Atherosclerosis

The build-up of plaque in artery walls that narrows and stiffens them.

Atherosclerosis is the build up of plaque inside artery walls: cholesterol carrying particles enter the wall, are retained there, provoke an inflammatory response, and gradually form a deposit that narrows the vessel and stiffens it.

The dangerous event is usually not the narrowing itself. Most heart attacks happen when a plaque ruptures or erodes and a clot forms on it, abruptly blocking a vessel that may have been only moderately narrowed the day before. That is why a stress test that looks acceptable is not a guarantee.

It begins far earlier than most people assume, with early lesions detectable in young adults, and it develops silently over decades. By the time it produces symptoms the process has been running for a very long time.

The causal role of LDL is one of the better established facts in medicine. A European consensus panel weighed genetic studies, cohorts, Mendelian randomisation and randomised trials together and concluded that LDL causes atherosclerotic cardiovascular disease, with cumulative exposure over years being what matters rather than any single reading.

The other major contributors are well characterised: smoking, high blood pressure, diabetes and insulin resistance, Lp(a), and inflammation. Most are modifiable and several are silent, which is the argument for measuring rather than feeling.

Because it accumulates, early modest control beats late aggressive control. Holding a reasonable LDL from your thirties does more than achieving an excellent one at sixty, which is an unwelcome message and a true one.

In practice, know your blood pressure, LDL or ApoB, HbA1c and, once, your Lp(a), and put them into our heart age calculator rather than guessing from how you feel.

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