Relationship between Lipoprotein (a) and Both Stroke and Carotid Atheroma
Key result
Lipoprotein (a) concentrations did not significantly differ between patients with stroke or transient ischaemic attack and controls (median 0.10 vs 0.12 g/L; P=0.34).
Why the study?
Is there an association between Lipoprotein (a) concentrations and stroke, transient ischaemic attack, or carotid atheroma?
Population
164 patients studied at least 21 days after stroke or transient ischaemic attack, and 91 controls.
Design
Case-control
Authors
Discussion
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Implication
Lp(a) concentrations were not associated with stroke or TIA; leaves open its cerebrovascular role and requires prospective confirmation.
Study Design
Type
Case-Control (n=255)
Structured PICO
Is there an association between Lipoprotein (a) concentrations and stroke, transient ischaemic attack, or carotid atheroma?
P
Population
255 participants, including 164 patients evaluated at least 21 days after stroke or transient ischaemic attack and 91 controls, assessed for lipoprotein (a) concentrations.
C
Comparator
Controls without stroke or transient ischaemic attack
O
Outcome
Difference in Lipoprotein (a) [Lp(a)] concentration between cases and controlssurrogate
Main Result
Absolute Event Rate: 0.1% vs 0.12%
p-value: p=0.34
In an unselected population of men studied >3 weeks post-event, there is no significant relationship between Lp(a) concentrations and stroke, TIA, or carotid atheroma.
Cite This Study
Markus et al. (1997) conducted a case-control in Stroke or transient ischaemic attack (n=255). Lipoprotein (a) concentrations vs. Controls without stroke or transient ischaemic attack was evaluated on Lipoprotein (a) concentration (p=0.34). Lipoprotein (a) concentrations did not significantly differ between patients with stroke or transient ischaemic attack and controls (median 0.10 vs 0.12 g/L; P=0.34).