2025: The year in cardiovascular disease - the year of triglyceride lowering therapies. Can we effectively reduce triglyceride-related residual cardiovascular disease and pancreatitis risk?
Abstract
This state-of-the-art review surveys the rapidly advancing field of triglyceride-lowering therapies as of 2025, positioning hypertriglyceridemia (HTG) as both a residual driver of atherosclerotic cardiovascular disease (ASCVD) and a key precipitant of acute pancreatitis. After outlining the pathophysiological role of elevated triglycerides - via remnant lipoproteins, inflammation and endothelial dysfunction, often within the lipid triad of low high-density lipoprotein-cholesterol (HDL-C) and small, dense low-density lipoprotein (LDL) - we evaluate established and emerging pharmacologic options. Fenofibrate, a PPAR-α activator, remains a cornerstone for mixed dyslipidemia, improving micro- and macrovascular outcomes in diabetes. Purified eicosapentaenoic acid (icosapent ethyl) is highlighted for its robust reduction of major adverse cardiovascular events despite neutral triglyceride thresholds, albeit with a modest increase in atrial fibrillation risk. Novel agents targeting apolipoprotein C-III (volanesorsen, olezarsen, plozasiran) achieve profound triglyceride declines and substantially mitigate pancreatitis in familial chylomicronemia syndrome (FCS), while angiopoietin-like 3 (ANGPTL3) inhibitors and fibroblast growth factor 21 (FGF21) agonists demonstrate early promise in broad atherogenic-lipid reduction and metabolic modulation. The paper emphasizes the importance of genetic testing to differentiate FCS from multifactorial chylomicronemia syndrome, guiding personalized…
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