Objective: Despite the link between positive coronary remodelling and acute ischaemic events, no data exist about the impact of arterial remodelling on subsequent progression of coronary atherosclerosis. The objective of this study was to examine whether extent and direction of arterial remodelling are predictors of progression of coronary atherosclerosis.
Design, setting and patients: From the Reversal of Atherosclerosis with Aggressive Lipid Lowering (REVERSAL) trial, 210 focal coronary lesions (single lesion per patient) were identified with ⩽50% angiographic diameter stenosis at baseline intravascular ultrasound (IVUS). Remodelling was categorised using the remodelling index.
Main outcome measures: Lesion sites were matched to the 18-month follow-up IVUS examination and change in atheroma area was calculated. Additionally, change in atheroma volume of the whole imaged artery was calculated.
Results: There were no relationships between baseline remodelling index and change in atheroma area at the lesion site (r = 0.004, p = 0.96) or change in atheroma volume in the whole artery (r = 0.06, p = 0.37). Change in atheroma area was not significantly different in lesions with positive, negative or no remodelling at baseline (0.4 (SD 2.1) vs 0.7 (SD 1.7) vs 0.6 (SD 1.8) mm2, p = 0.76). Similarly, change in atheroma volume in the whole artery was not significantly different among the three remodelling categories (2.2 (SD 25.0) vs 1.4 (SD 31.2) vs 2.4 (SD 27.1) mm3, p = 0.98).
Conclusions: Extent and direction of arterial remodelling do not predict subsequent progression of coronary atherosclerosis. Although positively remodelled lesions are associated with unstable clinical presentation, they are not associated with accelerated progression of atherosclerosis during lipid lowering therapy.
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Funding: The REVERSAL (Reversal of Atherosclerosis with Aggressive Lipid Lowering) trial was funded by Pfizer. This substudy is partially funded by a National Institutes of Health, National Center for Research Resources, General Clinical Research Center Grant MO1 RR-018390. PS was supported by a postdoctoral fellowship grant of the Ohio Affiliate of the American Heart Association. A Ralph Reader Overseas Research Fellowship from the National Heart Foundation of Australia supports SJN.
Competing interests: IS received lecture honoraria and an educational grant from Pfizer. EMT received grant support from Pfizer and Takeda and lecture honoraria from Pfizer. SJN has received lecture honoraria from Pfizer and AstraZeneca. PS has consulted for Takeda without financial compensation. All honoraria are paid directly to higher education, so that neither income nor any tax deduction is received. SEN has received research support from AstraZeneca, Eli Lilly, Pfizer, Takeda, Sankyo and Sanofi-Aventis. He has also consulted for a number of pharmaceutical companies without financial compensation. All honoraria, consulting fees, or other payments from any for-profit entity are paid directly to charity, so that neither income nor any tax deduction is received.
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