Letter by Sutton et al Regarding Article, “Effect of Rosuvastatin Therapy on Coronary Artery Stenoses Assessed by Quantitative Coronary Angiography: A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound–Derived Coronary Atheroma Burden”
To the Editor:
Dr Ballantyne and colleagues report modest regression of atherosclerosis after 24 months of rosuvastatin, 40 mg, as measured by quantitative coronary angiography (QCA) in a follow-up analysis of the A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound–Derived Coronary Atheroma Burden (ASTEROID) trial.1 The authors conclude that a decrease in minimal lumen diameter and percentage diameter stenosis by QCA correlate with and support the decrease in atheroma volume previously reported with intravascular ultrasound (IVUS).
The QCA changes seen in the study, though statistically significant, are exceedingly small. Previous work by Nissen and others has indicated that “plaque progression and regression are not closely related to luminal size,”2 suggesting that serial angiography may not be a reliable modality for studying the impact of aggressive statin therapy on atherosclerosis.
In previous IVUS analyses of plaque progression using atorvastatin 80 mg, a pattern of constrictive remodeling has been observed.3 How do the authors account for differences in vessel expansion or changes in the minimal lumen diameter at the lesion site compared with the “reference” segment in this study using QCA? No data on reference vessel minimal lumen diameter are presented, yet these values are used to calculate percentage stenosis.
Secondly, no data on absolute changes in lumen cross-sectional area were provided in the ASTEROID study.4 Can the authors comment on changes observed in this QCA study compared with absolute lumen cross-sectional area values obtained by IVUS in the ASTEROID trial?
Third, how do the authors explain different results observed in this study compared with trials using apolipoprotein A-I Milano in which lumen area assessed by IVUS did not significantly increase?5
We agree that plaque stabilization may be a more important metric than gross anatomic changes. The true significance of both the IVUS- and QCA-based analyses will not be known until clinical outcomes data are available. It remains to be seen whether or not these modalities, which yield surrogate end points, will add clinically relevant information.
Ballantyne CM, Raichlen JS, Nicholls SJ, Erbel R, Tardiff JC, Brener SJ, Cain VA, Nissen SE. Effect of rosuvastatin therapy on coronary artery stenoses assessed by quantitative coronary angiography: A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden. Circulation. 2008; 117: 2458–2466.
Schoenhagen P, Tuzcu EM, Apperson-Hansen C, Wang C, Wolski K, Lin S, Sipahi I, Nicholls SJ, Magyar WA, Loyd A, Churchill T, Crowe T, Nissen SE. Determinants of arterial wall remodeling during lipid-lowering therapy: serial intravascular ultrasound observations from the Reversal of Atherosclerosis With Aggressive Lipid Lowering Therapy (REVERSAL) Trial. Circulation. 2006; 113: 2826–2834.
Nissen SE, Nicholls SJ, Sipahi I, Libby P, Raichlen JS, Ballantyne CM, Davignon J, Erbel R, Fruchart JC, Tardif J, Schoenhagen P, Crowe T, Cain V, Wolski K, Goormastic M, Tuzcu EM. Effect of Very high-intensity statin therapy on regression of coronary atherosclerosis: the ASTEROID trial. JAMA. 2006; 295: 1556–1565.