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REFLECTIONS
Dyslipidaemia
Dyslipidaemia Global Newsletter #8 2024

This review delves into historical perspectives, physiology,
pathophysiology, genetic causality evidence, epidemiology, the Dyslipidaemia
role in familial hypercholesterolemia and diabetes, management,
screening, diagnosis, measurement, prevention, and the future
of Lp(a)-lowering drugs.

In terms of pathophysiology, the authors explain that
lipoprotein(a) particles could, via kringle structures, attach to
fibrin in the thrombus and inhibit plasmin-driven fibrinolysis,
leading to thrombus growth and cardiovascular disease.
Lipoprotein(a) could also deliver cholesterol for tissue repair and
wound healing.

Individuals with Lp(a) concentrations in the top 5% (>90 mg/dL
or >190 nmol/L) have a significantly increased risk of various CV
conditions, with 3-fold increased risk of myocardial infarction and
aortic valve stenosis.

Current guidelines recommend measuring Lp(a) at least once
in a lifetime, particularly for individuals at high cardiovascular
risk. While no approved Lp(a)-lowering drugs are available,
managing other CV risk factors (e.g., LDL-C, blood pressure) is
crucial.

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