George Touma: ApoB Should Be Central to All Lipid Guidlines
George Touma, Interventional Cardiologist at St George Private Cardiology, shared a post on LinkedIn:
“ApoB Should Be Central to All Lipid Guidlines.
We have spent decades asking: ‘What is the LDL-C?’
The more important question is: ‘How many atherogenic particles are actually circulating?’
I learnt approximately 12 years from Dr Allan Snidermans pioneering paper that:
- LDL-C measures the amount of cholesterol carried within LDL particles.
- ApoB reflects the number of circulating atherogenic particles.
And there is essentially one ApoB molecule per atherogenic particle — LDL, IDL, VLDL remnants and Lp(a).
This is important because atherosclerosis is driven by the retention of atherogenic lipoprotein particles within the arterial wall, not by cholesterol existing in isolation.
Two patients can have exactly the same LDL-C and very different ApoB concentrations. Their cholesterol concentration may look identical. Their atherogenic particle burden is not.
This becomes particularly important in:
- metabolic syndrome and diabetes
- hypertriglyceridaemia
- obesity
- low HDL-C states
- patients with LDL-C or non-HDL-C discordance
- patients who have achieved an apparently ‘optimal’ LDL-C but retain substantial residual risk
We have confused what is convenient to measure with what is biologically most relevant to our patients. Unfortunately, guidelines continue to conflate these measures relying on LDL cholesterol targets
The future of lipid guidelines and management should be ApoB as the central underlying particle-based measure of atherogenic burden.
If our objective is to prevent atherosclerosis, particle number must be at the centre of the conversation.
So its perplexing to me why the 2026 ACC/AHA guideline did not specifically recognises that apoB must be central.
Because apoB is commonly reported in g/L in my country of Australia:
- 100 mg/dL is 1.00 g/L
- 80 mg/dL is 0.80 g/L
- 70 mg/dL is 0.70 g/L
- 65 mg/dL is 0.65 g/L
- 55 mg/dL is 0.55 g/L
The important point for secondary prevention in my patients, I target ApoB less than 0.65 g/L as my minimum target for very-high-risk ASCVD and ApoB less than 0.55 g/L as an aggressive target when residual risk is substantial.
The following alogorithm from Dr Sniderman et al is all you need to diagnose and treat most clinically relevant hyperlipidemia.
Hope you find it useful. Please share it around.”
Stay updated with Hemostasis Today.
-
Nov 9, 2026, 10:08Ibrahim Mansoor: Rare Tests, Common Diseases – Rethinking Autoimmune Diagnostics
-
Nov 9, 2026, 09:29Veronica Sanchez: A Framework for Woman’s Health
-
Nov 8, 2026, 19:31Anna Kajaste-Rudnitski: Presenting AAV-Induced p53 Signalling in Human CNS Cells at ESGCT 26
-
Nov 8, 2026, 19:29David McIntosh: Cybersecurity Matters, but Blood Availability Remains the Bigger Challenge
-
Nov 8, 2026, 19:26Wenxue Ma: An Integrative Framework for Macrophage-Mediated Therapeutic Resistance in Cancer
-
Nov 8, 2026, 19:25Yildiz Yigit: Presenting a Polycythemia Vera Case at the MPN Subcommittee Session
-
Nov 8, 2026, 18:56Denis Oduor: Strengthening the Regulation and Delivery of Blood Transfusion and Transplantation Services
-
Nov 8, 2026, 18:28Raghavendra Rao: A Narrative Review on Chronic Venous Disease during Pregnancy
-
Nov 8, 2026, 17:57Dhiren Patel: PLD1-Derived Phospholipids Regulate NAD Kinase and ROS Production in Neutrophils