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These studies suggest that high LDL-C is associated with increased risks of peripheral arterial disease and chronic kidney disease, while lowering LDL-C improves clinical outcomes and reduces cardiovascular events.
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High levels of low-density lipoprotein cholesterol (LDL-C) are strongly associated with an increased risk of coronary artery disease (CAD) and other cardiovascular conditions. LDL-C is often referred to as "bad cholesterol" because it contributes to the buildup of plaque in the arteries, leading to atherosclerosis. This condition can result in heart attacks, strokes, and other serious cardiovascular events .
Recent studies have expanded our understanding of the impact of high LDL-C beyond coronary artery disease. High LDL-C levels have been linked to an increased risk of peripheral arterial disease (PAD) and chronic kidney disease (CKD). Observational and genetic analyses indicate that higher LDL-C levels are causally related to these conditions, suggesting that managing LDL-C is crucial for preventing a broad spectrum of vascular diseases.
Statin therapy is a cornerstone in the management of high LDL-C. High-intensity statin regimens aim to reduce LDL-C levels by 50% or more, which has been shown to significantly lower the risk of first cardiovascular events. The effectiveness of statins in reducing LDL-C and improving cardiovascular outcomes supports current guidelines that advocate for both absolute LDL-C targets and percentage reduction goals .
While high-density lipoprotein cholesterol (HDL-C) is traditionally seen as "good cholesterol," recent research emphasizes the importance of HDL functionality over its concentration. HDL's ability to promote cholesterol efflux from macrophages, a process known as cholesterol efflux capacity (CEC), is a critical factor in its protective role against atherosclerosis. This functionality is more predictive of cardiovascular health than HDL-C levels alone.
The scavenger receptor class B type I (SR-BI) has been identified as a key receptor for HDL. SR-BI facilitates the selective uptake of cholesterol from HDL into cells, distinguishing its mechanism from that of LDL receptors. This receptor plays a significant role in HDL metabolism and its atheroprotective functions.
Interestingly, both low LDL-C and high HDL-C levels have been associated with elevated liver enzymes, indicating potential liver dysfunction. This finding suggests a complex relationship between lipid metabolism and liver health, highlighting the need for comprehensive evaluation in individuals with dyslipidemia.
Managing high LDL cholesterol is crucial for reducing the risk of cardiovascular and peripheral vascular diseases. Statin therapy remains a highly effective strategy for lowering LDL-C levels and improving clinical outcomes. Additionally, the functionality of HDL cholesterol, rather than its concentration, plays a significant role in cardiovascular protection. Understanding these dynamics can help in the development of more targeted and effective treatments for dyslipidemia and its associated health risks.
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