Lp(a) tends to accumulate in artery walls, promoting plaque formation and potentially triggering atherosclerosis progression through prothrombotic or antifibrinolytic effects. High Lp(a) levels correlate with calcific aortic stenosis and atherothrombosis risk. L5 can induce endothelial cell apoptosis and increase vascular permeability, inflammation, and atherogenesis, playing a key role in initiating atherosclerosis. Elevated L5 levels in certain high-risk populations may serve as a distinctive predictor of ASCVD. L5 and Lp(a) are both atherogenic lipoproteins contributing to ASCVD through distinct mechanisms. Lp(a) has garnered attention, but equal consideration should be given to L5.
Keyphrases
- cardiovascular disease
- aortic stenosis
- transcatheter aortic valve replacement
- ejection fraction
- aortic valve replacement
- transcatheter aortic valve implantation
- aortic valve
- endothelial cells
- oxidative stress
- coronary artery disease
- left ventricular
- type diabetes
- working memory
- cell proliferation
- metabolic syndrome
- cardiovascular events
- atrial fibrillation
- cardiovascular risk factors