The role of lipoprotein (a) in the development of cerebral atherosclerosis.

OBJECTIVE

Aim: To review information sources on this issue in order to provide up-to-date knowledge on the pathogenesis of this condition.

PATIENTS AND

METHODS

Materials and

Methods

The PubMed, Embase, and the Cochrane Library databases were searched for studies from inception to April 16, 2022, without language restrictions. Databases were searched for studies from inception 2010 to December, 2024, without language restrictions. Key words for search: Lipoprotein(a), Lp[a], dyslipidemia, classical vascular risk factors, cardiovascular disease, cardiovascular risk, cardiovascular risk factor, cerebral atherosclerosis. More than 37 sources was analyzed.

CONCLUSION

Conclusions

Cardiovascular diseases remain the leading cause of disability and mortality globally. While dyslipidemia is a well-established risk factor for coronary atherosclerosis and myocardial infarction, its role in the development of intracranial atherosclerosis is less well characterized. Current evidence suggests that plasma measurement of lipoprotein(a) [Lp(a)] using validated assays is sufficient for cardiovascular risk stratification, obviating the need for genetic testing of Lp(a). Advanced diagnostic methods have demonstrated that elevated Lp(a) levels are associated with increased vascular wall inflammation, reinforcing its causal role in atherogenesis. Intracranial atherosclerosis, a major cause of ischemic stroke, is linked to a heightened risk of recurrent cerebrovascular events and the progression of vascular cognitive impairment. Although Lp(a) is a recognized risk factor for stroke, its predictive value appears to be lower than that for coronary heart disease or composite cardiovascular outcomes. Therefore, the clinical implications of elevated Lp(a) levels in relation to carotid and intracranial atherosclerosis merit further investigation, particularly in the context of stroke prevention and vascular dementia.