2026· Medicinska istrazivanja· pp. 29-29· 0 citations· 32 references
TL;DR
It is concluded that secondary causes must be ruled out upon diagnosis and non-HDL cholesterol is highlighted as a critical secondary therapeutic target for comprehensive cardiovascular risk management.
Abstract
Despite significant advances in lowering LDL cholesterol, a substantial residual risk for atherosclerotic cardiovascular disease (ASCVD) persists, largely driven by triglyceride-rich lipoproteins (TRLs). This narrative review emphasizes the importance of hypertriglyceridemia in the development of atherosclerotic cardiovascular disease and acute pancreatitis and clarifies the diagnostic dilemmas and current therapeutic options. This narrative review explores the pathophysiology, diagnostic criteria, and epidemiological impact of hypertriglyceridemia. TRLs, including chylomicrons and VLDL, contribute to atherosclerosis through the accumulation of cholesterol-rich "remnant particles" and apolipoprotein B (Apo B) in the subendothelial space. Recent epidemiological data, including findings from the Copenhagen General Population Study and the SIMETAP-HTG study, confirm that mild-to-moderate hypertriglyceridemia (1.7-5.6 mmol/L) is prevalent in approximately 25% of the population and is strongly associated with increased risks of myocardial infarction, heart failure, and multiorgan diseases such as diabetes and MASLD. Conversely, severe hypertriglyceridemia (≥10 mmol/L) significantly elevates the risk of acute pancreatitis. Current guidelines emphasize measuring fasting triglycerides, though non-fasting levels are increasingly recognized for screening. The paper concludes that secondary causes must be ruled out upon diagnosis and highlights non-HDL cholesterol as a critical secondary therapeutic target for comprehensive cardiovascular risk management. The final part of the review is focused on novel therapeutic options and emerging therapies for increased TRL.
ABSTRACT Managing hypertriglyceridemia (HTG) requires more than lowering triglyceride (TG) levels. Two related but clinically distinct risk domains often guide management: residual atherosclerotic cardiovascular disease (ASCVD) risk and acute pancreatitis (AP) risk. Their relative importance varies among patients and m...
The role of low-density lipoprotein cholesterol (LDL-C) in the excess cardiovascular risk associated with CKD is addressed and the impact of both traditional and novel LDL-C-lowering therapies across the entire spectrum of CKD is examined.
R. Minutolo, M. Ravera, M. Cozzolino et al.· Giornale Italiano di Nefrolo...· 0 citations
An overview of domestic and international guidelines for dyslipidemia is provided and the association between dyslipidemia and ischemic stroke is summarized from the perspectives of pathophysiology, pathological findings, and imaging and blood biomarker.
Junya Aoki· Journal of atherosclerosis a...· 0 citations
BACKGROUND
Homozygous familial hypercholesterolemia (HoFH) causes severe lifelong low-density lipoprotein-cholesterol (LDL-C) elevation and accelerated atherosclerosis from childhood.
CASE SUMMARY
A 10-year-old boy presented with extensive tuberous xanthomas and was diagnosed with HoFH due to bi-allelic pathogenic va...
D. Zachariah, A. Thomas, Lindinkululeko Nkheli et al.· JACC Case Reports· 0 citations
BACKGROUND
Familial hypercholesterolemia is characterized by lifelong elevations in low-density lipoprotein cholesterol (LDL-C) that, when left untreated, markedly increase the risk of premature atherosclerotic cardiovascular disease (ASCVD). Although ASCVD is common in adults with familial hypercholesterolemia, events...
V. Thorsen, George Slim, Navaneetha Saskikumar et al.· JACC Case Reports· 0 citations
It is demonstrated that hyperuricemia is independently associated with angiographically documented CAD after adjustment for conventional cardiovascular risk factors, and it is suggested that serum uric acid may serve as a marker of overall atherosclerotic burden rather than merely indicating the presence of coronary st...
Ahmad Fawad· Pakistan Heart Journal· 0 citations
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