A5012608208- Cardiac Fibrosis and Remodeling
- Peptidase Inhibition and Analysis
- Signaling Pathways in Disease
- Cardiac Structural Anomalies and Repair
- Cardiovascular Disease and Adiposity
- Neuroinflammation and Neurodegeneration Mechanisms
- Cardiac Imaging and Diagnostics
- S100 Proteins and Annexins
- Adenosine and Purinergic Signaling
- Chemokine receptors and signaling
- GDF15 and Related Biomarkers
- Cell Adhesion Molecules Research
- Tissue Engineering and Regenerative Medicine
- Protease and Inhibitor Mechanisms
- Atherosclerosis and Cardiovascular Diseases
- Immune cells in cancer
- Viral Infections and Immunology Research
- Radiopharmaceutical Chemistry and Applications
- Advanced MRI Techniques and Applications
- Congenital Heart Disease Studies
- Cardiac Ischemia and Reperfusion
- Inflammation biomarkers and pathways
- Coronary Artery Anomalies
- Cardiac electrophysiology and arrhythmias
- Kawasaki Disease and Coronary Complications
Medizinische Hochschule Hannover
2018-2025
InLeaVe
2020
University Hospital in Motol
2003
Deutsches Herzzentrum der Charité
2003
Istituti Clinici di Perfezionamento
2003
Deutsches Herzzentrum München
2003
Fundação Universitária de Cardiologia
2003
Hôpital Necker-Enfants Malades
2003
Assistance Publique – Hôpitaux de Paris
2003
Roche (Switzerland)
2003
Abstract Aims Balance between inflammatory and reparative leucocytes allows optimal healing after myocardial infarction (MI). Interindividual heterogeneity evokes variable functional outcome complicating targeted therapy. We aimed to characterize infarct chemokine CXC-motif receptor 4 (CXCR4) expression using positron emission tomography (PET) establish its relationship cardiac outcome. tested whether image-guided early CXCR4 directed therapy attenuates chronic dysfunction. Methods results...
Abstract Purpose Myocardial infarction (MI) triggers a local inflammatory response which orchestrates cardiac repair and contributes to concurrent neuroinflammation. Angiotensin-converting enzyme (ACE) inhibitor therapy not only attenuates remodeling by interfering with the neurohumoral system, but also influences acute leukocyte mobilization from hematopoietic reservoirs. Here, we seek dissect anti-inflammatory anti-remodeling contributions of ACE inhibitors benefit heart brain outcomes...
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Background: Myocardial infarction (MI) evokes an organized remodeling process characterized by the activation and transdifferentiation of quiescent cardiac fibroblasts to generate a stable collagen rich scar.Early fibroblast may be amenable targeted therapy, but is challenging identify in vivo.We aimed non-invasively image active fibrosis targeting protein (FAP) expressed activated (myo)fibroblasts, using novel positron emission tomography (PET) radioligand [ 68 Ga]MHLL1 after acute...
Rationale: Acute myocardial infarction (MI) triggers a systemic inflammatory response including crosstalk along the heart-kidney axis.We employed radionuclide-based inflammation-targeted wholebody molecular imaging to identify potential cardio-renal after MI in translational setup.Methods: Serial whole-body positron emission tomography (PET) with specific CXCR4 ligand 68 Ga-Pentixafor was performed mice.Tracer retention kidneys and heart compared hematopoietic organs evaluate inflammation,...
Persistent inflammation following myocardial infarction (MI) precipitates adverse outcome including acute ventricular rupture and chronic heart failure. Molecular imaging allows longitudinal assessment of immune cell activity in the infarct territory predicts severity remodeling. We utilized a multiparametric platform to assess response cardiac healing MI mice. Suppression circulating macrophages prior paradoxically resulted higher total leukocyte content heart, demonstrated by increased CXC...
Abstract Purpose Myocardial infarction (MI) triggers complex cellular responses essential for tissue repair and remodeling, including myofibroblast activation. Fibroblast activation protein alpha (FAP) identifies activated myofibroblasts post-MI, however its spatial distribution relative to the scar area at risk (AAR) is unclear. Non-invasive FAP-imaging with PET radiotracer 68 Ga-FAPI-46 shows uptake beyond infarct scar. We therefore aimed characterize FAP expression in AAR using a...
Acute myocardial infarction (MI) triggers a local and systemic inflammatory response. We recently showed microglia involvement using translocator protein imaging. Here, we evaluated whether <sup>11</sup>C-methionine provides further insight into heart–brain inflammation networking. <b>Methods:</b> Male C57BL/6 mice underwent permanent coronary artery ligation followed by PET at 3 7 d (<i>n</i> = 3). In subgroups, leukocyte homing was blocked integrin antibodies 5). The cellular substrate for...
The immune-fibrosis axis plays a critical role in cardiac remodeling after acute myocardial infarction. Imaging approaches to monitor temporal inflammation and fibroblast activation mice have seen wide application recent years. However, the repeatability of quantitative measurements remains challenging, particularly across multiple imaging centers. We aimed determine reproducibility images acquired at 2 facilities infarction mice. <b>Methods:</b> Mice underwent coronary artery ligation...
Abstract Background/Introduction Myeloid-derived inflammatory macrophages expressing CCR2 are crucial for scar formation and repair after myocardial infarction (MI). Interference with macrophage dynamics impairs healing promotes intraventricular thrombus formation, but the precise of in left ventricle (LV) under these conditions remain unclear. Purpose We investigated impact depletion on infarct expression, microcalcification, cardiac functional outcome mice reperfused MI. Methods Male...
Abstract Objectives Myocardial infarction evokes inflammation and activation of quiescent cardiac fibroblasts, leading to heart failure progression. We hypothesized that targeted molecular imaging fibroblast protein (FAP) on activated fibroblasts could predict subsequent remodeling monitor response anti-inflammatory therapy. Methods In vitro uptake 68Ga-FAPI-46 was assessed in human stimulated by supernatant from inflammatory macrophages. C57Bl/6 mice underwent 60min left coronary artery...
Abstract Introduction Following myocardial infarction (MI), orchestrated infiltration of diverse leukocyte subtypes contributes to local repair. Systemic and concurrent neuroinflammation is thought contribute cognitive impairment after MI. We have demonstrated that macrophage depletion impairs ventricle healing exacerbates early MI, with persistence cardiac neutrophils. Purpose aimed explore the role neutrophils in post-MI macrophage-depleted mice using timed anti-neutrophil antibody dosing...
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Background:AS-amyloid is common in elderly patients being considered for transcatheter aortic valve implantation (TAVI) and represents the coexistence of cardiac amyloid with severe stenosis (AS).The significance clinical impact this dual pathology unclear.Methods: Patients aged ≥75 referred TAVI at two tertiary centres underwent 99mTc-3,3-diphosphono-1,2-propanodicarboxylic acid (DPD)scintigraphy addition to routine care, which was reported using Perugini grading system (0 negative, 1-3...
Abstract Background/Introduction Myocardial infarction (MI) triggers local inflammation to support endogenous healing and repair. Recent imaging studies of the macrophage- microglia-expressed mitochondrial translocator protein (TSPO) identified concurrent neuroinflammation after acute MI in chronic heart failure. The source this its relationship cardiac function early late are unknown. Purpose We aimed characterize cellular basis TSPO PET signal by modulating via clodronate-mediated...
Background:Recent evidence indicates that acute myocardial infarction (MI) evokes concurrent cardiac and neuroinflammation.18F-GE180 PET imaging of the translocator protein (TSPO) identified activated microglia in brain early after MI.The amino acid 11C-methionine exhibits a low background signal heart compared to 18F-FDG, it is known accumulate inflammatory cells, with an albeit different profile TSPO markers.Purpose:We aimed evaluate feasibility image inflammation following MI.Methods:Male...
Ziel/Aim Cardiorenal syndrome is characterized by bidirectional interaction between the failing heart and kidneys. We speculated that inflammation contributes to this crosstalk sought obtain further mechanistic insights into retrospective analysis of CXCR4-targeted images in myocardial infarction (MI).
Ziel/Aim The 18kD mitochondrial translocator protein (TSPO) is physiologically expressed in kidneys, myocardium and immune cells, where it contributes to the cellular stress response. Here, we used whole-body, targeted PET for obtaining insights into TSPO pathology heart their interrelation, following myocardial infarction (MI).