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Editorial
April 24, 2019

Using Genetics to Plan Future Randomized Trials of Lipoprotein(a) Lowering—How Much Reduction, for How Long, and in Whom?

Author Affiliations
  • 1Preventive and Genomic Cardiology, McGill University Health Center and Research Institute, Montreal, Quebec, Canada
JAMA Cardiol. 2019;4(6):513-514. doi:10.1001/jamacardio.2019.1107

Imagine the case of a previously healthy middle-aged patient who has experienced an anterior ST-elevation myocardial infarction. A physician measures the patient’s lipoprotein(a) (Lp[a]) levels at 386 mg/dL, almost 25 times the mean Lp(a) level in North America and in the upper 99th percentile of Lp(a) distribution. This level of Lp(a) was likely the major contributor to the early myocardial infarction and leaves the patient at a very high risk for recurrent events. How should the physician proceed? Statins and most lipid-lowering therapies (except niacin, apheresis, and proprotein convertase subtilisin/kexin type 9 inhibitors) have no meaningful effect on Lp(a) levels. In addition, until very recently, there were no targeted therapies to lower Lp(a). But even with such therapies in development, how much would we need to lower the Lp(a), and for how long, to avoid future events? This is a key question for clinicians treating patients with high Lp(a), as well as clinical trialists planning future randomized clinical trials (RCTs) of Lp(a) lowering.

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