factor; current status. Eur Heart J 2010, 31(23):2844-2853