CBS - The 17th Left Main & Coronary Bifurcation Summit, CBS2025

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Incidence of Adverse Events at 3 Months Versus at 12 Months After Dual Antiplatelet Therapy Cessation in Patients Treated With Thin Stents With Unprotected Left Main or Coronary Bifurcations Volumetric characterization of human coronary calcification by frequency-domain optical coherence tomography Meta-Analysis of Death and Myocardial Infarction in the DEFINE-FLAIR and iFR-SWEDEHEART Trials Mortality after coronary artery bypass grafting versus percutaneous coronary intervention with stenting for coronary artery disease: a pooled analysis of individual patient data The Relation Between Optical Coherence Tomography-Detected Layered Pattern and Acute Side Branch Occlusion After Provisional Stenting of Coronary Bifurcation Lesions Reply: Will Pulmonary Artery Denervation Really Have a Place in the Armamentarium of the Pulmonary Hypertension Specialist? Two-year outcomes of everolimus vs. paclitaxel-eluting stent for the treatment of unprotected left main lesions: a propensity score matching comparison of patients included in the French Left Main Taxus (FLM Taxus) and the LEft MAin Xience (LEMAX) registries Left main coronary artery disease: importance, diagnosis, assessment, and management Histopathological validation of optical coherence tomography findings of the coronary arteries Diagnostic accuracy of fractional flow reserve from anatomic CT angiography

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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.

科研文章

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Myocardial Inflammation Predicts Remodeling and Neuroinflammation After Myocardial Infarction

ABSTRACT