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Circulation Dec 2022The "2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease" provides recommendations to guide clinicians in the diagnosis, genetic evaluation and...
2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines.
AIM
The "2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease" provides recommendations to guide clinicians in the diagnosis, genetic evaluation and family screening, medical therapy, endovascular and surgical treatment, and long-term surveillance of patients with aortic disease across its multiple clinical presentation subsets (ie, asymptomatic, stable symptomatic, and acute aortic syndromes).
METHODS
A comprehensive literature search was conducted from January 2021 to April 2021, encompassing studies, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Library, CINHL Complete, and other selected databases relevant to this guideline. Additional relevant studies, published through June 2022 during the guideline writing process, were also considered by the writing committee, where appropriate. Structure: Recommendations from previously published AHA/ACC guidelines on thoracic aortic disease, peripheral artery disease, and bicuspid aortic valve disease have been updated with new evidence to guide clinicians. In addition, new recommendations addressing comprehensive care for patients with aortic disease have been developed. There is added emphasis on the role of shared decision making, especially in the management of patients with aortic disease both before and during pregnancy. The is also an increased emphasis on the importance of institutional interventional volume and multidisciplinary aortic team expertise in the care of patients with aortic disease.
Topics: Female; Humans; Pregnancy; American Heart Association; Aortic Diseases; Bicuspid Aortic Valve Disease; Cardiology; Research Report; United States
PubMed: 36322642
DOI: 10.1161/CIR.0000000000001106 -
Heart (British Cardiac Society) Oct 2021Broadly defined, aortitis refers to inflammation of the aorta and incorporates both infectious and non-infectious aetiologies. As advanced imaging modalities are... (Review)
Review
Broadly defined, aortitis refers to inflammation of the aorta and incorporates both infectious and non-infectious aetiologies. As advanced imaging modalities are increasingly incorporated into clinical practice, the phenotypic spectrum associated with aortitis has widened. The primary large vessel vasculitides, giant cell arteritis and Takayasu arteritis, are the most common causes of non-infectious aortitis. Aortitis without systemic disease or involvement of other vascular territories is classified as clinically isolated aortitis. Periaortitis, where inflammation spreads beyond the aortic wall, is an important disease subset with a distinct group of aetiologies. Infectious aortitis can involve bacterial, viral or fungal pathogens and, while uncommon, can be devastating. Importantly, optimal management strategies and patient outcomes differ between aortitis subgroups highlighting the need for a thorough diagnostic workup. Monitoring disease activity over time is also challenging as normal inflammatory markers do not exclude significant vascular inflammation, particularly after starting treatment. Additional areas of unmet clinical need include clear disease classifications and improved short-term and long-term management strategies. Some of these calls are now being answered, particularly with regard to large vessel vasculitis where our understanding has advanced significantly in recent years. Work extrapolated from temporal artery histology has paved the way for targeted biological agents and, although glucocorticoids remain central to the management of non-infectious aortitis, these may allow reduced glucocorticoid reliance. Future work should seek to clarify disease definitions, improve diagnostic pathways and ultimately allow a more stratified approach to patient management.
Topics: Aorta; Aortitis; Humans; Tomography, X-Ray Computed
PubMed: 33593995
DOI: 10.1136/heartjnl-2020-318085 -
Circulation Research Jan 2023Giant cell arteritis is an autoimmune disease of medium and large arteries, characterized by granulomatous inflammation of the three-layered vessel wall that results in... (Review)
Review
Giant cell arteritis is an autoimmune disease of medium and large arteries, characterized by granulomatous inflammation of the three-layered vessel wall that results in vaso-occlusion, wall dissection, and aneurysm formation. The immunopathogenesis of giant cell arteritis is an accumulative process in which a prolonged asymptomatic period is followed by uncontrolled innate immunity, a breakdown in self-tolerance, the transition of autoimmunity from the periphery into the vessel wall and, eventually, the progressive evolution of vessel wall inflammation. Each of the steps in pathogenesis corresponds to specific immuno-phenotypes that provide mechanistic insights into how the immune system attacks and damages blood vessels. Clinically evident disease begins with inappropriate activation of myeloid cells triggering the release of hepatic acute phase proteins and inducing extravascular manifestations, such as muscle pains and stiffness diagnosed as polymyalgia rheumatica. Loss of self-tolerance in the adaptive immune system is linked to aberrant signaling in the NOTCH pathway, leading to expansion of NOTCH1CD4 T cells and the functional decline of NOTCH4 T regulatory cells (Checkpoint 1). A defect in the endothelial cell barrier of adventitial vasa vasorum networks marks Checkpoint 2; the invasion of monocytes, macrophages and T cells into the arterial wall. Due to the failure of the immuno-inhibitory PD-1 (programmed cell death protein 1)/PD-L1 (programmed cell death ligand 1) pathway, wall-infiltrating immune cells arrive in a permissive tissues microenvironment, where multiple T cell effector lineages thrive, shift toward high glycolytic activity, and support the development of tissue-damaging macrophages, including multinucleated giant cells (Checkpoint 3). Eventually, the vascular lesions are occupied by self-renewing T cells that provide autonomy to the disease process and limit the therapeutic effectiveness of currently used immunosuppressants. The multi-step process deviating protective to pathogenic immunity offers an array of interception points that provide opportunities for the prevention and therapeutic management of this devastating autoimmune disease.
Topics: Humans; Giant Cell Arteritis; Inflammation; Arteries; Immunity, Innate; Giant Cells
PubMed: 36656970
DOI: 10.1161/CIRCRESAHA.122.322128 -
Journal of the American College of... Dec 2022The "2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease" provides recommendations to guide clinicians in the diagnosis, genetic evaluation and...
2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease: A Report of the American Heart Association/American College of Cardiology Joint Committee on Clinical Practice Guidelines.
AIM
The "2022 ACC/AHA Guideline for the Diagnosis and Management of Aortic Disease" provides recommendations to guide clinicians in the diagnosis, genetic evaluation and family screening, medical therapy, endovascular and surgical treatment, and long-term surveillance of patients with aortic disease across its multiple clinical presentation subsets (ie, asymptomatic, stable symptomatic, and acute aortic syndromes).
METHODS
A comprehensive literature search was conducted from January 2021 to April 2021, encompassing studies, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Library, CINHL Complete, and other selected databases relevant to this guideline. Additional relevant studies, published through June 2022 during the guideline writing process, were also considered by the writing committee, where appropriate.
STRUCTURE
Recommendations from previously published AHA/ACC guidelines on thoracic aortic disease, peripheral artery disease, and bicuspid aortic valve disease have been updated with new evidence to guide clinicians. In addition, new recommendations addressing comprehensive care for patients with aortic disease have been developed. There is added emphasis on the role of shared decision making, especially in the management of patients with aortic disease both before and during pregnancy. The is also an increased emphasis on the importance of institutional interventional volume and multidisciplinary aortic team expertise in the care of patients with aortic disease.
Topics: United States; Humans; American Heart Association; Universities; Aortic Diseases
PubMed: 36334952
DOI: 10.1016/j.jacc.2022.08.004 -
Clinics in Chest Medicine Sep 2019Immunoglobulin G4 (IgG4)-Related Disease (IgG4-RD) can cause fibroinflammatory lesions in nearly any organ and lead to organ dysfunction and irreversible damage. In... (Review)
Review
Immunoglobulin G4 (IgG4)-Related Disease (IgG4-RD) can cause fibroinflammatory lesions in nearly any organ and lead to organ dysfunction and irreversible damage. In addition to frequent involvement of the salivary glands, lacrimal glands, and/or pancreas, IgG4-RD often affects the chest. Thoracic manifestations include lung nodules and consolidations, pleural thickening, aortitis, and lymphadenopathy. The diagnosis is made after careful clinicopathologic correlation because there is no single diagnostic test with excellent sensitivity or specificity. Biopsy of pulmonary lesions can be useful for distinguishing IgG4-RD from common mimickers. Immunosuppressive regimens, such as glucocorticoids and/or glucocorticoid-sparing agents, form the cornerstone of treatment.
Topics: Humans; Immunoglobulin G4-Related Disease; Lung
PubMed: 31376893
DOI: 10.1016/j.ccm.2019.05.005 -
Circulation Research Jan 2020Through localized delivery of rapamycin via a biomimetic drug delivery system, it is possible to reduce vascular inflammation and thus the progression of vascular...
RATIONALE
Through localized delivery of rapamycin via a biomimetic drug delivery system, it is possible to reduce vascular inflammation and thus the progression of vascular disease.
OBJECTIVE
Use biomimetic nanoparticles to deliver rapamycin to the vessel wall to reduce inflammation in an in vivo model of atherosclerosis after a short dosing schedule.
METHODS AND RESULTS
Biomimetic nanoparticles (leukosomes) were synthesized using membrane proteins purified from activated J774 macrophages. Rapamycin-loaded nanoparticles were characterized using dynamic light scattering and were found to have a diameter of 108±2.3 nm, a surface charge of -15.4±14.4 mV, and a polydispersity index of 0.11 +/ 0.2. For in vivo studies, ApoE mice were fed a high-fat diet for 12 weeks. Mice were injected with either PBS, free rapamycin (5 mg/kg), or rapamycin-loaded leukosomes (Leuko-Rapa; 5 mg/kg) once daily for 7 days. In mice treated with Leuko-Rapa, flow cytometry of disaggregated aortic tissue revealed fewer proliferating macrophages in the aorta (15.6±9.79 %) compared with untreated mice (30.2±13.34 %) and rapamycin alone (26.8±9.87 %). Decreased macrophage proliferation correlated with decreased levels of MCP (monocyte chemoattractant protein)-1 and IL (interleukin)-b1 in mice treated with Leuko-Rapa. Furthermore, Leuko-Rapa-treated mice also displayed significantly decreased MMP (matrix metalloproteinases) activity in the aorta (mean difference 2554±363.9, =9.95122×10). No significant changes in metabolic or inflammation markers observed in liver metabolic assays. Histological analysis showed improvements in lung morphology, with no alterations in heart, spleen, lung, or liver in Leuko-Rapa-treated mice.
CONCLUSIONS
We showed that our biomimetic nanoparticles showed a decrease in proliferating macrophage population that was accompanied by the reduction of key proinflammatory cytokines and changes in plaque morphology. This proof-of-concept showed that our platform was capable of suppressing macrophage proliferation within the aorta after a short dosing schedule (7 days) and with a favorable toxicity profile. This treatment could be a promising intervention for the acute stabilization of late-stage plaques.
Topics: 1,2-Dipalmitoylphosphatidylcholine; Animals; Aorta; Aortitis; Apolipoproteins E; Atherosclerosis; Biomimetics; C-Reactive Protein; Cryoelectron Microscopy; Cytokines; Drug Evaluation, Preclinical; Macrophage Activation; Macrophages; Mechanistic Target of Rapamycin Complex 1; Membrane Proteins; Mice; Mice, Inbred C57BL; Nanoparticles; Neovascularization, Pathologic; Organ Specificity; Phosphatidylcholines; Plaque, Atherosclerotic; Random Allocation; Sirolimus
PubMed: 31647755
DOI: 10.1161/CIRCRESAHA.119.315185 -
Science Translational Medicine Sep 2023Autoimmune vasculitis of the medium and large elastic arteries can cause blindness, stroke, aortic arch syndrome, and aortic aneurysm. The disease is often refractory to...
Autoimmune vasculitis of the medium and large elastic arteries can cause blindness, stroke, aortic arch syndrome, and aortic aneurysm. The disease is often refractory to immunosuppressive therapy and progresses over decades as smoldering aortitis. How the granulomatous infiltrates in the vessel wall are maintained and how tissue-infiltrating T cells and macrophages are replenished are unknown. Single-cell and whole-tissue transcriptomic studies of immune cell populations in vasculitic arteries identified a CD4 T cell population with stem cell-like features. CD4 T cells supplying the tissue-infiltrating and tissue-damaging effector T cells survived in tertiary lymphoid structures around adventitial vasa vasora, expressed the transcription factor T cell factor 1 (TCF1), had high proliferative potential, and gave rise to two effector populations, Eomesodermin (EOMES) cytotoxic T cells and B cell lymphoma 6 (BCL6) T follicular helper-like cells. TCF1CD4 T cells expressing the interleukin 7 receptor (IL-7R) sustained vasculitis in serial transplantation experiments. Thus, TCF1CD4 T cells function as disease stem cells and promote chronicity and autonomy of autoimmune tissue inflammation. Remission-inducing therapies will require targeting stem-like CD4 T cells instead of only effector T cells.
Topics: Humans; Tertiary Lymphoid Structures; Vasculitis; Arteries; Inflammation; CD4-Positive T-Lymphocytes
PubMed: 37672564
DOI: 10.1126/scitranslmed.adh0380 -
Ugeskrift For Laeger Aug 2023In this case report, we present a 70-year-old male who was brought to our hospital with signs of upper gastrointestinal bleeding. The patient was diagnosed with aortitis...
In this case report, we present a 70-year-old male who was brought to our hospital with signs of upper gastrointestinal bleeding. The patient was diagnosed with aortitis two and a half months prior. We suspected upper gastrointestinal bleeding, and the patient was taken to the operating room for an acute endoscopy, which showed blood in the oesophagus, ventricle, and duodenum, but no bleeding source. CT angiography showed erosion of aortic aneurism, at the site of known aortitis, with bleeding into the lung and pleura. The patient was transported to the nearest university hospital for thoracic endovascular repair and survived.
Topics: Male; Humans; Aged; Hematemesis; Hemoptysis; Aortitis; Gastrointestinal Hemorrhage; Aortic Aneurysm; Hospitals, University
PubMed: 37767877
DOI: No ID Found -
BMJ Case Reports Jan 2020A 72-year-old man was admitted with complaints of sudden-onset oppressive precordial pain radiating to the back for 1 hour. He had hypotension, peripheral cyanosis and...
A 72-year-old man was admitted with complaints of sudden-onset oppressive precordial pain radiating to the back for 1 hour. He had hypotension, peripheral cyanosis and cold extremities. An initial assessment was done and acute coronary syndrome was excluded. After the patient was admitted, he developed fever and increased levels of inflammatory markers. Data obtained from CT angiography and transoesophageal echocardiogram revealed diffuse parietal thickening of the arch and the descending thoracic aorta, as well as dilatation of the aortic root and the proximal ascending aorta. In addition, the test for was positive, and the patient was diagnosed with Lyme vasculitis of the thoracic aorta. He was treated with doxycycline for 3 weeks. Two months later, the patient exhibited a Stanford type A aortic dissection (clinically stable), which was treated by prosthesis replacement. The patient has remained asymptomatic for 1 year after the episode, performing his routine daily activities.
Topics: Aged; Aortic Dissection; Aortic Aneurysm, Thoracic; Aortitis; Blood Vessel Prosthesis Implantation; Borrelia burgdorferi; Diagnosis, Differential; Humans; Lyme Disease; Male
PubMed: 31941668
DOI: 10.1136/bcr-2019-231957