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
- aortic valve
- endothelial cells
- transcatheter aortic valve implantation
- left ventricular
- oxidative stress
- coronary artery disease
- cell proliferation
- working memory
- heart failure
- metabolic syndrome
- atrial fibrillation