A prospective, multicenter, randomized trial to assess efficacy of pioglitazone on in-stent neointimal suppression in type 2 diabetes: POPPS (Prevention of In-Stent Neointimal Proliferation by Pioglitazone Study).
OBJECTIVE
The aim of this study was to clarify whether pioglitazone suppresses in-stent neointimal proliferation and reduces restenosis and target lesion revascularization (TLR) after percutaneous coronary intervention (PCI).


BACKGROUND
Previous single-center studies have demonstrated the anti-restenotic effect of a peroxisome proliferator-activated receptor gamma agonist, pioglitazone, after PCI.


METHODS
A total of 97 patients with type 2 diabetes mellitus (T2DM) undergoing PCI (bare-metal stents only) were enrolled. After PCI, patients were randomly assigned to either the pioglitazone group (n = 48) or the control group (n = 49). Angiographical and intravascular ultrasound (IVUS) imaging were performed at baseline and repeated at 6-month follow-up. Primary end points included angiographical restenosis and TLR at 6 months follow-up. Secondary end point was in-stent neointimal volume by IVUS.


RESULTS
Baseline glucose level and glycosylated hemoglobin (HbA1c) level were similar between the pioglitazone group and the control group. Angiographical restenosis rate was 17% in the pioglitazone group and 35% in control group (p = 0.06). The TLR was significantly lower in pioglitazone group than in control group (12.5% vs. 29.8%, p = 0.04). By IVUS (n = 56), in-stent neointimal volume at 6 months showed a trend toward smaller in the pioglitazone group than in the control group (48.0 +/- 30.2 mm(3) vs. 62.7 +/- 29.0 mm(3), p = 0.07). Neointimal index (neointimal volume/stent volume x 100) was significantly smaller in the pioglitazone group than in the control group (31.1 +/- 14.3% vs. 40.5 +/- 12.9%, p = 0.01).


CONCLUSIONS
Pioglitazone treatment might suppress in-stent neointimal proliferation and reduce incidence of TLR after PCI in patients with T2DM.
Takagi
Tsutomu
T
Division of Cardiology, Takagi Cardiology Clinic, Kyoto, Japan.
Okura
Hiroyuki
H
Kobayashi
Yoshiki
Y
Kataoka
Toru
T
Taguchi
Haruyuki
H
Toda
Iku
I
Tamita
Koichi
K
Yamamuro
Atsushi
A
Sakanoue
Yuji
Y
Ito
Akira
A
Yanagi
Shiro
S
Shimeno
Kenji
K
Waseda
Katsuhisa
K
Yamasaki
Masao
M
Fitzgerald
Peter J
PJ
Ikeno
Fumiaki
F
Honda
Yasuhiro
Y
Yoshiyama
Minoru
M
Yoshikawa
Junichi
J
D000368:Aged; D015906:Angioplasty, Balloon, Coronary / Q000009:adverse effects / Q000295:instrumentation* / Q000401:mortality; D001786:Blood Glucose / Q000187:drug effects; D002140:California; D049109:Cell Proliferation / Q000187:drug effects; D017023:Coronary Angiography; D023903:Coronary Restenosis / Q000209:etiology / Q000401:mortality / Q000473:pathology / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000401:mortality; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006331:Heart Diseases / Q000209:etiology / Q000517:prevention & control; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007564:Japan; D008297:Male; D008670:Metals; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000209:etiology / Q000401:mortality / Q000628:therapy*; D000077205:Pioglitazone; D011446:Prospective Studies; D011474:Prosthesis Design; D015607:Stents; D045162:Thiazolidinediones / Q000627:therapeutic use*; D013997:Time Factors; D016896:Treatment Outcome; D017539:Tunica Intima / Q000187:drug effects* / Q000473:pathology; D018084:Ultrasonography, Interventional
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents; D008670:Metals; D000077205:Pioglitazone; D045162:Thiazolidinediones; C517652:hemoglobin A1c protein, human