title: Coronary artery calcification as a new predictor of non-target lesion revascularization during the chronic phase after successful percutaneous coronary intervention.
abstract: In the drug-eluting stent era, the outcome of patients undergoing percutaneous coronary intervention (PCI) has remarkably improved. Nevertheless, non-target lesion revascularization (non-TLR) is often performed even after successful PCI and optimized medical therapy. This study aimed to determine the predictor of non-TLR. In all, 125 consecutive patients with stable angina pectoris underwent intravascular ultrasound (IVUS)-guided PCI and were followed up for 3.3 ± 0.5 years. We performed oral glucose-tolerance tests in patients with no history of known diabetes mellitus (DM) to investigate glucose tolerance. To evaluate the severity of coronary artery calcification (CAC), we calculated CAC score by multiplying the arc (degree) with the length (mm) of the superficial calcium deposit detected by IVUS. Fourteen patients underwent non-TLR (non-TLR group); the remaining 111 did not (reference group). Glycosylated hemoglobin (HbA1c; %) and prevalence of known DM were similar in both groups, but the non-TLR group had higher fasting blood glucose (103 ± 16 vs. 94 ± 11 mg/dl, p = 0.04) and blood glucose (196 ± 60 vs. 149 ± 48 μU/ml, p = 0.01) and insulin at 2 h (184 ± 241 vs. 67 ± 49 μU/ml, p < 0.01) than did the reference group. CAC score was significantly higher in the non-TLR group (788 ± 585 vs. 403 ± 466, p = 0.01). Multiple logistic analysis indicated that CAC score is an independent predictor of non-TLR (p = 0.008). Non-TLR-free rate was significantly higher for patients with CAC score ≥400 than for those with CAC score <400 (p = 0.01). Non-TLR is associated with abnormal glucose tolerance and CAC score; CAC score is an independent predictor of non-TLR. Secondary prevention is especially important in patients with high CAC scores.
authors.affiliation: Gunma Prefectural Cardiovascular Center, 3-12, Kameizumi-machi, Maebashi, Gunma, 371-0004, Japan, rum-tum-tugger.1218@hotmail.co.jp.
authors.forename: Yohsuke
authors.initials: Y
authors.lastname: Honda
authors.forename: Takuji
authors.initials: T
authors.lastname: Toyama
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Miyaishi
authors.forename: Hakuken
authors.initials: H
authors.lastname: Kan
authors.forename: Ren
authors.initials: R
authors.lastname: Kawaguchi
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Adachi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hoshizaki
authors.forename: Shigeru
authors.initials: S
authors.lastname: Oshima
mesh_terms: D000368:Aged; D060050:Angina, Stable / Q000601:surgery*; D001786:Blood Glucose / Q000378:metabolism; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000209:etiology; D023903:Coronary Restenosis / Q000175:diagnosis* / Q000209:etiology; D054855:Drug-Eluting Stents; D005260:Female; D005500:Follow-Up Studies; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000379:methods*; D012189:Retrospective Studies; D012307:Risk Factors; D015996:Survival Rate; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional; D061205:Vascular Calcification / Q000175:diagnosis* / Q000209:etiology
chemical_list: D001786:Blood Glucose; D006442:Glycated Hemoglobin; C517652:hemoglobin A1c protein, human