title: Comparison of the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by tissue characterization using serial virtual histology intravascular ultrasound.
abstract: Thin-cap fibroatheroma (TCFA) is the most common type of vulnerable plaque and is the precursor of plaque rupture. However, rupture of a TCFA is not the only mechanism underlying thrombus formation or acute coronary syndrome. Although statin therapy changes the composition of coronary artery plaques, the effects of statins, particularly different types of statins, on plaque phenotype have not been fully examined. This study compared the effects of pitavastatin versus pravastatin on coronary artery plaque phenotype assessed by virtual histology (VH) intravascular ultrasound (IVUS) in patients with angina pectoris (AP). Coronary atherosclerosis in nonculprit lesions was evaluated using VH-IVUS at baseline and 8 months after statin therapy; analyzable IVUS data were obtained from 83 patients with stable AP (39 patients treated with pitavastatin and 44 with pravastatin) and 36 patients with unstable AP (19 patients treated with pitavastatin and 17 with pravastatin). Pitavastatin had a strong effect on reducing pathologic intimal thickening (PIT), especially in patients with unstable AP, but had no impact on VH-TCFA or fibroatheroma (FA). By contrast, pravastatin had weak effects on reducing PIT, VH-TCFA, or FA. Increases in the number of calcified plaques were observed for both statins. In conclusion, pitavastatin and pravastatin changed coronary artery plaque phenotype as assessed by VH-IVUS in patients with AP. However, the effects of these statins on coronary artery plaque phenotype were different.
authors: Division of Cardiology, Department of Internal Medicine, Yokohama Sakae Kyosai Hospital, Federation of National Public Service Personnel Mutual Associations, 132 Katsura-cho, Sakae-ku, Yokohama, 247-8581, Japan, nozue2493@yahoo.co.jp.
authors: Tsuyoshi
authors: T
authors: Nozue
authors: Shingo
authors: S
authors: Yamamoto
authors: Shinichi
authors: S
authors: Tohyama
authors: Kazuki
authors: K
authors: Fukui
authors: Shigeo
authors: S
authors: Umezawa
authors: Yuko
authors: Y
authors: Onishi
authors: Tomoyuki
authors: T
authors: Kunishima
authors: Akira
authors: A
authors: Sato
authors: Toshihiro
authors: T
authors: Nozato
authors: Shogo
authors: S
authors: Miyake
authors: Youichi
authors: Y
authors: Takeyama
authors: Yoshihiro
authors: Y
authors: Morino
authors: Takao
authors: T
authors: Yamauchi
authors: Toshiya
authors: T
authors: Muramatsu
authors: Kiyoshi
authors: K
authors: Hibi
authors: Mitsuyasu
authors: M
authors: Terashima
authors: Ichiro
authors: I
authors: Michishita
mesh_terms: D054058:Acute Coronary Syndrome / Q000000981:diagnostic imaging / Q000188:drug therapy*; D000368:Aged; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000188:drug therapy*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D010641:Phenotype; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000188:drug therapy*; D017035:Pravastatin / Q000627:therapeutic use*; D011446:Prospective Studies; D011804:Quinolines / Q000627:therapeutic use*; D018084:Ultrasonography, Interventional
chemical_list: D011804:Quinolines; D017035:Pravastatin; C108475:pitavastatin