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This editorial refers to ‘Coronary atheroma volume and cardiovascular events during maximally intensive statin therapy’†, by R. Puri et al., on page 3182

Hydroxymethylglutaryl (HMG) CoA-reductase inhibitors, or statins, play an important role in the primary and secondary prevention of coronary heart disease. By inhibiting the enzyme HMG-CoA reductase, statins lower the production of cholesterol in the liver, resulting in lower LDL cholesterol levels. Besides lowering cholesterol levels, statin therapy slows down plaque progression and in some patients even causes plaque regression.

In the beginning of the 1990s, the first trials were initiated to assess the effect of statin therapy on plaque dynamics. Randomized trials, such as MARS and REGRESS, used (quantitative) invasive coronary angiography (ICA) to assess luminal stenosis characteristics. Since ICA only allows assessment of the coronary lumen, differences in minimal lumen diameters (MLDs) and mean segment diameters (MSDs) between baseline and follow-up were assessed as a measurement of coronary plaque change.1,2 These early studies demonstrated that moderate dose statin therapy on average reduces plaque progression. Importantly, this was associated with a reduction of major adverse cardiovascular events (MACEs). Of note, it was shown that the beneficial effect of statin therapy is more pronounced in more severe lesions.1

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