Inflammation Drives CVD
Cholesterol loads the gun, inflammation pulls the trigger
You can have elevated ApoB for decades without a cardiovascular event. What converts stable plaque to rupture — the actual heart attack — is usually inflammation. This is why measuring hsCRP (high-sensitivity C-reactive protein) alongside lipids gives you a more complete picture of risk.
The CANTOS proof
The CANTOS trial showed that lowering inflammation with canakinumab (an IL-1β antibody) reduced cardiovascular events by 15% — without moving cholesterol a single mg/dL. The inflammation hypothesis of CVD isn't a hypothesis anymore; it's mechanism.
hsCRP tracks the residual risk
After lipids are optimised, hsCRP is the best single marker of residual cardiovascular risk. Target: under 1 mg/L. 1–3 is moderate concern. Over 3 mg/L consistently suggests chronic inflammation worth investigating — could be anything from periodontal disease to obesity to autoimmunity.
What lowers hsCRP?
Select every intervention with strong evidence for reducing inflammation markers.
This step is interactive — open the Thier app to try it.
Low-dose colchicine — the new anti-inflammatory tool
Colchicine, an old gout drug, became the first specifically anti-inflammatory CV drug to win FDA approval (June 2023, brand: Lodoco). The COLCOT and LoDoCo2 trials showed 0.5 mg daily reduces major cardiovascular events ~30 % in patients with established disease — on top of statins. It works by dampening the IL-1β / IL-6 inflammatory pathway downstream of NLRP3. Not currently used in primary prevention; ask your cardiologist if you have prior MI / stable CAD and persistent hsCRP > 2.
Key Takeaway
ApoB tells you how much plaque you're depositing. hsCRP tells you how ready it is to rupture. Both numbers matter, and both are independently modifiable. Aim for ApoB under 80 mg/dL and hsCRP under 1 mg/L as the dual target. Low-dose colchicine is now an FDA-approved option for residual inflammation in established CAD.