Is inflammation the real cause of heart attacks or is it cholesterol?

The correct answer is both, operating through a specific sequence. LDL and ApoB particles are the raw material of atherosclerotic plaque: they cross the endothelial barrier, lodge in the arterial wall, and form plaque. This process is the primary driver of plaque buildup over decades. Inflammation, measured as hs-CRP and driven by the cytokines that macrophages release inside plaques, is the accelerant that determines whether a stable plaque ruptures and causes a heart attack.

Think of it this way: ApoB determines how much plaque accumulates. Inflammation determines whether that plaque kills you this year or ten years from now. The man who dies at 53 from a heart attack with an LDL of 105 died because his plaque was inflamed and vulnerable, not because his LDL was catastrophic. The JUPITER trial proved that reducing inflammation in men with normal LDL reduced cardiac events by 44%. That finding does not make cholesterol irrelevant; it makes inflammation a co-equal priority. Managing both gives you the best outcome. (Ridker PM, NEJM, 2008)

Cardiologist's calibrated position, Solid (1) for the two-pathway framework. This is the current mechanistic consensus in cardiovascular medicine.

What to do: Do not let a debate between "cholesterol" and "inflammation" delay your action on both. Test ApoB and hs-CRP on the same panel. They are complementary, not competing.

For the full picture, read Inflammation's Invoice.