MDCTにおける遅延造影所見は急性心筋梗塞患者の微小循環障害や左室リモデリングを予測する

筑波大学 (University of Tsukuba)201

Preventive effect of statin pretreatment on contrast-induced acute kidney injury in patients undergoing coronary angioplasty: Propensity score analysis from a multicenter registry

BackgroundThe prophylactic benefit of statins in reducing the incidence of contrast-induced acute kidney injury (CI-AKI) has been investigated in several studies with conflicting results. We sought to investigate whether statin pretreatment prevents CI-AKI in coronary artery disease (CAD) patients undergoing percutaneous coronary intervention (PCI).MethodsA total of 2198 CAD patients who underwent PCI, except for those undergoing dialysis or who died within 7 days after angioplasty, were analyzed from the ICAS (Ibaraki Cardiovascular Assessment Study) multicenter registry. Analyzed subjects were divided into 2 groups according to statin pretreatment: statin pretreatment (n = 839) and non-statin pretreatment (n = 1359). Selection bias of statin pretreatment was adjusted by propensity score-matching method: pretreatment statin (n = 565) and non-statin pretreatment (n = 565). CI-AKI was defined as an increase in serum creatinine of ≥ 25% or 0.5 mg/dl from baseline within 1 week of contrast medium exposure.ResultsA total of 192 (8.7%) patients developed CI-AKI. No significant differences were observed in baseline patient characteristics between the statin and non-statin pretreatment groups after propensity score matching. In the propensity score-matched groups, the incidence of CI-AKI was significantly lower in patients with statin pretreatment than in those without statin pretreatment (3.5% vs.10.6%, odds ratio [OR]: 0.31, 95% confidence interval [CI]: 0.18–0.52, P < 0.001). Multivariate logistic regression analysis showed that statin pretreatment remained an independent negative predictor of CI-AKI (OR: 0.31, 95% CI: 0.18–0.53, P < 0.001) among propensity score-matched subjects.ConclusionsStatin pretreatment was associated with a significant decrease in the risk of CI-AKI in CAD patients undergoing PCI in the ICAS Registry

Impact of Coronary Plaque Composition on Cardiac Troponin Elevation After Percutaneous Coronary Intervention in Stable Angina Pectoris : A Computed Tomography Analysis

ObjectivesThe authors used multidetector computed tomography (MDCT) to study the relation between culprit plaque characteristics and cardiac troponin T (cTnT) elevation after percutaneous coronary intervention (PCI).BackgroundPercutaneous coronary intervention is often complicated by post-procedural myocardial necrosis manifested by elevated cardiac biomarkers.MethodsStable angina patients (n = 107) with normal pre-PCI cTnT levels underwent 64-slice MDCT before PCI to evaluate plaque characteristics of culprit lesions. Patients were divided into 2 groups according to presence (group I, n = 36) or absence (group II, n = 71) of post-PCI cTnT elevation ≥3 times the upper limit of normal (0.010 ng/ml) at 24 h after PCI.ResultsComputed tomography attenuation values were significantly lower in group I than in group II (43.0 [26.5 to 75.7] HU vs. 94.0 [65.0 to 109.0] HU, p 1.05; odds ratio: 4.54; 95% confidence interval: 1.36 to 15.9; p = 0.014) and spotty calcification (odds ratio: 4.27; 95% confidence interval: 1.30 to 14.8; p = 0.016) were statistically significant independent predictors for cTnT elevation. For prediction of cTnT elevation, the presence of all 3 variables (CT attenuation value 1.05, and spotty calcification) showed a high positive predictive value of 94%, and their absence showed a high negative predictive value of 90%.ConclusionsMDCT may be useful in detecting which lesions are at high risk for myocardial necrosis after PCI

高校生の生徒文化と学校経営(I)

日本教育社会学会第32回大会, 1980年9月(東北大学), 一般研究Ⅲ-3部会 高校教

Mitochonic Acid 5 (MA-5) Facilitates ATP Synthase Oligomerization and Cell Survival in Various Mitochondrial Diseases

Mitochondrial dysfunction increases oxidative stress and depletes ATP in a variety of disorders. Several antioxidant therapies and drugs affecting mitochondrial biogenesis are undergoing investigation, although not all of them have demonstrated favorable effects in the clinic. We recently reported a therapeutic mitochondrial drug mitochonic acid MA-5 (Tohoku J. Exp. Med., 2015). MA-5 increased ATP, rescued mitochondrial disease fibroblasts and prolonged the life span of the disease model “Mitomouse” (JASN, 2016). To investigate the potential of MA-5 on various mitochondrial diseases, we collected 25 cases of fibroblasts from various genetic mutations and cell protective effect of MA-5 and the ATP producing mechanism was examined. 24 out of the 25 patient fibroblasts (96%) were responded to MA-5. Under oxidative stress condition, the GDF-15 was increased and this increase was significantly abrogated by MA-5. The serum GDF-15 elevated in Mitomouse was likewise reduced by MA-5. MA-5 facilitates mitochondrial ATP production and reduces ROS independent of ETC by facilitating ATP synthase oligomerization and supercomplex formation with mitofilin/Mic60. MA-5 reduced mitochondria fragmentation, restores crista shape and dynamics. MA-5 has potential as a drug for the treatment of various mitochondrial diseases. The diagnostic use of GDF-15 will be also useful in a forthcoming MA-5 clinical trial