2 responses to “Elevated Lipoprotein (a) is a common reason for unexplained premature or recurrent coronary heart disease and stroke”

  1. Thank you for this interesting summary of evidence which is mostly new to me. This is an exciting idea but I’m not completely certain whether measurement of Lp(a) is “ready for prime time” based on the evidence presented.

    In 2015 very sensible lipid management guidelines were published in the Canadian Family Physician Journal (http://www.cfp.ca/content/61/10/857). It was based on good evidence that:
    1) Lipid lowering therapy should be based on overall cardiovascular risk, not lipid levels.
    2) Treating to target is not evidence based, as statin therapy of a given intensity (i.e. low- medium- or high-dose) confers the same relative risk reduction regardless of initial lipid levels.

    With regard to the above article, if we bear in mind the very sensibile and evidence-based principles described in that guideline it seems to me that the following conclusions can be drawn:

    – Since secondary prevention patients should always be on the highest intensity statin therapy they can tolerate, there is no need to check the Lp(a) levels in those patients regardless of their age at first MI.

    – Non-statin lipid lowering therapies (e.g. Niacin, as mentioned in the article) have never been shown to reduce CVD, another important reminder of the fallacy of the treat-to-target approach.

    – the evidence for primary prevention of CVD with statins is very weak in all but the highest risk groups, even though presumably 20% of the patients in those primary prevention trials would have had elevated Lp(a) based on the epidemiological evidence presented above.

    Thus, we conclude that 1) patients at low baseline risk will likely not benefit or benefit minimally from statin therapy regardless of Lp(a) level; 2) patients at high risk should already be on maximal statin therapy regardless of Lp(a) level; and 3) the only question is whether measuring Lp(a) in patients at moderate risk who are not currently on a statin might nudge them into the higher risk category and justify starting statin therapy. It seems to me that this question is interesting but far from answered.

  2. Thank you for your feedback. The Canadian Family Physician Lipid Guidelines published in 2015 are aimed at primary prevention patients, and do not address patients with inherited hyperlipidemia of which high Lp(a) is one type. Regardless of the lipid guidelines you choose to follow, the point of the article is that if you encounter premature coronary heart disease or stroke in a patient in whom obvious other reasons are not present, you should consider measuring Lp(a) to help understand the etiology of the early CVD. If you have a patient in whom premature CVD is present in their first degree relatives, and the patient is found to have high Lp(a), consideration should be given to starting the patient on a statin sooner to reduce the risk associated with the high Lp(a). The article does not propose measuring Lp(a) routinely in primary prevention patients, only those with such a history. The article also did not propose measuring Lp(a) routinely in secondary prevention patients, only in those with recurrent events despite adequate treatment with statins +/- other lipid lowering agents such as ezetimibe. In those cases is it optional to consider use of an agent like niacin to reduce the Lp(a), even though a good trial of this approach has not been done. It remains as part of the “art” of medicine and works very well in individual patients. Regarding your other points, while percent reduction of vascular events in patients with a given dose of a statin is similar in patients with varying levels of starting LDL-C, the actual event numbers remain much higher in those with higher starting LDL-C (as evidenced by the Heart Protection Study), suggesting lowering LDL-C further is beneficial. The non-statin therapy ezetimibe has been shown to have clear benefit in reducing CVD events when added to a statin (the IMPROVE-IT Trial, New Engl J Med 2015;372:2387-97). The Cochrane Collaboration concluded in their 2013 review that statins are indeed protective in primary prevention patients, including women (http://www.cochrane.org/CD004816/VASC_statins-primary-prevention-cardiovascular-disease).

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