CVD Risk and CKM Staging

1. The Secondary Prevention Hard Stop

AHA PREVENT and ASCVD PCE are validated for primary prevention only. In a patient who has already had a myocardial infarction or a stroke, or who has peripheral arterial disease, a ten-year risk score is not appropriate. The disease is proven, and secondary prevention with a high-intensity statin is indicated whatever the age or the lipid levels.

2. CKM Staging, and What It Changes

The 2024 AHA PREVENT equations introduce Cardio-Kidney-Metabolic staging, which recognises excess adiposity (stage 1), metabolic risk factors such as hypertension and chronic kidney disease (stage 2) and subclinical atherosclerosis (stage 3) as one continuum. This tool calculates the stage from your inputs. The point of it is that the target is not cholesterol alone but combined cardio-renal protection, which is what prompts an SGLT2 inhibitor or a GLP-1 receptor agonist.

3. When to Order a CAC Scan

Order it when the patient falls in the borderline or intermediate zone and you are genuinely uncertain about starting a statin.

• A CAC of zero in a non-diabetic patient is the strongest reason to defer pharmacotherapy and recheck in 5 years.
• A CAC of 100 or above settles it: start the statin.
• Do not order it in a patient with established ASCVD or one who is clearly high risk. It will not change management and adds unnecessary radiation.

4. The South Asian Paradox at the Bedside

A 45 year old Indian man with an LDL of 110 mg/dL and an ASCVD score of 4 per cent looks low risk on paper. He is not. South Asians develop myocardial infarction a decade earlier, at lower LDL thresholds, and with more vulnerable plaques. Always read the non-HDL cholesterol, which captures every atherogenic particle including VLDL remnants: where the triglycerides are high the LDL-C can look normal while the non-HDL-C shows the real atherogenic burden.

5. Interpreting Additional Biomarkers

LDL-C alone understates risk, because the same cholesterol can be spread across a greater number of particles and it is the particles that lodge in the artery wall.

• Apolipoprotein B counts those particles directly. ApoA1 reflects protective HDL capacity. An ApoB/ApoA1 ratio above 0.9 in men, or above 0.8 in women, marks an atherogenic lipid phenotype and calls for the stricter targets.
• Lipoprotein(a) is highly atherogenic and heavily genetically determined, and a value above 50 mg/dL carries a raised risk of premature ASCVD.
• Standard statin therapy does not lower Lp(a). Since that number will not move, drive the ApoB and the non-HDL-C down instead, to the most stringent targets the Lipid Association of India sets for the patient's risk group.