Comparison of Change in Coronary Atherosclerosis in Patients With Stable Versus Unstable Angina Pectoris Receiving Statin Therapy (from the Treatment With Statin on Atheroma Regression Evaluated by Intravascular Ultrasound With Virtual Histology [TRUTH] Study)

Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary artery disease, no reports have examined this. The purpose of the present study was to compare the changes in coronary atherosclerosis in pat...

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Published inThe American journal of cardiology Vol. 111; no. 7; pp. 923 - 929
Main Authors Nozue, Tsuyoshi, MD, Yamamoto, Shingo, MD, Tohyama, Shinichi, MD, Fukui, Kazuki, MD, Umezawa, Shigeo, MD, Onishi, Yuko, MD, Kunishima, Tomoyuki, MD, Sato, Akira, MD, Nozato, Toshihiro, MD, Miyake, Shogo, MD, Takeyama, Youichi, MD, Morino, Yoshihiro, MD, Yamauchi, Takao, MD, Muramatsu, Toshiya, MD, Hibi, Kiyoshi, MD, Terashima, Mitsuyasu, MD, Michishita, Ichiro, MD
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 01.04.2013
Elsevier Limited
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Abstract Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary artery disease, no reports have examined this. The purpose of the present study was to compare the changes in coronary atherosclerosis in patients with stable versus unstable angina pectoris (AP). The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology intravascular ultrasound, and analyzable intravascular ultrasound data were obtained from 119 patients (83 patients with stable AP and 36 with unstable AP). A significant decrease in plaque volume was observed in patients with unstable AP (−2.2%, p = 0.02) but not in patients with stable AP. A significant increase in the necrotic-core component (0.30 mm3 /mm, p = 0.009) was observed only in patients with unstable AP. Significant positive correlations were observed between the percentage of change in platelet-activating factor acetylhydrolase and the percentage of change in plaque volume (r = 0.346, p = 0.05) in patients with unstable AP. No significant correlations were observed in patients with stable AP. Multivariate regression analyses showed that a reduction in platelet-activating factor acetylhydrolase was associated with regression in coronary atherosclerosis, particularly of the fibrous component (β = 0.443, p = 0.003), in patients with unstable AP. In conclusion, regression of the coronary artery plaque volume was greater, although statin therapy did not halt the increases in plaque vulnerability, in patients with unstable AP compared to those with stable AP. A reduction in the serum platelet-activating factor acetylhydrolase level was associated with regression in coronary atherosclerosis, particularly the fibrous plaque volume, in patients with unstable AP.
AbstractList Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary artery disease, no reports have examined this. The purpose of the present study was to compare the changes in coronary atherosclerosis in patients with stable versus unstable angina pectoris (AP). The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology intravascular ultrasound, and analyzable intravascular ultrasound data were obtained from 119 patients (83 patients with stable AP and 36 with unstable AP). A significant decrease in plaque volume was observed in patients with unstable AP (-2.2%, p = 0.02) but not in patients with stable AP. A significant increase in the necrotic-core component (0.30 mm(3)/mm, p = 0.009) was observed only in patients with unstable AP. Significant positive correlations were observed between the percentage of change in platelet-activating factor acetylhydrolase and the percentage of change in plaque volume (r = 0.346, p = 0.05) in patients with unstable AP. No significant correlations were observed in patients with stable AP. Multivariate regression analyses showed that a reduction in platelet-activating factor acetylhydrolase was associated with regression in coronary atherosclerosis, particularly of the fibrous component (β = 0.443, p = 0.003), in patients with unstable AP. In conclusion, regression of the coronary artery plaque volume was greater, although statin therapy did not halt the increases in plaque vulnerability, in patients with unstable AP compared to those with stable AP. A reduction in the serum platelet-activating factor acetylhydrolase level was associated with regression in coronary atherosclerosis, particularly the fibrous plaque volume, in patients with unstable AP.
Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary artery disease, no reports have examined this. The purpose of the present study was to compare the changes in coronary atherosclerosis in patients with stable versus unstable angina pectoris (AP). The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology intravascular ultrasound, and analyzable intravascular ultrasound data were obtained from 119 patients (83 patients with stable AP and 36 with unstable AP). A significant decrease in plaque volume was observed in patients with unstable AP (-2.2%, p = 0.02) but not in patients with stable AP. A significant increase in the necrotic-core component (0.30 mm3/mm, p = 0.009) was observed only in patients with unstable AP. Significant positive correlations were observed between the percentage of change in platelet-activating factor acetylhydrolase and the percentage of change in plaque volume (r = 0.346, p = 0.05) in patients with unstable AP. No significant correlations were observed in patients with stable AP. Multivariate regression analyses showed that a reduction in platelet-activating factor acetylhydrolase was associated with regression in coronary atherosclerosis, particularly of the fibrous component (β = 0.443, p = 0.003), in patients with unstable AP. In conclusion, regression of the coronary artery plaque volume was greater, although statin therapy did not halt the increases in plaque vulnerability, in patients with unstable AP compared to those with stable AP. A reduction in the serum platelet-activating factor acetylhydrolase level was associated with regression in coronary atherosclerosis, particularly the fibrous plaque volume, in patients with unstable AP.
Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary artery disease, no reports have examined this. The purpose of the present study was to compare the changes in coronary atherosclerosis in patients with stable versus unstable angina pectoris (AP). The effects of 8-month statin therapy on coronary atherosclerosis were evaluated using virtual histology intravascular ultrasound, and analyzable intravascular ultrasound data were obtained from 119 patients (83 patients with stable AP and 36 with unstable AP). A significant decrease in plaque volume was observed in patients with unstable AP (−2.2%, p = 0.02) but not in patients with stable AP. A significant increase in the necrotic-core component (0.30 mm3/mm, p = 0.009) was observed only in patients with unstable AP. Significant positive correlations were observed between the percentage of change in platelet-activating factor acetylhydrolase and the percentage of change in plaque volume (r = 0.346, p = 0.05) in patients with unstable AP. No significant correlations were observed in patients with stable AP. Multivariate regression analyses showed that a reduction in platelet-activating factor acetylhydrolase was associated with regression in coronary atherosclerosis, particularly of the fibrous component (β = 0.443, p = 0.003), in patients with unstable AP. In conclusion, regression of the coronary artery plaque volume was greater, although statin therapy did not halt the increases in plaque vulnerability, in patients with unstable AP compared to those with stable AP. A reduction in the serum platelet-activating factor acetylhydrolase level was associated with regression in coronary atherosclerosis, particularly the fibrous plaque volume, in patients with unstable AP.
Author Onishi, Yuko, MD
Terashima, Mitsuyasu, MD
Umezawa, Shigeo, MD
Muramatsu, Toshiya, MD
Michishita, Ichiro, MD
Fukui, Kazuki, MD
Yamamoto, Shingo, MD
Miyake, Shogo, MD
Hibi, Kiyoshi, MD
Yamauchi, Takao, MD
Kunishima, Tomoyuki, MD
Takeyama, Youichi, MD
Morino, Yoshihiro, MD
Sato, Akira, MD
Tohyama, Shinichi, MD
Nozato, Toshihiro, MD
Nozue, Tsuyoshi, MD
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/23337838$$D View this record in MEDLINE/PubMed
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Snippet Although statin-induced regression in coronary atherosclerosis seems to be greater in patients with acute coronary syndrome than in those with stable coronary...
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SubjectTerms Aged
Angina pectoris
Angina, Stable - complications
Angina, Unstable - complications
Biomarkers - blood
Cardiovascular
Cardiovascular disease
Cholesterol
Coronary Artery Disease - complications
Coronary Artery Disease - diagnostic imaging
Coronary Artery Disease - drug therapy
Coronary vessels
Female
Heart attacks
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use
Japan
Lipids - blood
Male
Plaque, Atherosclerotic - complications
Plaque, Atherosclerotic - diagnostic imaging
Plaque, Atherosclerotic - drug therapy
Pravastatin - therapeutic use
Quinolines - therapeutic use
Regression Analysis
Treatment Outcome
Ultrasonography, Interventional
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Title Comparison of Change in Coronary Atherosclerosis in Patients With Stable Versus Unstable Angina Pectoris Receiving Statin Therapy (from the Treatment With Statin on Atheroma Regression Evaluated by Intravascular Ultrasound With Virtual Histology [TRUTH] Study)
URI https://www.clinicalkey.es/playcontent/1-s2.0-S0002914912025507
https://dx.doi.org/10.1016/j.amjcard.2012.12.008
https://www.ncbi.nlm.nih.gov/pubmed/23337838
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