
Dr. Dapo
6.5K posts

Dr. Dapo
@DrDapo
Dapo Iluyomade MD MBA FACC FAHA 🫀 Preventive Cardiologist @BaptistHealthSF || Assistant Prof of Medicine @FIUmedicine || #cvPrev 🇳🇬 Tweets mine.





















Key updates to this guideline include: ➡️ The use of the American Heart Association PREVENT-ASCVD equations to guide primary-prevention and lipid-lowering therapy decisions. ➡️ Testing Lp(a) at least once in a lifetime and selective apolipoprotein B measurement to improve risk assessment and guide treatment ➡️ The return of LDL-C and non-high-density lipoprotein cholesterol treatment goals (with lower targets for higher-risk groups) ➡️ Expanded use of coronary artery calcium scoring to reclassify risk[ME1.1] ✍🏼 @rblument1 @tygluckman @RonBlankstein @PamelaBMorris @pnatarajanmd @AnnMarieNavar @SethShayMartin @APRN_CNS @nyulangone @DrMichaelShapir @kgradneyrd @eugeniagianos @virani_md @KellieMcLain1 @ijeomaheartdoc @SamiaMoraMD @DrHeatherJohn @dmljmd





















🧬 VLDL — The Central Particle Connecting Triglycerides, ApoB and LDL Within lipid metabolism, VLDL (Very Low Density Lipoprotein) represents the liver’s primary mechanism for exporting excess energy. It carries triglycerides and cholesterol from the liver to peripheral tissues and forms the starting point of the ApoB lipoprotein lifecycle. Understanding VLDL helps explain how triglycerides, HDL changes and LDL formation are interconnected. 🌿 VLDL Physiology — Why It Is Formed The liver produces VLDL when triglycerides accumulate from: • Dietary intake • Fatty acids released from adipose tissue • De novo lipogenesis These lipids are packaged with cholesterol and apolipoproteins — mainly ApoB-100 — allowing safe transport through circulation rather than hepatic storage. VLDL therefore represents energy distribution. 🧬 What VLDL Contains Each VLDL particle includes: • Triglycerides (major component) • Cholesterol • ApoB-100 (structural backbone) • ApoC proteins (regulate triglyceride utilisation) • ApoE (enables clearance) This integrates VLDL into the broader apolipoprotein network. 🌱 The VLDL Lifecycle As VLDL circulates: • Lipoprotein lipase removes triglycerides • The particle shrinks • It becomes IDL • Eventually contributes to LDL formation LDL is therefore a downstream product of VLDL metabolism. Under balanced conditions this process is efficient and transient. ⚠️ VLDL Pathophysiology — When Production Exceeds Utilisation When hepatic lipid input remains high or utilisation slows, VLDL production increases and clearance becomes less efficient. Common influences include: • Insulin resistance • Energy excess • Sedentary behaviour • Hormonal shifts • Inflammation and circadian disruption The system moves from turnover toward persistence. 🌿 What Persistent VLDL Leads To Prolonged circulation of triglyceride-rich particles results in: • Remnant particle accumulation • Lipid exchange with HDL altering its function • Increased ApoB particle burden • Formation of small dense LDL • Greater variability in LDL cholesterol despite similar particle numbers The disturbance extends across the lipid network. 🌱 Consequences of VLDL Imbalance When VLDL remains elevated: • Triglyceride levels rise • HDL patterns change • Remnant cholesterol becomes more relevant • Particle exposure to vascular tissue increases • Lipid profiles reflect persistence rather than efficient transport This explains why triglycerides often signal early metabolic change. 🌿 Why VLDL Matters Clinically VLDL reflects: • Hepatic metabolic state • ApoB particle production • Efficiency of triglyceride handling • Early cardiometabolic imbalance Changes in VLDL frequently precede significant LDL elevation and help interpret TG–HDL patterns. ✨ The Takeaway VLDL is not inherently harmful — it is essential for energy transport. Risk emerges when production, utilisation and clearance lose coordination, linking triglycerides, apolipoproteins, remnant particles and LDL transformation. Understanding VLDL shifts lipid interpretation from isolated numbers to dynamic metabolic processes.
