Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques

Effects of statin therapy on ruptured coronary plaque

Myeongki Hong, Gary S. Mintz, Cheol Whan Lee, Il Woo Suh, Eui Seok Hwang, Young Hoon Jeong, Duk Woo Park, Young Hak Kim, Ki Hoon Han, Sang Sig Cheong, Jae Joong Kim, Seong Wook Park, Seung Jung Park

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Abstract

Using serial intravascular ultrasound (IVUS), we evaluated the natural evolution of non-culprit/non-target lesion ruptured coronary plaques and assessed the impact of statin therapy. Twenty-eight patients with non-stenotic ruptured plaques underwent baseline and 12-month follow-up IVUS studies; half were treated with statins. Standard IVUS analyses were performed. Complete healing of ruptured plaques was observed in four (29%) statin-treated patients and no non-statin-treated patients (p = 0.049). Statin-treated patients had an increase in lumen area of 0.4 ± 0.8 mm 2 (versus a decrease in lumen area of -0.6 ± 1.0 mm 2 in non-statin-treated patients, p = 0.007) and no change in plaque area (versus an increase in plaque area of 0.6 ± 0.9 mm 2 , p = 0.051). During 1-year follow-up, target lesion revascularization was performed in three non-statin-treated patients (21%) and no statin-treated patient (p = 0.11). Compared to lesions that did not require revascularization, lesions requiring revascularization had a decrease in lumen area (-1.7 ± 1.4 mm 2 versus 0.1 ± 0.8 mm 2 , p = 0.001) as well as an increase in plaque area (1.6 ± 1.0 mm 2 versus 0.1 ± 0.7 mm 2 , p = 0.002). In conclusion, the current observational follow-up IVUS study showed beneficial effects of statin treatment on reduction of revascularization rates and stabilization of non-culprit/non-target lesion plaque ruptures without significant stenosis. Conversely, healing of non-statin-treated non-culprit/non-target lesion plaque ruptures can be responsible for lesion progression requiring revascularization.

Original languageEnglish
Pages (from-to)107-114
Number of pages8
JournalAtherosclerosis
Volume191
Issue number1
DOIs
Publication statusPublished - 2007 Mar 1

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Hydroxymethylglutaryl-CoA Reductase Inhibitors
Therapeutics
Rupture
Pathologic Constriction

All Science Journal Classification (ASJC) codes

  • Cardiology and Cardiovascular Medicine

Cite this

Hong, Myeongki ; Mintz, Gary S. ; Lee, Cheol Whan ; Suh, Il Woo ; Hwang, Eui Seok ; Jeong, Young Hoon ; Park, Duk Woo ; Kim, Young Hak ; Han, Ki Hoon ; Cheong, Sang Sig ; Kim, Jae Joong ; Park, Seong Wook ; Park, Seung Jung. / Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques : Effects of statin therapy on ruptured coronary plaque. In: Atherosclerosis. 2007 ; Vol. 191, No. 1. pp. 107-114.
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abstract = "Using serial intravascular ultrasound (IVUS), we evaluated the natural evolution of non-culprit/non-target lesion ruptured coronary plaques and assessed the impact of statin therapy. Twenty-eight patients with non-stenotic ruptured plaques underwent baseline and 12-month follow-up IVUS studies; half were treated with statins. Standard IVUS analyses were performed. Complete healing of ruptured plaques was observed in four (29{\%}) statin-treated patients and no non-statin-treated patients (p = 0.049). Statin-treated patients had an increase in lumen area of 0.4 ± 0.8 mm 2 (versus a decrease in lumen area of -0.6 ± 1.0 mm 2 in non-statin-treated patients, p = 0.007) and no change in plaque area (versus an increase in plaque area of 0.6 ± 0.9 mm 2 , p = 0.051). During 1-year follow-up, target lesion revascularization was performed in three non-statin-treated patients (21{\%}) and no statin-treated patient (p = 0.11). Compared to lesions that did not require revascularization, lesions requiring revascularization had a decrease in lumen area (-1.7 ± 1.4 mm 2 versus 0.1 ± 0.8 mm 2 , p = 0.001) as well as an increase in plaque area (1.6 ± 1.0 mm 2 versus 0.1 ± 0.7 mm 2 , p = 0.002). In conclusion, the current observational follow-up IVUS study showed beneficial effects of statin treatment on reduction of revascularization rates and stabilization of non-culprit/non-target lesion plaque ruptures without significant stenosis. Conversely, healing of non-statin-treated non-culprit/non-target lesion plaque ruptures can be responsible for lesion progression requiring revascularization.",
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Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques : Effects of statin therapy on ruptured coronary plaque. / Hong, Myeongki; Mintz, Gary S.; Lee, Cheol Whan; Suh, Il Woo; Hwang, Eui Seok; Jeong, Young Hoon; Park, Duk Woo; Kim, Young Hak; Han, Ki Hoon; Cheong, Sang Sig; Kim, Jae Joong; Park, Seong Wook; Park, Seung Jung.

In: Atherosclerosis, Vol. 191, No. 1, 01.03.2007, p. 107-114.

Research output: Contribution to journalArticle

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T1 - Serial intravascular ultrasound evidence of both plaque stabilization and lesion progression in patients with ruptured coronary plaques

T2 - Effects of statin therapy on ruptured coronary plaque

AU - Hong, Myeongki

AU - Mintz, Gary S.

AU - Lee, Cheol Whan

AU - Suh, Il Woo

AU - Hwang, Eui Seok

AU - Jeong, Young Hoon

AU - Park, Duk Woo

AU - Kim, Young Hak

AU - Han, Ki Hoon

AU - Cheong, Sang Sig

AU - Kim, Jae Joong

AU - Park, Seong Wook

AU - Park, Seung Jung

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AB - Using serial intravascular ultrasound (IVUS), we evaluated the natural evolution of non-culprit/non-target lesion ruptured coronary plaques and assessed the impact of statin therapy. Twenty-eight patients with non-stenotic ruptured plaques underwent baseline and 12-month follow-up IVUS studies; half were treated with statins. Standard IVUS analyses were performed. Complete healing of ruptured plaques was observed in four (29%) statin-treated patients and no non-statin-treated patients (p = 0.049). Statin-treated patients had an increase in lumen area of 0.4 ± 0.8 mm 2 (versus a decrease in lumen area of -0.6 ± 1.0 mm 2 in non-statin-treated patients, p = 0.007) and no change in plaque area (versus an increase in plaque area of 0.6 ± 0.9 mm 2 , p = 0.051). During 1-year follow-up, target lesion revascularization was performed in three non-statin-treated patients (21%) and no statin-treated patient (p = 0.11). Compared to lesions that did not require revascularization, lesions requiring revascularization had a decrease in lumen area (-1.7 ± 1.4 mm 2 versus 0.1 ± 0.8 mm 2 , p = 0.001) as well as an increase in plaque area (1.6 ± 1.0 mm 2 versus 0.1 ± 0.7 mm 2 , p = 0.002). In conclusion, the current observational follow-up IVUS study showed beneficial effects of statin treatment on reduction of revascularization rates and stabilization of non-culprit/non-target lesion plaque ruptures without significant stenosis. Conversely, healing of non-statin-treated non-culprit/non-target lesion plaque ruptures can be responsible for lesion progression requiring revascularization.

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