Gothala Sushma Chandrika, Kongi Kavyasudha and Yadala Prapurna Chandra
Dyslipidemia, defined as abnormal levels of blood lipids, is a significant risk factor for cardiovascular disease (CVD), the leading cause of death globally. It is commonly characterized by elevated low-density lipoprotein cholesterol (LDL-C) or triglycerides, reduced high-density lipoprotein cholesterol (HDL-C), or a combination of these abnormalities. Such lipid imbalances contribute to atherosclerosis, endothelial dysfunction, and plaque formation, ultimately increasing the risk of thrombotic events like myocardial infarction and stroke. The development of dyslipidemia is influenced by modifiable factors including diet, obesity, physical inactivity, smoking, alcohol consumption, diabetes, and hypertension as well as non-modifiable factors such as age, sex, and genetic predisposition. Excess LDL cholesterol can infiltrate the vascular endothelium, undergo oxidation, and activate inflammatory pathways, promoting foam cell formation and plaque progression. Management begins with lifestyle modifications, such as adopting a heart-healthy diet, engaging in regular physical activity, maintaining a healthy weight, avoiding tobacco, and moderating alcohol intake. Pharmacological therapy is essential for high-risk patients or those unresponsive to lifestyle interventions, with statins serving as first-line treatment. Other options include fibrates, bile acid sequestrants, ezetimibe, and PCSK9 inhibitors, which target various aspects of lipid metabolism. Despite these therapies, residual cardiovascular risk persists, necessitating innovative approaches. Emerging treatments, including small interfering RNA (siRNA), antisense oligonucleotides, gene-editing strategies, and lipoprotein (a)-targeted agents, offer promise for long-term and personalized lipid control. Integrating lifestyle measures, pharmacotherapy, and novel interventions is essential to achieve optimal outcomes and reduce global CVD morbidity and mortality.
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