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Lipoprotein (a)
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Beyond traditional lipid profiles, clinicians have a wide variety of studies for cardiovascular risk assessment available to choose from: highly sensitive C-reactive protein, nuclear magnetic resonance lipid particle assessment, apolipoprotein B, lipoprotein-associated phospholipase A2, lipoprotein (a), coronary calcium scoring, carotid intima-media thickness assessment and others. It can be difficult to decide which of these add to care vs. only add cost to care.
Lipoprotein (a) or Lp(a) is an LDL-like particle which is covalently linked to the glycoprotein apolipoprotein (a) by a disulfide bridge. Lp(a) has been shown to promote atherosclerosis in animal models. Apolipoprotein (a) shares structural homology with plasminogen which may result in impaired fibrinolysis and promote thrombosis. Epidemiologic studies suggest increased cardiovascular risk associated with higher levels of Lp(a). Elevated Lp(a) is most strongly associated with increased cardiovascular risk when other risk factors such as smoking, diabetes or hypertension are present.
A recent meta-analysis reviewed 36 eligible prospective studies. It found that levels of Lp(a) are independently associated with risk of coronary heart disease and stroke. However, the effects were modest, only about one-quarter as strong as non-HDL cholesterol.
Niacin is the most potent agent to lower Lp(a), reducing levels by as much as 20%. Statins may also lower cardiovascular risk in patients with elevated Lp(a), but longer-term prospective studies are lacking. Designing such studies is challenging because agents that have beneficial effects in regards to Lp(a) also reduce LDL cholesterol and raise HDL cholesterol. It can be difficult, if not impossible, to determine exactly which factor is promoting lower risk.
In my own practice, I order Lp(a) only in select patients. This includes those with personal or family history of premature coronary or vascular events without obvious risk factors. In those whom I find to have elevated Lp(a), I address other risk factors such as smoking and hypertension. I may also consider pharmacologic therapy with niacin and/or statin.
Instead of encouraging my colleagues to routinely order emerging studies such as Lp(a), I more strongly advocate for them to screen for traditional risk factors and address them. Too many of our patients are at increased cardiovascular risk and yet are not being identified and treated until after an event occurs.