CBS 2019
CBSMD教育中心
中 文

双重抗血小板治疗持续时间

Abstract

Recommended Article

Bleeding-Related Deaths in Relation to the Duration of Dual-Antiplatelet Therapy After Coronary Stenting Mortality Following Cardiovascular and Bleeding Events Occurring Beyond 1 Year After Coronary Stenting - A Secondary Analysis of the Dual Antiplatelet Therapy (DAPT) Study Benefit of switching dual antiplatelet therapy after acute coronary syndrome: the TOPIC (timing of platelet inhibition after acute coronary syndrome) randomized study Dual Antithrombotic Therapy with Dabigatran after PCI in Atrial Fibrillation Risk of Early Adverse Events After Clopidogrel Discontinuation in Patients Undergoing Short-Term Dual Antiplatelet Therapy: An Individual Participant Data Analysis Low-Dose Aspirin Discontinuation and Risk of Cardiovascular Events: A Swedish Nationwide, Population-Based Cohort Study Characterization of the Average Daily Ischemic and Bleeding Risk After Primary PCI for STEMI Patterns and associations between DAPT cessation and 2-year clinical outcomes in left main/proximal LAD versus other PCI: Results from the Patterns of Non-Adherence to Dual Antiplatelet Therapy in Stented Patients (PARIS) registry
|<< 1 2 3 4 5 6 7 ...>>|

Original Research2018 Jan 23;71(3):263-275.

JOURNAL：J Am Coll Cardiol. Article Link

Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction

Thackeray JT, Hupe HC, Bengel FM et al. Keywords: heart failure; inflammation; macrophages; myocardial infarction; neurodegeneration; positron emission tomography

ABSTRACT



Background - The local inflammatory tissue response after acute myocardial infarction (MI) determines subsequent healing. Systemic interaction may induce neuroinflammation as a precursor to neurodegeneration.


Objectives - This study sought to assess the influence of MI on cardiac and brain inflammation using noninvasive positron emission tomography (PET) of the heart-brain axis.


Methods - After coronary artery ligation or sham surgery, mice (n = 49) underwent serial whole-body PET imaging of the mitochondrial translocator protein (TSPO) as a marker of activated macrophages and microglia. Patients after acute MI (n = 3) were also compared to healthy controls (n = 9).



Results - Infarct mice exhibited elevated myocardial TSPO signal at 1 week versus sham (percent injected dose per gram: 8.0 ± 1.6 vs. 4.8 ± 0.9; p < 0.001), localized to activated CD68+ inflammatory cells in the infarct. Early TSPO signal predicted subsequent left ventricular remodeling at 8 weeks (rpartial = −0.687; p = 0.001). In parallel, brain TSPO signal was elevated at 1 week (1.7 ± 0.2 vs. 1.4 ± 0.2 for sham; p = 0.017), localized to activated microglia. After interval decline at 4 weeks, progressive heart failure precipitated a second wave of neuroinflammation (1.8 ± 0.2; p = 0.005). TSPO was concurrently up-regulated in remote cardiomyocytes at 8 weeks (8.8 ± 1.7, p < 0.001) without inflammatory cell infiltration, suggesting mitochondrial impairment. Angiotensin-converting enzyme inhibitor treatment lowered acute inflammation in the heart (p = 0.003) and brain (p = 0.06) and improved late cardiac function (p = 0.05). Patients also demonstrated elevation of cardiac TSPO signal in the infarct territory, paralleled by neuroinflammation versus controls.


Conclusions - The brain is susceptible to acute MI and chronic heart failure. Immune activation may interconnect heart and brain dysfunction, a finding that provides a foundation for strategies to improve heart and brain outcomes.


Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.





>CBS CBS 2019

> CBS 2019 REGISTRATION

> CBS 2019 PROGRAM

> CBS 2019 CALL FOR SCIENCE

> CBS 2019 SPOTLIGHTS

 CBSMD

> CBSMD WEBSITE REGISTRATION

> EDUCATION CENTER

> RECOMMANDED PAPER

> TOP 10 RESEARCH PAPER

> PRE-READING

CBS 2019 CBS 2019 FACULTY Education Resource CBSMD Scientific Library
Copyright ⓒ CBS MD Nanjing China. All rights reserved. 京ICP备16025898号-11
联系我们| Top