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Comparison in prevalence, predictors, and clinical outcome of VSR versus FWR after acute myocardial infarction: The prospective, multicenter registry MOODY trial-heart rupture analysis The Potential Use of the Index of Microcirculatory Resistance to Guide Stratification of Patients for Adjunctive Therapy in Acute Myocardial Infarction 2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: a stepped-wedge, cluster-randomised controlled trial Patient Characteristics Associated With Antianginal Medication Escalation and De-Escalation Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN CTO Registry Clinical and Angiographic Features of Patients With Out-of-Hospital Cardiac Arrest and Acute Myocardial Infarction Coronary Angiography in Patients With Out-of-Hospital Cardiac Arrest Without ST-Segment Elevation: A Systematic Review and Meta-Analysis Role of Low Endothelial Shear Stress and Plaque Characteristics in the Prediction of Nonculprit Major Adverse Cardiac Events: The PROSPECT Study A Combination of Allogeneic Stem Cells Promotes Cardiac Regeneration

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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.

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Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction

ABSTRACT