19 research outputs found

    Effects of eicosapentaenoic acid on peri-procedural (type IVa) myocardial infarction following elective coronary stenting

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    AbstractObjectivesThe aim of this study was to assess the effect of eicosapentaenoic acid (EPA) on peri-procedural (type IVa) myocardial infarction (MI) following elective percutaneous coronary intervention (PCI).Methods and resultsWe analyzed data from 165 of 178 consecutive patients with stable angina pectoris who underwent de novo successful stent implantation in the native coronary artery. Patients were assigned to receive statin therapy in combination with 1800mg/day of EPA or statin alone. Post-procedural index of microcirculatory resistance (IMR) values were calculated for 30 patients in the EPA group and 32 controls. In the multivariate logistic model, EPA administration, low kidney function, and the presence of slow flow/no reflow were significantly and independently associated with type IVa MI. Post-procedural IMR values were significantly lower in the EPA group [19.8 (6.4, 51.1) vs. 27.8 (8.2, 89.3), p=0.003] compared to the control group.ConclusionsPre-treatment with EPA in addition to statins significantly reduced the incidence of type IVa MI compared to statin therapy only, which may be attributed to the ability of EPA to reduce microvascular dysfunction induced by PCI

    Clustering of metabolic syndrome components attenuates coronary plaque regression during intensive statin therapy in patients with acute coronary syndrome: The JAPAN-ACS subanalysis study

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    金沢大学医薬保健研究域医学系Background: The JAPAN-ACS (Japan Assessment of Pitavastatin and Atorvastatin in Acute Coronary Syndrome) trial showed that intensive statin therapy could induce significant coronary plaque regression in acute coronary syndrome (ACS). We evaluated the impact of metabolic syndrome (MetS) and its components on coronary plaque regression in the JAPAN-ACS patients. Methods and Results: Serial intravascular ultrasound measurements over 8-12 months were performed in 242 ACS patients receiving pitavastatin or atorvastatin. Patients were divided into groups according to the presence of MetS or the number of MetS components. Although the percent change in plaque volume (%PV) was not significantly different between the MetS (n=119) and non-MetS (n=123) groups (P=0.50), it was significantly associated with an increasing number of MetS components (component 0: -24.0%, n=7; components 1: -20.8%, n=31; components 2: -16.1%, n=69; components 3: -18.7%, n=83; components 4: -13.5%, n=52; P=0.037 for trend). The percent change in body mass index (%BMI) significantly correlated with %PV (r=0.15, P=0.021), especially in the MetS components 4 group (r=0.35, P=0.017). In addition, %BMI was an independent predictor of plaque regression after adjustment for the changes of low- and high-density lipoprotein cholesterol, triglycerides and HbA1c. Conclusions: The clustering of MetS components, but not the presence of MetS itself, could attenuate coronary plaque regression during intensive statin therapy in ACS patients. Therefore, to achieve a greater degree of plaque regression, it is necessary to treat to each MetS component and use lifestyle modification.出版者照会後に全文公
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