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tions resulted in fewer adverse events in PROVE IT the discordance between only modest regression
[16] and also in the absence of plaque progression of plaque size on the one hand vs. profound clinical
in REVERSAL in atorvastatin-treated patients, sug- improvement on the other hand and, even more in-
gesting parallel favorable effects of intensive statin triguingly, the minor or absent improvement of pre-
therapy on coronary atheroma burden and patient sumed high-risk plaque morphology in response to
outcomes. intensive statin treatment. While the use of in vivo
intracoronary imaging has revolutionized our under-
In a post hoc pooled analysisof six serial IVUS stud- standing of serial changes of coronary plaque in re-
ies, Nicholls et al. found that PAV progression was an sponse to risk factors and pharmacologic interven-
independent predictor of major adverse cardiovascu- tions, it is possible that our current armamentarium
lar events over a mean 21-month follow-up; the vast may capture only in part the complex pathobiology of
majority of events included repeat revascularization, plaque progression, stabilization, or regression. Given
and no impact of plaque progression on mortality the complementary information provided by different
was reported.
modalities separately, efforts should continue to fo-
In summary, the association between serial reduction cus on both the combined use of these techniques
of atheroma burden (which has been consistently and more robust validation.
quantified around only 1%) and major cardiovascular
events (which are reduced annually by over one-fifth REFERENCES :
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CONCULSION 11. Bayturan O, Kapadia S, Nicholls SJ, Tuzcu EM, Shao M, Uno K, et al. Clin-
Anti-atherosclerotic medications can halt or even ical predictors of plaque progression despite very low levels of low-density
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unaddressed questions remain, however, including
GCDC 2017

