Lipoprotein (a) used to be the forgotten lipid. Not anymore.

human heart low poly color

Lipoprotein (a) — or its abbreviation, Lp(a), pronounced “el-pee-little-a” — is emerging from obscurity. And for good reason. Among them, Bob Harper, the TV famous trainer from The Biggest Loser, has helped bring Lp(a) to national attention after his heart attack in 2017. Put simply, Lp(a) is a version of LDL that is more dangerous. It is more pro-inflammatory and more pro-thrombotic.

Studies show that elevated Lp(a) levels correlate with increased cardiac risk. So, it makes sense that we would want to lower patients’ elevated Lp(a) levels to reduce cardiac risk, right? So far, that hasn’t been very successful.

Unfortunately, Lp(a) does not respond well to lifestyle changes. Its level is almost entirely genetically determined and cannot be easily manipulated with environmental exposures (nutrition and exercise) the way that LDL can. The best treatments for lowering Lp(a) are niacin and a drug class called CETP inhibitors. The problem, however, is that despite lowering Lp(a), these treatments have not been shown to reduce the outcomes we care about — the risk of heart attack and death.

The conventional wisdom, therefore, is to treat other risk factors more aggressively in those with elevated Lp(a). Top on the list, of course, is treating LDL with statin medications.

That may now change. A new study published in the Lancet looked back at seven statin trials including over 29,000 subjects. The authors found that even with statin treatment, Lp(a) levels above 50mg/dL were still associated with increased cardiac risk. This was despite the reduction of LDL on average by almost 40%. (With Lp(a), it is important to note the units since it is also often reported as a particle count, in nmol/L.)

The Lancet: Baseline and on-statin treatment lipoprotein(a) levels for prediction of cardiovascular events: individual patient-data meta-analysis of statin outcome trials

It does not appear that statin therapy significantly lowers the risk of cardiovascular disease events in those with elevated Lp(a). The authors concluded that the study “provides rationale for evaluating drugs to specifically lower Lp(a) in cardiovascular outcome trials.” On the one hand, this conclusion makes sense based on the trial data. On the other hand, it should come as no surprise that the trial was sponsored by the pharmaceutical company Novartis, which just happens to have an investigational drug targeting Lp(a), which presents a clear conflict of interest.

Future studies may or may not prove that lowering Lp(a) with drugs reduces cardiac risk. However, we know for certain that regardless of Lp(a) levels, healthy lifestyle habits are always first-line therapy for improving our cardiovascular risks. No matter what drugs we may or may not take, nutrition, exercise, stress management, and other lifestyle interventions are the best place to start.

Thanks for reading,
Bret Scher, MD FACC


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