scholarly journals Neurodegeneration and microvascular dysfunction

2022 ◽  
Author(s):  
Frank Cornelis Theodorus van der Heide
Keyword(s):  
Microvascular Dysfunction

Clinical and Morphological Features of Myocardial Damage and the Course of Fulminant Myocarditis on the Background of СOVID-19, Diagnosis and Treatment Tactics

2020 ◽  
Vol 75 (5S) ◽  
pp. 414-425
Author(s):  
Olga S. Oynotkinova ◽  
Evgenii L. Nikonov ◽  
Oleg V. Zayratyants ◽  
Elena V. Rzhevskaya ◽  
Evgenii V. Krukov ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Myocardial Damage ◽  
Heart Rhythm ◽  
Microvascular Dysfunction ◽  
Symptomatic Treatment ◽  
Clinical Situation ◽  
Diagnosis And Treatment ◽  
Screening Tests ◽  
Fulminant Myocarditis ◽  
Heart Rhythm Disorders

In a review article based on my own clinical experience of managing patients with acute myocardial injury and fulminant myocarditis, taking into account expert recommendations on the clinical treatment of myocardial damage associated with novel coronavirus infection a National clinical geriatric medical research center, division of cardiovascular diseases, the Chinese geriatrics society, Department of cardiology, Beijing Medical Association and European clinics discusses the pathogenesis, diagnosis and treatment of myocardial damage and FM patients, infected with SARS-CoV-2 in the context of the COVID-19 pandemic. Clinical features and diagnostic criteria are presented, including screening tests of markers of myocardial damage in the form of a highly sensitive troponin test, a natriuretic peptide. The article discusses in detail the pathogenesis and mechanisms of myocardial damage, including immune mechanisms, cytokine storm, systemic inflammation with macro- and microvascular dysfunction and the development of myocardial dysfunction with acute heart failure, hypotension, cardiogenic shock and/or life-threatening heart rhythm disorders caused by hypoxia and metabolic disorders at the cellular level. Features of the clinical course of fulminant myocarditis in infected patients (SARS-CoV-2) in the conditions of the COVID-19 pandemic are presented. For the first time, a detailed histo-morphological analysis of pathological myocardial injuries and complications is presented on the basis of unique autopsy material on post-mortem diagnostics of various pathoanatomic autopsies of those who died from COVID-19 in Moscow. Based on the clinical, functional and morphological material, the Protocol of etiopathogenetic treatment is presented. The basis of standard therapy is considered antiviral drugs, immunoglobulin G, the use of monoclonal antibodies to interleukin-6, anticoagulants, glucocorticoids, depending on the clinical situation, cardioprotectors and symptomatic treatment are recommended to maintain the heart, which in combination can achieve a certain clinical effectiveness. As adjuvant cardioprotective targeted therapy, the sodium salt of phosphocreatine is considered in order to preserve the myocardium, maintain its contractility and vital activity.

Coronary microvascular dysfunction

2020 ◽  
Vol 68 (2) ◽  
Author(s):  
Vincenzo Sucato ◽  
Giuseppina Novo ◽  
Antonino Saladino ◽  
Salvatore Evola ◽  
Alfredo R. Galassi
Keyword(s):  
Microvascular Dysfunction ◽  
Coronary Microvascular Dysfunction

Microvascular (dys)Function in Stable Coronary Artery Disease: Cross Talk with Epicardial Segments

2018 ◽  
Vol 24 (25) ◽  
pp. 2900-2905
Author(s):  
Lucian Calmac ◽  
Vlad Bataila ◽  
Bogdan Dragoescu ◽  
Cosmin Mihai ◽  
Alexandru Scafa-Udriste ◽  
...  
Keyword(s):  
Coronary Flow ◽  
Stable Coronary Artery Disease ◽  
Microvascular Dysfunction ◽  
Complex Interaction ◽  
Diagnostic Tools ◽  
Pathological State ◽  
Hemodynamic Parameters ◽  
Artery Disease ◽  
Epicardial Stenosis ◽  
Current Guidelines

Myocardial ischemia is the consequence of an unbalance between coronary flow that can be achieved and myocardial metabolic needs. Pathological state of both epicardial and intramyocardial vessels may be responsible for inducing ischemia. However, revascularization decision should be based on the severity of each epicardial lesion that is evaluated. There are different diagnostic tools that may help for the evaluation of each compartment which is based on the measurement of coronary hemodynamics. Pressure-derived indices are recommended by current guidelines for evaluation of epicardial stenosis significance. We assess the complex interaction between hemodynamic parameters in order to understand how different parameters are influenced in the settings of microvascular dysfunction.

scholarly journals CD40/CD40L contributes to hypercholesterolemia-induced microvascular inflammation

2009 ◽  
Vol 296 (3) ◽  
pp. H689-H697 ◽  
Author(s):  
Karen Y. Stokes ◽  
LeShanna Calahan ◽  
Candiss M. Hamric ◽  
Janice M. Russell ◽  
D. Neil Granger
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
T Cell ◽  
Blood Cell ◽  
Cell Function ◽  
Inflammatory Responses ◽  
Microvascular Dysfunction ◽  
Cd40 Ligand ◽  
Scid Mice ◽  
Endothelial Cell Function

Hypercholesterolemia is associated with phenotypic changes in endothelial cell function that lead to a proinflammatory and prothrombogenic state in different segments of the microvasculature. CD40 ligand (CD40L) and its receptor CD40 are ubiquitously expressed and mediate inflammatory responses and platelet activation. The objective of this study was to determine whether CD40/CD40L, in particular T-cell CD40L, contributes to microvascular dysfunction induced by hypercholesterolemia. Intravital microscopy was used to quantify blood cell adhesion in cremasteric postcapillary venules, endothelium-dependent vasodilation responses in arterioles, and microvascular oxidative stress in wild-type (WT) C57BL/6, CD40-deficient (−/−), CD40L−/−, or severe combined immune deficient (SCID) mice placed on a normal (ND) or high-cholesterol (HC) diet for 2 wk. WT-HC mice exhibited an exaggerated leukocyte and platelet recruitment in venules and impaired vasodilation responses in arterioles compared with ND counterparts. A deficiency of CD40, CD40L, or lymphocytes attenuated these responses to HC. The HC phenotype was rescued in CD40L−/− and SCID mice by a transfer of WT T cells. Bone marrow chimeras revealed roles for both vascular- and blood cell-derived CD40 and CD40L in the HC-induced vascular responses. Hypercholesterolemia induced an oxidative stress in both arterioles and venules of WT mice, which was abrogated by either CD40 or CD40L deficiency. The transfer of WT T cells into CD40L−/− mice restored the oxidative stress. These results implicate CD40/CD40L interactions between circulating cells and the vascular wall in both the arteriolar and venular dysfunction elicited by hypercholesterolemia and identify T-cell-associated CD40L as a key mediator of these responses.

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