{ "groups": [ { "id": "signals", "title": "Sensing & mediators", "question": "How is danger recognised and communicated?", "color": "#c8d9af" }, { "id": "cells", "title": "Immune cells", "question": "Which cells recognise, respond and cooperate?", "color": "#9dcbbb" }, { "id": "tissue", "title": "Regulation & repair", "question": "What restrains injury and shapes recovery?", "color": "#e8cc91" }, { "id": "clinical", "title": "Clinical phenotypes", "question": "Which mechanism fits this clinical context?", "color": "#e7a184" }, { "id": "connections", "title": "Organ interfaces", "question": "Which connections are supported by evidence?", "color": "#c7bddb" }, { "id": "methods", "title": "Observation & translation", "question": "How do we observe, test and translate a claim?", "color": "#aacbe4" } ], "topics": [ { "id": "innate", "title": "Pattern recognition", "group": "signals", "idea": "Pattern-recognition receptors detect microbial structures and damage-associated signals in immune and cardiac-resident cells. Their signalling initiates context-dependent innate responses.", "heart": "TLRs, cytosolic nucleic-acid sensors and downstream pathways connect infection or sterile injury to inflammatory activation.", "evidence": "Receptor expression is not proof of pathway activation. Viral and sterile injury can share sensors while requiring different interpretations.", "sources": [], "related": [ "autoinflammation", "macrophages", "cardio-infectiology", "cardiomyocytes", "complement", "dendritic-cells", "microbiome", "inflammasome", "trained-immunity" ], "book": null, "immune": "Innate sensing", "question": "What is being sensed: a pathogen, damaged tissue, or both?", "reading": "sensing", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "complement", "title": "Complement", "group": "signals", "idea": "A regulated protein cascade: classical, lectin and alternative activation converge on C3. Opsonisation, inflammatory signalling and the terminal complex are key outputs.", "heart": "Connects host defence with tissue injury; cardiovascular research includes ischaemia–reperfusion and vascular inflammation.", "evidence": "Mechanistic involvement does not establish benefit from complement inhibition in every cardiac disease.", "sources": [], "related": [ "autoantibodies", "cardio-infectiology", "immunothrombosis", "neutrophils", "innate", "transplantation", "vasculitis" ], "book": null, "immune": "Innate effector · adaptive interface", "question": "Which pathway, fragment and disease stage are implicated?", "reading": "complement", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "inflammasome", "title": "Inflammasome", "group": "signals", "idea": "Intracellular protein complexes that can activate caspase-1 and promote maturation of IL-1β and IL-18.", "heart": "A bridge between cellular danger signals and inflammatory pathways studied in cardiovascular injury.", "evidence": "Distinguish evidence about a specific inflammasome from evidence about its downstream cytokines.", "sources": [], "related": [ "atherosclerosis", "autoinflammation", "cell-death", "clonal-haematopoiesis", "interleukins", "innate" ], "book": null, "immune": "Innate sensing & amplification", "question": "Is the evidence about inflammasome assembly, a cytokine, or pyroptosis?", "reading": "inflammasome", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "interleukins", "title": "Cytokine networks", "group": "signals", "idea": "Cytokines form context-dependent networks between immune, vascular and stromal cells. IL-1, IL-6 and other interleukins have distinct sources, receptors and effects.", "heart": "Cytokine inhibition tests a specific target in a defined population; it does not test all inflammation at once.", "evidence": "A fall in CRP or another biomarker does not establish a reduction in cardiovascular events.", "sources": [], "related": [ "biomarkers", "causal-evidence", "immunometabolism", "inflammasome", "mast-cells", "nk-ilc", "pericarditis" ], "book": null, "immune": "Innate ↔ adaptive communication", "question": "Which ligand, receptor and patient population are being studied?", "reading": "cytokines", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "immunometabolism", "title": "Immunometabolism", "group": "tissue", "idea": "The interaction between metabolic state and immune-cell function.", "heart": "Helps frame inflammatory responses to ischaemic injury and cardiometabolic stress.", "evidence": "A promising translational field; changing a cellular metabolic pathway is not automatically a validated therapy.", "sources": [], "related": [ "atherosclerosis", "macrophages", "interleukins", "microbiome", "trained-immunity" ], "book": null, "immune": "Innate ↔ adaptive regulation", "question": "Is altered metabolism driving cell function, reflecting injury, or both?", "reading": "metabolism", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "microbiome", "title": "Gut–heart axis", "group": "connections", "idea": "Microbial communities and their metabolites interact with host physiology and immunity.", "heart": "The gut–heart axis connects diet, microbial metabolism and cardiovascular phenotypes.", "evidence": "A prospective association or a predictive model does not show that changing the microbiome prevents cardiovascular disease.", "sources": [], "related": [ "atherosclerosis", "immunometabolism", "innate" ], "book": null, "immune": "Microbial–metabolic interface", "question": "Does the study show association, prediction or a causal intervention?", "reading": "microbiome", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "macrophages", "title": "Cardiac macrophages", "group": "cells", "idea": "Resident and recruited macrophage populations participate in surveillance, clearance and repair. Ontogeny, tissue niche and activation state all matter; a simple M1/M2 split is insufficient.", "heart": "Cardiac macrophages interact with cardiomyocytes, vessels and fibroblasts. Their roles vary between homeostasis, acute injury and chronic disease.", "evidence": "Much mechanistic evidence comes from models; origin alone does not fully define a cell’s function.", "sources": [], "related": [ "chemokines", "clonal-haematopoiesis", "dendritic-cells", "efferocytosis", "fibroblasts", "immunometabolism", "neutrophils", "innate", "regeneration", "remodeling", "resolution", "single-cell-spatial", "trained-immunity" ], "book": null, "immune": "Innate cells", "question": "Which origin, state, niche and time after injury?", "reading": "macrophages", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19", "terms": "macrophages monocytes résidents recrutés moelle CCR2 ontogénie état niche temporalité M1 M2" }, { "id": "lymphocytes", "title": "T lymphocytes", "group": "cells", "idea": "T cells support antigen-specific effector, memory and regulatory responses. CD4, CD8, regulatory and unconventional populations differ in their receptors, state and tissue functions.", "heart": "Antigen specificity distinguishes targeted cardiac immune responses from a nonspecific inflammatory infiltrate.", "evidence": "Cell identity, activation state and tissue context matter; “lymphocyte” is not one uniform mechanism.", "sources": [], "related": [ "adaptive", "b-cells", "cardio-oncology", "dendritic-cells", "tolerance", "myocarditis", "transplantation" ], "book": null, "immune": "Adaptive cells", "question": "Which subset, antigen specificity and tissue compartment?", "reading": "tcells", "terms": "lymphocytes T CD4 CD8 Treg Th1 Th2 Th17 Tfh gamma delta MAIT mémoire cytotoxicité", "subtopics": [ "lymphocytes", "T", "CD4", "CD8", "Treg", "Th1", "Th2", "Th17", "Tfh", "gamma", "delta", "MAIT", "mémoire", "cytotoxicité" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "dendritic-cells", "title": "Dendritic cells", "group": "cells", "immune": "Innate cells · adaptive priming", "question": "Which dendritic-cell subset, maturation state and antigen?", "idea": "Dendritic cells integrate danger sensing, antigen processing and T-cell priming. Their subset, maturation state and tissue niche influence immunity or tolerance.", "heart": "Cardiac antigen sampling and presentation provide a bridge between local tissue injury, draining lymph nodes and adaptive responses.", "evidence": "Conventional and plasmacytoid subsets have different functions. Benefits of engineered cells in experimental models do not establish a clinical treatment.", "related": [ "adaptive", "lymphatics", "macrophages", "tolerance", "innate", "lymphocytes" ], "reading": "dc", "sources": [], "book": null, "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "neutrophils", "title": "Neutrophils & NETs", "group": "cells", "immune": "Innate cells · immunothrombosis", "question": "Which neutrophil state and which evidence of NET formation?", "idea": "Neutrophils coordinate antimicrobial defence, acute inflammation and interactions with platelets and other immune cells. Extracellular traps are one effector mechanism, not a synonym for all neutrophil activity.", "heart": "NET-associated processes connect thrombosis, reperfusion injury and repair, while timing and tissue context shape the effects of neutrophils.", "evidence": "Circulating NET-associated markers do not uniquely identify tissue NET formation or show that NET-directed treatment improves clinical outcomes.", "related": [ "atherosclerosis", "macrophages", "complement", "immunothrombosis", "platelets", "vasculitis" ], "reading": "neutrophils", "sources": [], "book": null, "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "adaptive", "title": "Antigen presentation", "group": "signals", "idea": "Antigen-presenting cells process proteins and display peptides to T cells. Dendritic cells, macrophages and B cells differ in how they prime, sustain or regulate responses.", "heart": "Presentation of cardiac antigens links tissue injury to T-cell activation or tolerance. Antigen release alone is not evidence of pathogenic autoimmunity.", "evidence": "Distinguish antigen presentation, demonstrable antigen-specific responses and proof that those responses cause disease.", "sources": [], "related": [ "b-cells", "dendritic-cells", "tolerance", "myocarditis", "neuro", "lymphocytes" ], "book": null, "immune": "Innate ↔ adaptive bridge", "question": "Who presents which antigen, through which MHC and co-signals?", "reading": "dc", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "tolerance", "title": "Immune tolerance", "group": "tissue", "idea": "Mechanisms that prevent or restrain immune responses against self. Central selection and peripheral control are complementary safeguards.", "heart": "A conceptual bridge to autoimmune disease, graft rejection and adverse effects of immune therapies.", "evidence": "Tolerance is not simply the absence of inflammation or general immunosuppression.", "sources": [], "related": [ "adaptive", "b-cells", "cardio-oncology", "rheumatology", "dendritic-cells", "neuro", "eye", "kidney", "systemic", "lymphocytes", "therapeutic-targets", "transplantation" ], "book": null, "immune": "Adaptive regulation · innate support", "question": "Which protective control is lost, preserved or being restored?", "reading": "treg", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "resolution", "title": "Resolution", "group": "tissue", "idea": "Active containment and ending of an inflammatory response, rather than merely a fall in inflammatory markers.", "heart": "Timely resolution and clearance of the infiltrate are important for organised cardiac repair.", "evidence": "Stopping inflammation and restoring functional tissue are related but different outcomes.", "sources": [], "related": [ "lymphatics", "macrophages", "efferocytosis", "fibrosis", "nk-ilc", "regeneration", "remodeling" ], "book": null, "immune": "Active inflammatory control", "question": "Has inflammation resolved, and has tissue function recovered?", "reading": "resolution", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "remodeling", "title": "Remodeling", "group": "tissue", "idea": "Changes in cardiac structure and function after injury or persistent stress.", "heart": "Inflammatory and reparative responses contribute to the trajectory after myocardial injury.", "evidence": "Remodelling describes a process; it is not synonymous with inflammation or proof of its cause.", "sources": [], "related": [ "lymphatics", "macrophages", "fibrosis", "heart-failure", "resolution" ], "book": null, "immune": "Immune–stromal response", "question": "Which structural change, at which phase after injury?", "reading": "repair", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "fibrosis", "title": "Fibrosis", "group": "tissue", "idea": "Accumulation and reorganisation of extracellular matrix, including scar formation after tissue loss.", "heart": "A scar can preserve integrity, while persistent or diffuse fibrosis may impair function.", "evidence": "Active fibroblast signalling, accumulated scar and potential reversibility are different quantities. An imaging signal needs validation against the biological process it is claimed to measure.", "sources": [], "related": [ "amyloidosis", "aortic-disease", "fibroblasts", "mast-cells", "myocarditis", "regeneration", "remodeling", "resolution", "arrhythmias", "valvular-disease" ], "book": null, "immune": "Stromal response", "question": "Active fibroblast signalling, matrix deposition or established scar?", "reading": "fibrosis", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "regeneration", "title": "Regeneration", "group": "tissue", "idea": "Replacement of lost functional tissue; distinct from repair by scar formation.", "heart": "Experimental cardiac repair studies investigate how inflammatory and stromal responses affect recovery.", "evidence": "Results in mice do not establish restoration of human myocardium or a ready-to-use treatment.", "sources": [], "related": [ "macrophages", "fibroblasts", "fibrosis", "resolution" ], "book": null, "immune": "Repair–regeneration interface", "question": "Is functional myocardium replaced, or is scar formation modified?", "reading": "regeneration", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "atherosclerosis", "title": "Atherosclerosis", "group": "clinical", "idea": "Arterial plaque disease in which lipids and inflammatory processes interact.", "heart": "A major cardiovascular setting for studying the consequences of immune activation.", "evidence": "Inflammation is one component of risk, alongside other established contributors.", "sources": [], "related": [ "causal-evidence", "clonal-haematopoiesis", "microbiome", "immunometabolism", "immunothrombosis", "inflammasome", "neutrophils", "therapeutic-targets" ], "book": null, "immune": "Lipid–immune disease", "question": "Does target engagement translate into fewer clinical events?", "reading": "atherosclerosis", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "pericarditis", "title": "Pericarditis", "group": "clinical", "idea": "Inflammation of the pericardium, the sac surrounding the heart.", "heart": "Shows why anatomical site, disease course and cause should be considered separately.", "evidence": "Clinical assessment and disease-specific guidance are needed; a pathway alone does not define management.", "sources": [], "related": [ "autoinflammation", "interleukins", "myocarditis" ], "book": null, "immune": "Pericardial inflammation", "question": "Which cause, inflammatory phenotype and recurrence pattern?", "reading": "pericarditis", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "myocarditis", "title": "Myocarditis", "group": "clinical", "idea": "Inflammation involving the heart muscle.", "heart": "Distinct from pericarditis, although the two may overlap.", "evidence": "The cause, clinical presentation and evidence of tissue injury need individual assessment.", "sources": [], "related": [ "adaptive", "autoantibodies", "cardiac-imaging", "cardio-infectiology", "cardio-oncology", "cardiomyocytes", "eosinophils", "fibrosis", "pericarditis", "arrhythmias", "sarcoidosis", "lymphocytes" ], "book": null, "immune": "Myocardial inflammation", "question": "What establishes inflammation, its cause and the risk profile?", "reading": "esc", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "sarcoidosis", "title": "Sarcoidosis", "group": "clinical", "idea": "A multisystem disease characterised by granulomatous inflammation.", "heart": "Cardiac involvement is a distinct concern within a disease that may affect several organs.", "evidence": "A diagnosis in one organ does not by itself define the presence or severity of cardiac involvement.", "sources": [], "related": [ "cardiac-imaging", "myocarditis", "eye", "pulmonary", "arrhythmias", "systemic" ], "book": null, "immune": "Granulomatous disease", "question": "Active inflammation, scar, or a combination of both?", "reading": "sarcoidosis", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "amyloidosis", "title": "Amyloidosis", "group": "clinical", "idea": "Misfolded proteins accumulate in tissue. Cardiac AL amyloidosis and transthyretin amyloidosis are biologically distinct entities.", "heart": "Included at the boundary of the map: AL involves an immunoglobulin-producing clone, whereas ATTR is not primarily an immune-mediated myocarditis.", "evidence": "AL and transthyretin amyloidosis are distinct; infiltration must not be equated with active immune inflammation.", "sources": [], "related": [ "fibrosis", "heart-failure", "systemic" ], "book": null, "immune": "Protein deposition · differential diagnosis", "question": "Which amyloid protein is demonstrated?", "reading": "amyloidosis", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "systemic", "title": "Systemic diseases", "group": "clinical", "idea": "Immune-mediated diseases may involve several organs rather than one isolated tissue.", "heart": "Lupus, for example, can involve the heart as well as other organs.", "evidence": "Mechanisms and organ patterns differ between diseases; extrapolation requires care.", "sources": [], "related": [ "amyloidosis", "rheumatology", "tolerance", "neuro", "eye", "pulmonary-hypertension", "pulmonary", "kidney", "sarcoidosis", "valvular-disease", "vasculitis" ], "book": null, "immune": "Multiorgan immune disease", "question": "What is established in the heart, rather than inferred from another organ?", "reading": "systemic", "terms": "lupus sclérodermie myosite Sjögren polyarthrite autoimmunité systémique connective tissue disease", "subtopics": [ "lupus", "sclérodermie", "myosite", "Sjögren", "polyarthrite", "autoimmunité", "systémique", "connective", "tissue", "disease" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "vasculitis", "title": "Vasculitis", "group": "clinical", "idea": "Inflammation affecting blood vessels, with manifestations depending on the vessels and organs involved.", "heart": "Connects vascular injury with questions about the heart and other organs.", "evidence": "The vasculitis subtype matters; a general label does not determine a patient’s organ involvement.", "sources": [], "related": [ "aortic-disease", "rheumatology", "complement", "eosinophils", "neutrophils", "kidney", "systemic" ], "book": { "label": "Read issue 1 · The Silent Heart", "url": "revue/n1-the-silent-heart.html" }, "immune": "Vascular inflammation", "question": "Which subtype, vessel size, activity and cardiac manifestation?", "reading": "vasculitis", "terms": "vascularites ANCA GPA MPA EGPA Behçet Kawasaki petits moyens gros vaisseaux", "subtopics": [ "vascularites", "ANCA", "GPA", "MPA", "EGPA", "Behçet", "Kawasaki", "petits", "moyens", "gros", "vaisseaux" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "autoinflammation", "title": "Autoinflammation", "group": "clinical", "idea": "Disorders characterised by inappropriate activation of innate inflammatory pathways.", "heart": "Offers a framework for understanding recurrent inflammatory syndromes and their interfaces.", "evidence": "Autoinflammation and autoimmunity overlap in some settings but are not interchangeable terms.", "sources": [], "related": [ "inflammasome", "innate", "pericarditis" ], "book": null, "immune": "Dysregulated innate inflammation", "question": "What supports an autoinflammatory rather than an infectious or autoimmune mechanism?", "reading": "pericarditis", "terms": "auto-inflammation FMF TRAPS CAPS Still fièvre périodique IL-1", "subtopics": [ "auto-inflammation", "FMF", "TRAPS", "CAPS", "Still", "fièvre", "périodique", "IL-1" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "pulmonary-hypertension", "title": "Pulmonary hypertension", "group": "clinical", "idea": "Elevated pressure in the pulmonary circulation, arising through different disease groups.", "heart": "Connects pulmonary vascular disease with the workload of the right heart.", "evidence": "The underlying group and cause matter; inflammation is not the sole explanation for pulmonary hypertension.", "sources": [], "related": [ "endothelium", "heart-failure", "pulmonary", "systemic" ], "book": null, "immune": "Pulmonary vascular–right heart interface", "question": "Which haemodynamic group, and what evidence of immune involvement?", "reading": "ph", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "heart-failure", "title": "Heart failure & cardiomyopathy", "group": "clinical", "idea": "A clinical syndrome with multiple possible causes.", "heart": "Provides a shared clinical outcome in which vascular, myocardial and systemic processes may converge.", "evidence": "Heart failure is not one immune disease; identifying a mechanism requires more than the syndrome label.", "sources": [], "related": [ "amyloidosis", "clonal-haematopoiesis", "immune-ageing", "pulmonary-hypertension", "remodeling" ], "book": null, "immune": "Syndrome · heterogeneous mechanisms", "question": "Which cause and phenotype explain the immune signal?", "reading": "hf", "terms": "insuffisance cardiaque HFpEF HFrEF cardiomyopathie dilatée DCM ACM génétique péripartum diabète obésité sexes ventricule droit oreillette", "subtopics": [ "insuffisance", "cardiaque", "HFpEF", "HFrEF", "cardiomyopathie", "dilatée", "DCM", "ACM", "génétique", "péripartum", "diabète", "obésité", "sexes", "ventricule", "droit", "oreillette" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "cardio-oncology", "title": "Cardio-oncology", "group": "clinical", "idea": "The cardiovascular consequences of cancer and its treatments.", "heart": "Immune therapies are an important interface, alongside other cancer-related cardiovascular effects.", "evidence": "Risk and management depend on the treatment and clinical setting; mechanisms cannot be generalised across agents.", "sources": [], "related": [ "tolerance", "myocarditis", "lymphocytes" ], "book": null, "immune": "Treatment–immune interface", "question": "Which therapy, immune lesion and competing diagnosis?", "reading": "ici", "terms": "ICI inhibiteurs checkpoints immunitaires CAR-T syndrome libération cytokines CRS cancer radiothérapie toxicité immunothérapie", "subtopics": [ "ICI", "inhibiteurs", "checkpoints", "immunitaires", "CAR-T", "syndrome", "libération", "cytokines", "CRS", "cancer", "radiothérapie", "toxicité", "immunothérapie" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "cardio-infectiology", "title": "Cardio-infectiology", "group": "clinical", "idea": "The cardiovascular interfaces of infection, including infective endocarditis.", "heart": "Connects pathogen, host response and cardiac tissue or device involvement.", "evidence": "The selected influenza study combines human observations with mechanistic animal work. It does not explain every infection-related cardiac syndrome.", "sources": [], "related": [ "complement", "myocarditis", "nk-ilc", "innate", "valvular-disease" ], "book": null, "immune": "Pathogen–host interface", "question": "What distinguishes pathogen persistence from immune-mediated damage?", "reading": "infection", "terms": "infection virus influenza SARS-CoV-2 VIH Chagas endocardite sepsis post-infectieux", "subtopics": [ "infection", "virus", "influenza", "SARS-CoV-2", "VIH", "Chagas", "endocardite", "sepsis", "post-infectieux" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "transplantation", "title": "Transplantation", "group": "clinical", "idea": "Replacement of a failing heart with a donor organ, with continuing attention to immune rejection.", "heart": "Makes recognition of non-self and its regulation clinically tangible.", "evidence": "Rejection, infection and graft dysfunction are distinct problems requiring specialist evaluation.", "sources": [], "related": [ "autoantibodies", "complement", "tolerance", "lymphocytes" ], "book": null, "immune": "Alloimmune recognition", "question": "Cellular rejection, antibody-mediated injury, infection or another graft problem?", "reading": "transplant", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "eye", "title": "Ocular immunity", "group": "connections", "idea": "Immune-mediated and infectious inflammation of the eye; uveitis is one example.", "heart": "A cross-organ perspective for reading multisystem inflammation, rather than a claim of a universal eye–heart mechanism.", "evidence": "An inflammatory sign in the eye does not establish a cardiac diagnosis.", "sources": [], "related": [ "tolerance", "sarcoidosis", "systemic" ], "book": null, "immune": "Cross-organ comparison", "question": "Which ocular mechanism is demonstrated, and can it be extrapolated?", "reading": "eye", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "kidney", "title": "Renal immunity", "group": "connections", "idea": "Immune injury in the kidney, illustrated by lupus nephritis.", "heart": "Offers a cross-organ way to think about systemic disease and organ-specific damage.", "evidence": "The selected human study identifies signatures in lupus nephritis. Its findings cannot diagnose cardiac involvement or establish a cardiac therapeutic target.", "sources": [], "related": [ "biomarkers", "tolerance", "systemic", "hypertension", "vasculitis" ], "book": null, "immune": "Cross-organ comparison", "question": "Do circulating signatures reflect kidney injury, cardiac injury or systemic activity?", "reading": "kidney", "terms": "rein rénal néphrite cardiorénal lupus complément urémie", "subtopics": [ "rein", "rénal", "néphrite", "cardiorénal", "lupus", "complément", "urémie" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "neuro", "title": "Neuroimmune axis", "group": "connections", "idea": "Interactions between immunity and the nervous system; multiple sclerosis is a familiar example of immune-mediated damage.", "heart": "Included as a neighbouring discipline for comparing tissue context and organ vulnerability.", "evidence": "This conceptual connection does not imply a common cardiac mechanism or treatment.", "sources": [], "related": [ "adaptive", "tolerance", "arrhythmias", "systemic", "hypertension" ], "book": null, "immune": "Neural–immune communication", "question": "Which neural circuit, immune effector and cardiac outcome are linked?", "reading": "neuro", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "pulmonary", "title": "Pulmonary immunity", "group": "connections", "idea": "Immune processes in the lung, including granulomatous inflammation in sarcoidosis.", "heart": "Connects a multisystem perspective with pulmonary and cardiovascular questions.", "evidence": "Shared inflammatory vocabulary does not mean identical organ behaviour.", "sources": [], "related": [ "pulmonary-hypertension", "sarcoidosis", "systemic" ], "book": null, "immune": "Lung–heart interface", "question": "Is cardiac stress secondary to pulmonary vascular disease or direct cardiac involvement?", "reading": "ph", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "rheumatology", "title": "Cardio-rheumatology", "group": "connections", "idea": "Systemic immune-mediated diseases may involve joints, skin and internal organs.", "heart": "Lupus illustrates why cardiovascular questions belong within a wider organ assessment.", "evidence": "Troponin indicates myocardial injury in context; assay interference and non-inflammatory causes must also be considered.", "sources": [], "related": [ "tolerance", "systemic", "vasculitis" ], "book": null, "immune": "Systemic–cardiac interface", "question": "Inflammatory injury, vascular disease, treatment effect or an analytical interference?", "reading": "rheum", "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "clonal-haematopoiesis", "title": "Clonal haematopoiesis", "group": "connections", "immune": "Bone marrow–cardiovascular interface", "question": "Which driver mutation, clone size and clinical endpoint?", "idea": "Somatic mutations can expand a haematopoietic clone and alter the inflammatory behaviour of its blood-cell descendants. Different driver genes do not produce one uniform immune phenotype.", "heart": "Clonal haematopoiesis links ageing, myeloid biology and cardiovascular risk, including atherosclerosis and heart failure.", "evidence": "Risk associations and mechanistic models do not establish routine population screening or a validated clone-directed cardiovascular treatment.", "related": [ "atherosclerosis", "macrophages", "heart-failure", "immune-ageing", "inflammasome", "trained-immunity" ], "reading": "chip", "sources": [], "book": null, "subtopics": [], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "chemokines", "title": "Chemokines & trafficking", "group": "signals", "immune": "Recruitment & positioning", "question": "Which cell is recruited, through which receptor and into which compartment?", "idea": "Chemokine gradients and adhesion signals position immune cells within tissues. Expression, migration and retention are distinct observations.", "heart": "CCL2–CCR2 and CXCL-family pathways help frame the recruitment of myeloid and lymphoid cells to injured myocardium.", "evidence": "Chemokine abundance alone cannot identify its cellular source, demonstrate a functional gradient or establish benefit from receptor blockade.", "reading": "chemokines", "related": [ "lymphatics", "macrophages", "endothelium", "fibroblasts" ], "terms": "chimiokines recrutement migration adhésion CCL2 CCR2 CXCL9 CXCL10 CXCR3", "sources": [], "book": null, "subtopics": [ "chimiokines", "recrutement", "migration", "adhésion", "CCL2", "CCR2", "CXCL9", "CXCL10", "CXCR3" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "autoantibodies", "title": "Autoantibodies", "group": "signals", "immune": "Humoral immunity", "question": "Does the antibody bind, alter function, or cause disease?", "idea": "Autoantibodies may bind cardiac antigens or influence receptor signalling. Their presence and their functional effects need separate assays.", "heart": "Humoral mechanisms are studied in myocardial disease, systemic autoimmunity and graft injury.", "evidence": "Association, functional activity and pathogenic causality are different claims. A positive antibody test does not by itself justify immune therapy.", "reading": "autoantibodies", "related": [ "b-cells", "complement", "immunothrombosis", "myocarditis", "transplantation" ], "terms": "autoanticorps autoimmunité humorale immunoglobulines récepteurs complexes immuns Fc", "sources": [], "book": null, "subtopics": [ "autoanticorps", "autoimmunité", "humorale", "immunoglobulines", "récepteurs", "complexes", "immuns", "Fc" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "trained-immunity", "title": "Trained immunity", "group": "signals", "immune": "Innate memory & reprogramming", "question": "Which earlier exposure leaves which durable change?", "idea": "Some innate cells and their progenitors retain altered responsiveness after an earlier stimulus through metabolic and epigenetic reprogramming.", "heart": "Persistent myeloid responses provide a framework for studying vascular inflammation after metabolic or infectious exposures.", "evidence": "This is not antigen-specific adaptive memory. Demonstrating a chromatin signature alone does not establish a clinically useful intervention.", "reading": "trained", "related": [ "macrophages", "clonal-haematopoiesis", "immunometabolism", "innate" ], "terms": "immunité entraînée mémoire innée épigénétique tolérance innée moelle progéniteurs", "sources": [], "book": null, "subtopics": [ "immunité", "entraînée", "mémoire", "innée", "épigénétique", "tolérance", "innée", "moelle", "progéniteurs" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "b-cells", "title": "B cells & plasma cells", "group": "cells", "immune": "Adaptive cells", "question": "Which B-cell state, specificity and function are implicated?", "idea": "B cells can present antigen and produce cytokines; differentiated plasma cells secrete antibodies. Regulatory and effector functions depend on state and context.", "heart": "B-cell responses and receptor repertoires are studied in myocarditis and other cardiac immune settings.", "evidence": "B-cell depletion and suppression of long-lived plasma cells are not equivalent. Findings in experimental myocarditis do not establish a broadly effective cardiac treatment.", "reading": "bcells", "related": [ "adaptive", "autoantibodies", "tolerance", "lymphocytes" ], "terms": "lymphocytes B plasmocytes BCR Breg mémoire centres germinatifs", "sources": [], "book": null, "subtopics": [ "lymphocytes", "B", "plasmocytes", "BCR", "Breg", "mémoire", "centres", "germinatifs" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "nk-ilc", "title": "NK cells & ILCs", "group": "cells", "immune": "Innate lymphoid cells", "question": "Which lineage, activation state and target are being examined?", "idea": "Natural killer cells and helper innate lymphoid populations differ in cytotoxicity and cytokine programmes. They lack the rearranged antigen receptors of conventional B and T cells.", "heart": "These populations participate in experimental responses to infection, injury and tissue repair in the heart.", "evidence": "NK, NKT and ILC subsets should not be conflated. A circulating cell count cannot establish the function of a tissue-resident population.", "reading": "sensing", "related": [ "cardio-infectiology", "interleukins", "resolution" ], "terms": "cellules NK lymphoïdes innées ILC1 ILC2 ILC3 NKT cytotoxicité perforine granzymes", "sources": [], "book": null, "subtopics": [ "cellules", "NK", "lymphoïdes", "innées", "ILC1", "ILC2", "ILC3", "NKT", "cytotoxicité", "perforine", "granzymes" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "eosinophils", "title": "Eosinophils", "group": "cells", "immune": "Innate granulocytes", "question": "Which cause and which evidence of eosinophilic tissue injury?", "idea": "Eosinophils release granule proteins and lipid mediators. Blood eosinophilia and eosinophilic myocardial infiltration describe different findings.", "heart": "Hypersensitivity, eosinophilic granulomatosis with polyangiitis and hypereosinophilic disorders can be associated with cardiac injury.", "evidence": "A normal blood count does not exclude tissue disease. Imaging can suggest a phenotype but cannot by itself establish its histological cause.", "reading": "eosinophils", "related": [ "cell-death", "myocarditis", "vasculitis" ], "terms": "éosinophiles EGPA hyperéosinophilie hypersensibilité myocardite éosinophilique", "sources": [], "book": null, "subtopics": [ "éosinophiles", "EGPA", "hyperéosinophilie", "hypersensibilité", "myocardite", "éosinophilique" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "mast-cells", "title": "Mast cells", "group": "cells", "immune": "Innate tissue sentinels", "question": "Which mediator and which phase of the response?", "idea": "Mast cells are tissue-resident immune cells with granule-derived mediators, cytokines and proteases. Their functions vary across local environments.", "heart": "Experimental work links cardiac mast cells to vascular responses, matrix remodelling and inflammatory regulation.", "evidence": "Many functional claims remain preclinical. Cell abundance, degranulation and the effect of a particular mediator require different measurements.", "reading": "mast", "related": [ "interleukins", "endothelium", "fibrosis" ], "terms": "mastocytes histamine tryptase chymase allergie Kounis basophiles", "sources": [], "book": null, "subtopics": [ "mastocytes", "histamine", "tryptase", "chymase", "allergie", "Kounis", "basophiles" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "platelets", "title": "Platelets", "group": "cells", "immune": "Haemostatic & immune interface", "question": "Which platelet activity links haemostasis to immunity?", "idea": "Platelets are anucleate blood elements that combine haemostatic functions with mediator release and interactions with immune cells.", "heart": "Platelet–leukocyte interactions provide a bridge between vascular injury, inflammation and thrombus formation.", "evidence": "Platelet activation is not one uniform state. A circulating activation marker does not demonstrate a causal tissue interaction.", "reading": "platelets", "related": [ "endothelium", "immunothrombosis", "neutrophils" ], "terms": "plaquettes agrégation thrombo-inflammation vésicules extracellulaires CD40L", "sources": [], "book": null, "subtopics": [ "plaquettes", "agrégation", "thrombo-inflammation", "vésicules", "extracellulaires", "CD40L" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "endothelium", "title": "Endothelium", "group": "cells", "immune": "Vascular resident cells", "question": "Which vascular bed and which endothelial state?", "idea": "Endothelial cells regulate barrier function, leucocyte recruitment and signals exchanged with their tissue environment.", "heart": "Coronary and pulmonary microvascular states can influence the distribution and consequences of cardiac inflammation.", "evidence": "An endothelial transcriptomic signature needs functional validation. The heart and lung do not share one uniform endothelial programme.", "reading": "endothelium", "related": [ "aortic-disease", "chemokines", "mast-cells", "platelets", "pulmonary-hypertension", "single-cell-spatial", "hypertension" ], "terms": "endothélium microcirculation glycocalyx perméabilité adhésion péricytes cellules musculaires lisses", "sources": [], "book": null, "subtopics": [ "endothélium", "microcirculation", "glycocalyx", "perméabilité", "adhésion", "péricytes", "cellules", "musculaires", "lisses" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "cardiomyocytes", "title": "Cardiomyocytes", "group": "cells", "immune": "Cardiac resident responders", "question": "Is the myocyte a sensor, a target, or both?", "idea": "Cardiomyocytes respond to injury and can activate innate sensing, cytokine and regulated cell-death pathways. Their contractile role does not make them immunologically passive.", "heart": "In viral myocarditis, direct infection and host-mediated injury can converge on the same cardiac cell.", "evidence": "A pathogen signal or an inflammatory transcript is not enough to separate direct cytotoxicity from immune-mediated damage.", "reading": "sensing", "related": [ "cell-death", "myocarditis", "innate" ], "terms": "cardiomyocytes mitochondries stress réticulum autophagie cardiotoxicité", "sources": [], "book": null, "subtopics": [ "cardiomyocytes", "mitochondries", "stress", "réticulum", "autophagie", "cardiotoxicité" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "fibroblasts", "title": "Fibroblast niches", "group": "tissue", "immune": "Immune–stromal interface", "question": "Which fibroblast state and which local partners?", "idea": "Cardiac fibroblasts maintain extracellular matrix and organise niches. Injury can change their inflammatory, reparative and matrix-producing programmes.", "heart": "Their interactions with immune and myocardial cells connect tissue integrity, inflammatory positioning and fibrosis.", "evidence": "A fibroblast marker or a predicted ligand–receptor pair does not establish a functional interaction. Reducing scar formation and restoring contractile tissue are different outcomes.", "reading": "fibroblasts", "related": [ "macrophages", "chemokines", "fibrosis", "immune-ageing", "regeneration", "single-cell-spatial" ], "terms": "fibroblastes stroma niches matrice TGF bêta FAP mécanobiologie périvasculaire", "sources": [], "book": null, "subtopics": [ "fibroblastes", "stroma", "niches", "matrice", "TGF", "bêta", "FAP", "mécanobiologie", "périvasculaire" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "lymphatics", "title": "Cardiac lymphatics", "group": "tissue", "immune": "Drainage & immune trafficking", "question": "What leaves the tissue, and where does it go?", "idea": "Lymphatic vessels drain interstitial fluid and support movement of immune cells and antigens towards lymph nodes.", "heart": "Experimental myocardial injury studies connect lymphatic remodelling with inflammatory clearance and recovery.", "evidence": "More lymphatic vessels do not automatically mean effective drainage. Translational benefit needs demonstration beyond vessel density in animal tissue.", "reading": "lymphatics", "related": [ "chemokines", "dendritic-cells", "remodeling", "resolution" ], "terms": "lymphatiques ganglions drainage œdème circulation lymphatique lymphangiogenèse", "sources": [], "book": null, "subtopics": [ "lymphatiques", "ganglions", "drainage", "œdème", "circulation", "lymphatique", "lymphangiogenèse" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "efferocytosis", "title": "Efferocytosis", "group": "tissue", "immune": "Clearance of dying cells", "question": "Are dying cells recognised, engulfed and processed successfully?", "idea": "Phagocytes clear apoptotic cells through coordinated recognition, engulfment and processing. Failed clearance can prolong local injury.", "heart": "Efferocytosis helps frame resolution after myocardial infarction and clearance within atherosclerotic lesions.", "evidence": "Increased phagocyte numbers do not establish efficient clearance. A mechanistic rescue in a model does not establish clinical efficacy.", "reading": "efferocytosis", "related": [ "macrophages", "cell-death", "resolution" ], "terms": "efférocytose phagocytose MerTK CD47 apoptose eat-me clearance", "sources": [], "book": null, "subtopics": [ "efférocytose", "phagocytose", "MerTK", "CD47", "apoptose", "eat-me", "clearance" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "cell-death", "title": "Cell death & danger", "group": "tissue", "immune": "Injury–inflammation interface", "question": "Which death programme is demonstrated by which perturbation?", "idea": "Apoptosis, necroptosis, pyroptosis and ferroptosis describe distinct regulated processes. Their contributions can overlap in a diseased tissue.", "heart": "Cell death changes myocardial cell mass and can release signals that recruit or activate immune responses.", "evidence": "A single marker rarely identifies a unique death programme. PANoptosis describes proposed coordinated death circuitry and requires mechanistic evidence.", "reading": "cell-death", "related": [ "cardiomyocytes", "efferocytosis", "eosinophils", "inflammasome" ], "terms": "mort cellulaire apoptose nécroptose pyroptose ferroptose PANoptose DAMP", "sources": [], "book": null, "subtopics": [ "mort", "cellulaire", "apoptose", "nécroptose", "pyroptose", "ferroptose", "PANoptose", "DAMP" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "immune-ageing", "title": "Immune ageing", "group": "tissue", "immune": "Host context", "question": "How do age and senescence change the response?", "idea": "Immune ageing and cellular senescence can alter surveillance, inflammatory tone and tissue repair. Chronological age does not fully capture these processes.", "heart": "Senescent stromal, vascular and immune states are studied in age-associated cardiovascular dysfunction.", "evidence": "A senescence-associated marker is not a complete cell identity. Senolytic findings in models do not establish routine human cardiac treatment.", "reading": "ageing", "related": [ "clonal-haematopoiesis", "fibroblasts", "heart-failure" ], "terms": "vieillissement sénescence immunosénescence inflammaging SASP sexe genre hormones comorbidités", "sources": [], "book": null, "subtopics": [ "vieillissement", "sénescence", "immunosénescence", "inflammaging", "SASP", "sexe", "genre", "hormones", "comorbidités" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "hypertension", "title": "Systemic hypertension", "group": "clinical", "immune": "Vascular–renal–immune phenotype", "question": "What evidence supports immune involvement in this hypertensive setting?", "idea": "Experimental and human studies examine immune pathways alongside vascular, renal and neurohumoral regulation of blood pressure.", "heart": "Immune activation may contribute to vascular dysfunction and target-organ injury in selected contexts.", "evidence": "Most hypertension is not established as an autoimmune disease. Immune associations do not replace validated blood-pressure management or establish benefit from immunosuppression.", "reading": "hypertension", "related": [ "endothelium", "neuro", "kidney" ], "terms": "hypertension artérielle HTA pression sodium angiotensine aldostérone", "sources": [], "book": null, "subtopics": [ "hypertension", "artérielle", "HTA", "pression", "sodium", "angiotensine", "aldostérone" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "arrhythmias", "title": "Rhythm & conduction", "group": "clinical", "immune": "Electrical phenotype", "question": "Which inflammatory process is linked to which electrical outcome?", "idea": "Immune cells and inflammatory mediators can interact with electrical properties, tissue architecture and autonomic signals.", "heart": "Atrial fibrillation, conduction disease and ventricular arrhythmia are different clinical settings; inflammation and scar may contribute in different ways.", "evidence": "An inflammatory association does not prove an immune cause of an arrhythmia. Results in atrial fibrillation cannot be assumed to apply to every rhythm disorder.", "reading": "arrhythmias", "related": [ "fibrosis", "myocarditis", "neuro", "sarcoidosis" ], "terms": "arythmies fibrillation atriale conduction bloc ventriculaire mort subite", "sources": [], "book": null, "subtopics": [ "arythmies", "fibrillation", "atriale", "conduction", "bloc", "ventriculaire", "mort", "subite" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "valvular-disease", "title": "Valvular disease", "group": "clinical", "immune": "Valvular immune interfaces", "question": "Which valve process: post-infectious autoimmunity, calcification or another cause?", "idea": "Rheumatic valve disease provides an established setting in which an immune response after infection can contribute to valve injury. Other valve diseases have different mechanisms.", "heart": "Valve inflammation, fibrosis and calcification need to be distinguished from the haemodynamic consequence of a valve lesion.", "evidence": "Not every valve lesion is immune-mediated. A review of rheumatic disease does not establish the mechanism of degenerative calcific disease.", "reading": "valves", "related": [ "cardio-infectiology", "fibrosis", "systemic" ], "terms": "valves valvulopathies rhumatisme articulaire aigu endocardite Libman Sacks calcification", "sources": [], "book": null, "subtopics": [ "valves", "valvulopathies", "rhumatisme", "articulaire", "aigu", "endocardite", "Libman", "Sacks", "calcification" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "aortic-disease", "title": "Aorta & large vessels", "group": "clinical", "immune": "Arterial wall disease", "question": "Is the wall disease inflammatory, degenerative, genetic or mixed?", "idea": "Large-vessel vasculitis and clinically isolated aortitis can affect aortic structure. Aneurysm is an anatomical finding with several possible causes.", "heart": "Imaging, pathology and clinical context help separate active wall inflammation from established structural damage.", "evidence": "A growth-rate association in an observational cohort does not prove treatment efficacy. Genetic and degenerative aneurysms must not be relabelled as autoimmune disease.", "reading": "aorta", "related": [ "endothelium", "fibrosis", "vasculitis" ], "terms": "aorte aortite Takayasu artérite cellules géantes anévrisme dissection paroi", "sources": [], "book": null, "subtopics": [ "aorte", "aortite", "Takayasu", "artérite", "cellules", "géantes", "anévrisme", "dissection", "paroi" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "immunothrombosis", "title": "Immunothrombosis & APS", "group": "clinical", "immune": "Immune–coagulation interface", "question": "Which immune trigger contributes to which thrombotic event?", "idea": "Coagulation, platelets, complement and immune cells can interact. Antiphospholipid syndrome is a specific autoimmune setting within this wider interface.", "heart": "Arterial, venous and microvascular thrombosis have different contexts and consequences for the heart and circulation.", "evidence": "An isolated antiphospholipid antibody result does not establish antiphospholipid syndrome. Classification criteria and individual clinical diagnosis serve different purposes.", "reading": "aps", "related": [ "atherosclerosis", "autoantibodies", "complement", "neutrophils", "platelets" ], "terms": "immunothrombose SAPL antiphospholipides thrombose thromboembolie anticoagulation", "sources": [], "book": null, "subtopics": [ "immunothrombose", "SAPL", "antiphospholipides", "thrombose", "thromboembolie", "anticoagulation" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "cardiac-imaging", "title": "Cardiac imaging", "group": "methods", "immune": "Observation", "question": "Which biological process does the image actually measure?", "idea": "Echocardiography, magnetic resonance, CT and nuclear imaging measure different properties. Inflammation, extracellular expansion and active fibroblast signalling are not interchangeable signals.", "heart": "Multimodality imaging can locate injury and follow ventricular, vascular or tissue consequences in an appropriate clinical context.", "evidence": "An imaging pattern cannot automatically identify an immune cause. Molecular tracers require validation against the biological process they are claimed to measure.", "reading": "fibrosis", "related": [ "biomarkers", "myocarditis", "sarcoidosis" ], "terms": "imagerie échocardiographie IRM CMR TEP PET CT scanner strain LGE T1 T2 ECV", "sources": [], "book": null, "subtopics": [ "imagerie", "échocardiographie", "IRM", "CMR", "TEP", "PET", "CT", "scanner", "strain", "LGE", "T1", "T2", "ECV" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "biomarkers", "title": "Biomarkers & sampling", "group": "methods", "immune": "Measurement & interpretation", "question": "Which sample, assay, timing and clinical question?", "idea": "A biomarker is interpreted through its biological source, analytical method and intended clinical use. Diagnostic, prognostic and treatment-response claims require different evidence.", "heart": "Troponin, natriuretic peptides and inflammatory markers may inform complementary questions in cardiovascular disease.", "evidence": "A biomarker may reflect processes outside the heart. A statistical association does not establish clinical utility or a treatment threshold.", "reading": "rheum", "related": [ "cardiac-imaging", "interleukins", "kidney" ], "terms": "biomarqueurs troponine CRP BNP NT-proBNP prélèvement biopsie histologie immunohistochimie endomyocardique", "sources": [], "book": null, "subtopics": [ "biomarqueurs", "troponine", "CRP", "BNP", "NT-proBNP", "prélèvement", "biopsie", "histologie", "immunohistochimie", "endomyocardique" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19", "readingSecondary": [ "biomarkers" ] }, { "id": "single-cell-spatial", "title": "Single-cell & spatial", "group": "methods", "immune": "Cell states & tissue niches", "question": "Does proximity support a functional interaction?", "idea": "Single-cell, single-nucleus and spatial methods describe cell states and their anatomical arrangement. Human cardiac atlases provide reference populations and niches.", "heart": "These methods help formulate hypotheses about which immune, vascular and stromal cells may interact in the heart.", "evidence": "Dissociation, sampling and computational choices can alter the result. Proximity and inferred ligand–receptor pairing do not establish causality; developmental and adult tissues are distinct.", "reading": "single-cell", "related": [ "macrophages", "causal-evidence", "endothelium", "fibroblasts" ], "terms": "unicellulaire transcriptomique spatial omiques protéomique épigénomique scRNA snRNA données reproductibilité", "sources": [], "book": null, "subtopics": [ "unicellulaire", "transcriptomique", "spatial", "omiques", "protéomique", "épigénomique", "scRNA", "snRNA", "données", "reproductibilité" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "causal-evidence", "title": "Causal evidence", "group": "methods", "immune": "From mechanism to clinical effect", "question": "Which comparison would change the claim?", "idea": "Perturbation experiments and randomised clinical comparisons answer different causal questions. Each requires a defined intervention, comparison, population and outcome.", "heart": "Targeted IL-1β inhibition has been tested in selected patients with previous myocardial infarction and persistent inflammatory risk.", "evidence": "A positive trial supports its tested intervention and setting, not every anti-inflammatory strategy. Bias, transportability, adverse events and absolute effects remain part of interpretation.", "reading": "cantos", "related": [ "atherosclerosis", "interleukins", "single-cell-spatial", "therapeutic-targets" ], "terms": "causalité essais randomisés modèles animaux humains génétique Mendélienne biais preuve intervention", "sources": [], "book": null, "subtopics": [ "causalité", "essais", "randomisés", "modèles", "animaux", "humains", "génétique", "Mendélienne", "biais", "preuve", "intervention" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" }, { "id": "therapeutic-targets", "title": "Therapeutic translation", "group": "methods", "immune": "From target to patient", "question": "Does target engagement improve a patient-relevant outcome?", "idea": "Immune interventions differ in target, exposure, timing and consequences. Biomarker change and a reduction in clinical events are distinct outcomes.", "heart": "Trials of colchicine after acute myocardial infarction and in chronic coronary disease illustrate why the clinical setting remains part of the claim.", "evidence": "A neutral trial is not proof that immunity is irrelevant, and a positive trial does not validate all immune inhibition. Infection, toxicity and treatment interactions require separate assessment.", "reading": "clear", "related": [ "atherosclerosis", "causal-evidence", "tolerance" ], "terms": "thérapeutique colchicine canakinumab immunosuppression immunomodulation CAR-T anti IL-1 IL-6 IL-5 anti TNF JAK sécurité infection", "sources": [], "book": null, "subtopics": [ "thérapeutique", "colchicine", "canakinumab", "immunosuppression", "immunomodulation", "CAR-T", "anti", "IL-1", "IL-6", "IL-5", "anti", "TNF", "JAK", "sécurité", "infection" ], "evidenceLevel": "Selected reading; see design and limits", "lastReviewed": "2026-10-19" } ], "reviewed": "19 October 2026", "papers": { "sensing": { "title": "Antiviral innate immunity in myocarditis: mechanisms and emerging therapeutics", "journal": "Experimental & Molecular Medicine", "year": "2026", "kind": "Review", "url": "https://www.nature.com/articles/s12276-026-01822-z", "doi": "10.1038/s12276-026-01822-z", "access": "Open access · source licence applies", 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