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REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #4 2023
measured RC using nuclear magnetic resonance indicated Dyslipidaemia
that calculated RC was positively consistent with measured RC CLINICAL PEARLS FROM THE FACULTY
at high TG levels (≥150 mg/dL), but was poorly correlated with
measured RC when the TG levels were <150 mg/dL. In addition,
there are some controversies regarding the use of fasting or
non-fasting remnant lipid profiles to predict potential CVD risk.
Several current recommendations support the use of a random,
non-fasting lipid profile in clinical practice for CVD risk prediction,
and a subgroup analysis of the data in the publication showed
that regardless of the use of fasting or non-fasting RC, elevated
RC is associated with an elevated CVD risk. This will allow for
convenience in using non-fasting RC in clinic follow-ups.
WATCH
The authors suggest that it is reasonable to conclude that RC- PROF. FARNIER DISCUSS THE
lowering therapy can further reduce residual CVD risks. Statins RELEVANCE OF THESE RESULTS FOR
have been shown to reduce RC, and a combination of statin CLINICAL PRACTICE.
with ezetimibe was shown to reduce RC to a greater extent than
using ezetimibe or statins alone.
It is also unclear if the use of RC as a risk marker for initially CLICK HERE
identifying high-risk patients can improve the 10-year risk score. FOR THE LINK TO FULL ARTICLE
Further studies are needed to explore and validate the 10-year
risk score when using RC as a risk marker for CVD events.
Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis:
A European Atherosclerosis Society consensus statement.
Kronenberg F, et al. Eur Heart J. 2022;43(39):3925-3946.
Since the 2010 European Atherosclerosis Society (EAS) consensus statement, there has been extensive research on the role of
Lp(a) in ASCVD and aortic valve stenosis. The 2022 EAS lipoprotein(a) consensus statement, therefore, updates the evidence for
the role of Lp(a) in ASCVD and aortic valve stenosis, provides clinical guidance for testing and treating elevated Lp(a) levels, and
discusses inclusion of Lp(a) in global risk estimation.
Lp(a) concentration is predominantly determined by genetics (>90%), more than any other lipoprotein. The authors also noted
that Lp(a) level varies with ethnicity (in increasing order: Chinese, White, South Asian, and Black individuals). There are also sex
differences, with Lp(a) concentration generally ~5–10% higher in women than men, and while Lp(a) remains relatively constant
throughout the lifespan, women levels tend to increase at menopause.
Non-genetic factors may also influence Lp(a) concentration, including lifestyle, hormones and related conditions, chronic kidney
disease, hepatic impairment, and inflammation and related conditions (see table below for details within each category).
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