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Does spotty calcification attenuate the response of nonculprit plaque to statin therapy?: A serial optical coherence tomography study
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AbstractObjectivesThe aim of this study was to determine if spotty calcification decreases the response of plaque progression to statin therapy.BackgroundPrevious studies showed that the presence of spotty calcification is a marker of vulnerable plaque. However, the relationship between spotty calcification and plaque progression is not clear.MethodsNinety‐six nonculprit lipid‐rich plaques in 69 patients who received serial optical coherence tomography (OCT) imaging were included. Plaques were divided into three groups: spotty calcification (n = 38), calcified (n = 12) and noncalcified (n = 46) plaques. Spotty calcification was identified by the presence of a lesion <4 mm in length with an arc of calcification <90°. Changes in plaque characteristics and fibrous cap thickness (FCT) at 6 and 12 months under statin therapy were analyzed by OCT.ResultsThe increase of FCT was sustained from baseline to 6 and 12 months in three groups: spotty calcification (62.8 ± 20.9, 126.4 ± 84.9, and 169.2 ± 81.6 μm, respectively; P < .001), calcified (59.8 ± 17.0, 93.4 ± 51.4, and 155.2 ± 61.7 μm, respectively; P < .001) and noncalcified (60.0 ± 17.2, 125.5 ± 62.1, and 161.0 ± 80.5 μm, respectively; P < .001). Intensive statin induced a greater change in FCT at 12 months than moderate statin in the spotty calcification group (P = 0.034). The mean lipid arc decreased significantly at 12 months from baseline in the three groups (P = 0.004, P = 0.023, and P < .001, respectively).ConclusionsStatin therapy was effective for plaque stabilization in plaques with and without spotty calcification. Patients with spotty calcification benefitted more from intensive statin than from moderate statin therapy.
Title: Does spotty calcification attenuate the response of nonculprit plaque to statin therapy?: A serial optical coherence tomography study
Description:
AbstractObjectivesThe aim of this study was to determine if spotty calcification decreases the response of plaque progression to statin therapy.
BackgroundPrevious studies showed that the presence of spotty calcification is a marker of vulnerable plaque.
However, the relationship between spotty calcification and plaque progression is not clear.
MethodsNinety‐six nonculprit lipid‐rich plaques in 69 patients who received serial optical coherence tomography (OCT) imaging were included.
Plaques were divided into three groups: spotty calcification (n = 38), calcified (n = 12) and noncalcified (n = 46) plaques.
Spotty calcification was identified by the presence of a lesion <4 mm in length with an arc of calcification <90°.
Changes in plaque characteristics and fibrous cap thickness (FCT) at 6 and 12 months under statin therapy were analyzed by OCT.
ResultsThe increase of FCT was sustained from baseline to 6 and 12 months in three groups: spotty calcification (62.
8 ± 20.
9, 126.
4 ± 84.
9, and 169.
2 ± 81.
6 μm, respectively; P < .
001), calcified (59.
8 ± 17.
0, 93.
4 ± 51.
4, and 155.
2 ± 61.
7 μm, respectively; P < .
001) and noncalcified (60.
0 ± 17.
2, 125.
5 ± 62.
1, and 161.
0 ± 80.
5 μm, respectively; P < .
001).
Intensive statin induced a greater change in FCT at 12 months than moderate statin in the spotty calcification group (P = 0.
034).
The mean lipid arc decreased significantly at 12 months from baseline in the three groups (P = 0.
004, P = 0.
023, and P < .
001, respectively).
ConclusionsStatin therapy was effective for plaque stabilization in plaques with and without spotty calcification.
Patients with spotty calcification benefitted more from intensive statin than from moderate statin therapy.
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