Correction of Antithrombogenic Activity of the Vascular Wall and Insulin Provision in Patients with Ischemic Heart Disease

2001 ◽  
Vol 82 (3) ◽  
pp. 164-166
Author(s):  
M. Yu. Altshuler ◽  
E. Yu. Sazhina
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Fibrinolytic Activity ◽  
Combined Treatment ◽  
Vascular Wall ◽  
Ischemic Heart ◽  
C Peptide ◽  
Low Level ◽  
Healthy Persons

The antithrombogenic activity of the vascular wall during probe, insulin provision during the glucosotolerant test are studied in 50 patients with ischemic heart disease and in 18 healthy persons. The change of antiagregational, anticoagulant, fibrinolytic activity of the endothelial cells of the vascular wall is revealed. The essential hyperinsulinemia duruing the whole glucosotolerant test at the low level of C-peptide showing the disorder of transforming proinsulin into insulin is noted. The use of ticlide is recommended in combined treatment of patients with ischemic heart disease

Markers of Vascular Wall Fibrosis Metalloproteinase-9 and Tissue Inhibitor of Metalloproteinases-1 in Patients with Ischemic Heart Disease with and without Concomitant Type-2 Diabetes Mellitus

Kardiologiia ◽  
2019 ◽  
Vol 59 (5) ◽  
pp. 61-66
Author(s):  
Y. N. Belenkov ◽  
E. V. Privalova ◽  
A. O. Iusupova ◽  
A. V. Zhito
Keyword(s):  
Diabetes Mellitus ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Vascular Wall ◽  
Ischemic Heart ◽  
Tissue Inhibitor Of Metalloproteinases ◽  
Tissue Inhibitor ◽  
Dm Type 2 ◽  
Metalloproteinase 9

The prevalence of ischemic heart disease (IHD) and diabetes mellitus type 2 (DM type 2) is permanently increasing both worldwide and in theRussian Federation. That is why studies of mechanisms of pathogenesis of both diseases is continuing for prevention of complications and mortality. DM type 2 contributes a lot to deterioration of IHD. One of pathogenetic features these two pathologies share is pronounced blood vessel wall fibrosis. In this review we present analysis of studies devoted to the determination of the role of metalloproteinase-9 and tissue inhibitor of metalloproteinases-1 indevelopment of vascular wall fibrosis.   

scholarly journals Dynamics of endothelian function in different treatment strategies in stable ischemic heart disease

2019 ◽  
Vol 11 (1) ◽  
pp. 5-12
Author(s):  
Sergey A. Sayganov ◽  
Anastasiia M. Kuzmina-Krutetskaia
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Ischemic Heart Disease ◽  
Peripheral Blood ◽  
Ischemic Heart ◽  
Circulating Endothelial Cells ◽  
Lipid Lowering ◽  
Stable Ischemic Heart Disease

Aim. To assess the dynamics of endothelial function by determining circulating endothelial cells in peripheral blood in patients with stable ischemic heart disease within various treatment approaches. Material and methods. The study involved 98 patients with stable ischemic heart disease and 30 patients in the control group without coronary atherosclerosis. Endothelial function was assessed by determining the number of circulating endothelial cells in peripheral blood using flow cytofluorimetry with antibodies to cell surface markers: CD146+CD45– at the baseline. Depending on the treatment tactics, the study participants were divided into 3 groups: the medicamental therapy group, the group of coronary stenting, and the group of coronary bypass surgery. After 3 months from the baseline, dinamics assessment of endothelial dysfunction was performed. Results. Endothelial dysfunction was observed in all patients with obstructive lesions of the coronary blood flow and associated with effort angina class and anatomical severity of coronary disease. Improvement of endothelial function was facilitated by lipid-lowering therapy. Revascularization by coronary stenting impaired endothelial function in three months after the intervention. Mycoardial revascularization by coronary bypass did not impair endothelial function. Conclusion. Examination of endothelial dysfunction by determining the number of circulating endothelial cells in peripheral blood can be used to assess the severity of endothelial dysfunction in patients with IHD receiving lipid-lowering therapy and undergoing surgical revascularization.

ISOLATION AND CHARACTERISTICS OF COLONY-FORMING ENDOTHELIAL CELLS FROM PERIPHERAL BLOOD IN PATIENTS WITH ISCHEMIC HEART DISEASE

Tsitologiya ◽  
2018 ◽  
Vol 60 (8) ◽  
pp. 598-608
Author(s):  
V. G. Matveeva ◽  
◽  
M. Yu. Khanova ◽  
E. A. Velikanova ◽  
L. V. Antonova ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Peripheral Blood ◽  
Ischemic Heart

Earlier Onset of Ischemia After Exposure to Low Level Carbon Monoxide in Patients With Ischemic Heart Disease

1987 ◽  
Vol 7 (7) ◽  
pp. 352
Author(s):  
Adams KF ◽  
Chatterjee B ◽  
Koch G ◽  
Price CJ ◽  
Goldstein G ◽  
...  
Keyword(s):  
Carbon Monoxide ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Ischemic Heart ◽  
Low Level

Increase in perfused boundary region of endothelial glycocalyx is associated with higher prevalence of ischemic heart disease and lesions of microcirculation and vascular wall

2018 ◽  
Vol 25 (4) ◽  
pp. e12454 ◽  
Author(s):  
Alexander Y. Gorshkov ◽  
Marina V. Klimushina ◽  
Sergei A. Boytsov ◽  
Alexander Y. Kots ◽  
Nadezhda G. Gumanova
Keyword(s):  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Vascular Wall ◽  
Boundary Region ◽  
Ischemic Heart ◽  
Endothelial Glycocalyx

scholarly journals Differentiation, Survival, and Function of Embryonic Stem Cell Derived Endothelial Cells for Ischemic Heart Disease

Circulation ◽  
2007 ◽  
Vol 116 (11_suppl) ◽  
pp. I-46-I-54 ◽  
Author(s):  
Z. Li ◽  
J. C. Wu ◽  
A. Y. Sheikh ◽  
D. Kraft ◽  
F. Cao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Stem Cell ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Embryonic Stem Cell ◽  
Embryonic Stem ◽  
Ischemic Heart ◽  
And Function

scholarly journals THE PARTICIPATION OF IMMUNE AND INFLAMMATORY MECHANISMSIN THE PATHOGENESIS OF CORONARY ATHEROSCLEROSIS

2015 ◽  
Vol 7 (4) ◽  
pp. 13-23 ◽  
Author(s):  
V I Mazurov ◽  
S V Stolov ◽  
I B Belyaeva ◽  
E A Trofimov
Keyword(s):  
Rheumatoid Arthritis ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Coronary Atherosclerosis ◽  
Vascular Wall ◽  
Ischemic Heart ◽  
Additional Increase ◽  
Coronary Insufficiency ◽  
Immune Mediated ◽  
Autoimmune Pathology

It was revealed that in development of a coronary atherosclerosis, participate the immune-mediated mechanisms. In blood of patients with coronary atherosclerosis the maintenance of the basic classes cytokines (IL-1 β, IL-2, IL-6, IL-8, TNF-a) were increased. Development of acute coronary insufficiency is accompanied by additional increase of levels of the data cytokines. The accessory of the cytokine activity to a coronary atherosclerosis was confirmed at studying the maintenance mRNA cytokines in a vascular wall. Thus in a zone atheromatous (aorta) it was synthesized mainly mRNA IL-2, while in a zone lipomatosis (a beam radial artery) it is formed nonspecific immune reaction with development of the mRNA IL-1 and IL-6. For patients with rheumatoid arthritis typically more active defeat of a coronary arteries, in comparison with healthy persons. Chronic immune-mediated process in frameworks of the autoimmune pathology can serve a trigger for accelerated development ischemic heart disease. The General immune-inflammatory mechanisms which participate in pathogenesis of the ischemic heart disease and rheumatoid arthritis, allow to spend the certain parallels between atherosclerotic process and autoimmune pathology.

scholarly journals Ranolazine may exert its beneficial effects by increasing myocardial adenosine levels

2020 ◽  
Vol 318 (1) ◽  
pp. H189-H202 ◽  
Author(s):  
D. Elizabeth Le ◽  
Catherine M. Davis ◽  
Kevin Wei ◽  
Yan Zhao ◽  
Zhiping Cao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Heart Disease ◽  
Ischemic Heart Disease ◽  
Specific Activity ◽  
Venous Blood ◽  
Dobutamine Stress ◽  
Left Ventricular ◽  
Ischemic Heart ◽  
Metabolic Enzyme ◽  
Beneficial Effects

We hypothesized that ranolazine-induced adenosine release is responsible for its beneficial effects in ischemic heart disease. Sixteen open-chest anesthetized dogs with noncritical coronary stenosis were studied at rest, during dobutamine stress, and during dobutamine stress with ranolazine. Six additional dogs without stenosis were studied only at rest. Regional myocardial function and perfusion were assessed. Coronary venous blood was drawn. Murine endothelial cells and cardiomyocytes were incubated with ranolazine and adenosine metabolic enzyme inhibitors, and adenosine levels were measured. Cardiomyocytes were also exposed to dobutamine and dobutamine with ranolazine. Modeling was employed to determine whether ranolazine can bind to an enzyme that alters adenosine stores. Ranolazine was associated with increased adenosine levels in the absence (21.7 ± 3.0 vs. 9.4 ± 2.1 ng/mL, P < 0.05) and presence of ischemia (43.1 ± 13.2 vs. 23.4 ± 5.3 ng/mL, P < 0.05). Left ventricular end-systolic wall stress decreased (49.85 ± 4.68 vs. 57.42 ± 3.73 dyn/cm2, P < 0.05) and endocardial-to-epicardial myocardial blood flow ratio tended to normalize (0.89 ± 0.08 vs. 0.76 ± 0.10, P = nonsignificant). Adenosine levels increased in cardiac endothelial cells and cardiomyocytes when incubated with ranolazine that was reversed when cytosolic-5′-nucleotidase (cN-II) was inhibited. Point mutation of cN-II aborted an increase in its specific activity by ranolazine. Similarly, adenosine levels did not increase when cardiomyocytes were incubated with dobutamine. Modeling demonstrated plausible binding of ranolazine to cN-II with a docking energy of −11.7 kcal/mol. We conclude that the anti-adrenergic and cardioprotective effects of ranolazine-induced increase in tissue adenosine levels, likely mediated by increasing cN-II activity, may contribute to its beneficial effects in ischemic heart disease. NEW & NOTEWORTHY Ranolazine is a drug used for treatment of angina pectoris in patients with ischemic heart disease. We discovered a novel mechanism by which this drug may exhibit its beneficial effects. It increases coronary venous levels of adenosine both at rest and during dobutamine-induced myocardial ischemia. Ranolazine also increases adenosine levels in endothelial cells and cardiomyocytes in vitro, by principally increasing activity of the enzyme cytosolic-5′-nucleotidase. Adenosine has well-known myocardial protective and anti-adrenergic properties that may explain, in part, ranolazine’s beneficial effect in ischemic heart disease.

Myocardial infarction triggers Inflammatory deterioration of vascular niche by accelerating loss of a specific vessel subtype in bone

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Hoffmann ◽  
G Luxan ◽  
W.T Abplanalp ◽  
T Rasper ◽  
A.M Fischer ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Endothelial Cells ◽  
Heart Disease ◽  
Chronic Heart Failure ◽  
Ischemic Heart Disease ◽  
Ischemic Heart ◽  
Vessel Length ◽  
Vascular Niche ◽  
The Impact

Abstract Introduction The interface between heart and bone emerges as a key trigger of post-infarction inflammation and progression of chronic heart failure (CHF). However, our knowledge on the underlying mechanisms of this interaction is incomplete. Bone vasculature, specifically so-called H-type (Endomucinhigh) endothelial cells (EC), plays a crucial role in maintenance of the bone integrity and regulation of hematopoietic stem cells (HSC). While previous studies in mice showed the reduction of H-type vessels by aging, the impact of ischemic heart disease is unclear. Therefore, we aimed to investigate the effects of myocardial infarction (MI) and chronic heart failure on the vascular bone cell composition in mice and humans. Methods and results Flow cytometric analysis of harvested bones at the different timepoints after MI induction in mice revealed a gradual loss of H-type endothelial cells in the time-course of developing chronic heart failure (P&lt;0.05 at day 7 and 14 vs. control; P&lt;0.0001 at day 28 vs. control). This results were confirmed in immunostainings of tibia sections showing a significant decrease of H-type vessel length after MI (p&lt;0.05 at day 14 and 28, accordingly). The loss of type-H endothelium was accompanied by a significant expansion of long-term HSC in the bone (P=0.0005 at day 28 post MI vs. control). Importantly, type H ECs were also significantly reduced in the bone of ischemic post-infarct HF patients (n=16) compared with control subjects (n=8; P=0.0003). To gain insights into the mechanisms underlying the changes in the vascular niche, we performed single cells RNA sequencing of human BM ECs. These studies confirmed the decrease in Emcnexpressing ECs in ischemic HF patients, which was accompanied by significantly increased expression of inflammatory genes, including IL1b (P&lt;0.0001). Inflammatory EC phenotypes and IL1b expression in HF could be further confirmed at protein level using cytospin immunostainings. Murine studies further revealed an early induction IL-1b specifically in H-type vessels already at day 1 after MI induction, which preceded the loss of H-type endothelium within the following 4 weeks. By inhibiting IL-1b production using a specific Nlrp3 inflammasome inhibitor (MCC950) we could observe a partial restoration of H-type EC frequencies (P=0.033) and a significant increase in H-type vessel length (p=0.035) at day 28 day after MI. Conclusions Our data show for the first time an impact of myocardial infarction and chronic heart failure on the bone marrow vasculature. These changes seem to be strongly associated with inflammatory response in H-type vessels, which precedes its loss after MI. Specifically, the induction of the inflammatory cytokine IL1b may contribute to the disturbed phenotype. This suggest that inhibition of IL1b (e.g. by canakinumab) be used as a novel strategy to prevent or reverse the deterioration of the vascular bone function in ischemic heart disease. Funding Acknowledgement Type of funding source: None

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