Lipoprotein(a) and large artery atherosclerosis: Results from the BIOSIGNAL Study

BackgroundLipoprotein(a) (Lp(a)) is a causal risk-factor for atherosclerotic cardiovascular disease including acute ischemic stroke (AIS). The underlying pathomechanisms mediating this risk are less well understood, especially in AIS caused by large artery atherosclerosis (LAA). In this observational cohort study we evaluated the association of Lp(a) with markers of LAA, namely carotid intima media thickness (cIMT) and the presence of extra- or intracranial vessel narrowing plaques. MethodsAmong participants of the BIOSIGNAL cohort study we determined Lp(a) levels within 24h after symptom onset in 1161 AIS patients from the single center of Zurich. cIMT was determined using a semi-automated computerized edge tracking software, internal carotid artery (ICA) stenosis was graded according to the North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria, intracranial ultrasound was performed by transcranial color-coded duplex (TCCD). ResultsIn 1161 participants higher Lp(a) levels were not associated with an increased cIMT in univariable or multivariable regression models containing known cardiovascular risk-factors. Higher Lp(a) levels were not associated with the presence of neither extracranial high-grade ICA-stenosis nor significant intracranial stenosis assessed by neurovascular ultrasound. ConclusionIn AIS patients higher Lp(a) levels were not associated with clinical markers of arteriosclerotic burden despite its association with LAA-stroke etiology and an increased risk for stroke recurrence. RegistrationRegistration-URL: http://www.clinicaltrials.gov; Unique identifier: NCT-02274727