Im Ziel oder nicht? Wenn LDL, Non-HDL und ApoB Verschiedenes sagen

<h4>Background</h4>Cardiovascular risk in type 1 diabetes mellitus (T1DM) is frequently underestimated in daily clinical practice. The aim was therefore to evaluate lipid management in patients with T1DM according to current guidelines, and agreement in target attainment across three recommended lipid biomarkers.<h4>Methods</h4>Target attainment of (low-density lipoprotein cholesterol [LDL-C, estimated with the Friedewald formula], non-high-density lipoprotein cholesterol [non-HDL-C], and apolipoprotein B [apoB]) was determined based on the 2021 European Society of Cardiology Dyslipidemia guideline among adult patients with T1DM enrolled in SwissDiab.<h4>Results</h4>Median age of the 216 patients included was 43.6 years, diabetes duration 16 years, HbA1c 7.3% (56 mmol/mol), 39.4% were females, 75.0% were at high, and 11.6% at very high cardiovascular risk. Prescription of lipid-lowering therapy (LLT) was low (33.6%). LDL-C target attainment was poor (11.6%), while significantly more patients reached non-HDL-C (30.6%) and apoB (59.7%) targets (P-values <0.00001). Overall, 11.1% of the patients reached all three, and 39.8% none of the lipid targets.<h4>Conclusion</h4>Raised awareness of the importance of lipid management in T1DM is needed. However, the observed discordance in target attainment across lipid biomarkers can lead to uncertainties in clinical decision-making on how to best apply current lipid management recommendations for optimal cardiovascular risk prevention in T

Atherosclerotic cardiovascular disease (ASCVD) remains the leading global cause of morbidity and mortality, even in the era of aggressive low-density lipoprotein cholesterol (LDL-C) lowering. This persistent residual risk has prompted a reevaluation of atherogenic lipid markers, with non-high-density lipoprotein cholesterol (non-HDL-C) and apolipoprotein B (Apo B) emerging as superior indicators of the total atherogenic particle burden. Unlike LDL-C, non-HDL-C includes cholesterol from all atherogenic lipoproteins, while Apo B reflects the total number of atherogenic particles regardless of cholesterol content. Their clinical relevance is underscored in populations with diabetes, obesity, and hypertriglyceridemia, where LDL-C may not adequately reflect cardiovascular risk. This review explores the biological, clinical, and genetic foundations of non-HDL-C and Apo B as critical tools for risk stratification and therapeutic targeting. It highlights discordance analysis, inflammatory mechanisms in atherogenesis, the influence of metabolic syndromes, and their utility in specific populations, including those with chronic kidney disease and children with familial hypercholesterolemia. Additionally, the role of lipoprotein (a), glycation in diabetes, and hypertriglyceridemia are examined as contributors to residual risk. Clinical trials and genetic studies support Apo B and non-HDL-C as more robust predictors of cardiovascular events than LDL-C. Current guidelines increasingly endo

Apolipoprotein B (ApoB) has emerged as a central biomarker and mechanistic driver of atherosclerotic cardiovascular disease (ASCVD), outperforming traditional lipid metrics in both risk stratification and therapeutic targeting. In this article a critical evaluation of the information is presented on the molecular biology, metabolic regulation, and clinical relevance of ApoB isoforms, ApoB100 and ApoB48, which play their own distinct, yet complementary roles in hepatic and intestinal lipid transport. The ways in which ApoB particle density is influenced by insulin resistance, nutrient status, hepatic lipid flux, inflammation, and genetic variation, all of which contribute to dyslipoproteinemic phenotypes associated with ASCVD and metabolic syndrome. Importantly, ApoB levels provide a direct measure atherogenic particle number, offering superior predictive value over low-density lipoprotein cholesterol (LDL-C), particularly in cases of lipid discordance and among statin-treated patients with residual cardiovascular risk. Emerging evidence demonstrates therapies targeting ApoB reduction, including statins, PCSK9 inhibitors, and glucose-lowering agents such as GLP-1 receptor agonists, can significantly reduce major adverse cardiovascular events. However, the lipid-modulating effects of agents like SGLT2 inhibitors, metformin, and thiazolidinediones are variable or independent of ApoB changes. The classification of four ApoB-related dyslipoproteinemic phenotypes, normotriglyceride