Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study evaluates the effect of balanced ultrafiltration, modified ultrafiltration, and balanced ultrafiltration with modified ultrafiltration on inflammatory mediators in children's open-heart surgery. Eighty children with congenital heart disease were randomly divided into four groups: control group (C group); balanced ultrafiltration group (BUF group); modified ultrafiltration group (MUF group); and balanced ultrafiltration with modified ultrafiltration group (B+M group). Clinical data of these groups were similar. Tumor necrosis factor (TNF), interleukin-8(IL-8), and E-selectin were measured at the beginning of cardiopulmonary bypass (CPB), 30 min later, at the cessation of CPB, at the cessation of MUF (MUF group and B+M group), and 2 hours postoperatively. During CPB, the concentrations of TNF, IL-8, and E-selectin increased significantly in C and MUF groups and did not change significantly in BUF and B+M groups. In the period of MUF, TNF and IL-8 increased; whereas, E-selectin did not change. The study shows that ultrafiltration can filter out the inflammatory mediators, but only BUF can decrease the concentrations of them. Moreover, MUF only can concentrate blood. Combining both techniques has both effects, but the effect of BUF was offset by MUF.
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PMID:Balanced ultrafiltration, modified ultrafiltration, and balanced ultrafiltration with modified ultrafiltration in pediatric cardiopulmonary bypass. 1180 33

The targeting and recruitment of inflammatory cells to vascular endothelium in ischaemic heart diseases is mediated by Intercellular Adhesion Molecule-1 (ICAM-1), Vascular Cell Adhesion Molecule (VCAM-1) and E-selectin and proinflammatory cytokines. Accumulation of mononuclear cells to the endothelium is one of the earliest events in the formation of an atherosclerotic lesion. The aim of this study was to estimate the serum concentrations of soluble intercellular adhesion molecule-1 (sICAM-1), vascular adhesion molecule-1 (sVCAM-1), selectin E (sE-selectin) in patients with acute myocardial infarction (Group 1--n = 18 patients: 3 women and 15 men, mean age--60 years), unstable angina pectoris (Grupa 2--n = 31 patients: 8 women and 23 men, mean age--62 years and stable heart disease (Grupa 3--n = 25 patients: 14 women and 11 men, mean age--61 years. The control group (Group 4--n = 20) consist of twenty healthy patient without coronary risk factors. ELISA method was used to determine the concentration of adhesion molecules of acute inflammation parameters, and traditional risk factors with using standard methods. The serum levels of sICAM-1, sVCAM-1 were markedly elevated in patients with acute myocardial infarction, unstable angina pectoris and stable heart disease compared to control group (p < 0.001, p < 0.004, p < 0.0002 for sICAM-1, p < 0.007, p < 0.003, p < 0.004 for sVCAM-1). Serum concentration of sE-selectin in three groups was similar, we did not find statistically significant differences between them. Furthermore, serum concentrations of adhesion molecules correlated with serum concentrations of acute inflammation parameters and traditional coronary risk factor for example BMI, systolic and diastolic blood pressure and lipid concentration. Additional serum concentration of sICAM-1 was elevated in smoking patients compared to non-smokers. We conclude that evaluation of adhesion molecules (sICAM-1 and sVCAM-1 in patients with heart diseases can be unspecific markers of activity of inflammatory process in coronary vascular endothelium.
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PMID:[Assessment of serum levels of adhesion molecules (sICAM-1, sVCAM-1, sE-selectin) in stable and unstable angina and acute myocardial infarction]. 1475 Apr 16

Rho family GTPases are key signal transducers that regulate cell adhesion and migration and a variety of other cellular responses, including changes in gene expression. In this review, we discuss how Rho GTPases regulate signaling by endothelial cell receptors involved in leukocyte extravasation. First, Rho GTPases affect the expression of some leukocyte adhesion molecules on endothelial cells, such as intracellular adhesion molecule-1 and E-selectin, that can be induced by proinflammatory mediators, hypoxia, or shear stress. Second, Rho GTPases are activated by engagement of several leukocyte adhesion receptors and contribute to both early morphological changes and subsequent alterations in gene expression. Rho GTPases are therefore candidate targets for inhibiting leukocyte transendothelial migration in heart disease and chronic inflammatory disorders.
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PMID:Rho GTPases and leukocyte adhesion receptor expression and function in endothelial cells. 1657 16

Pulmonary hypertension (PH), a risk factor for mortality in sickle cell disease (SCD), has pathologic features of both pulmonary arterial hypertension (PAH) and PH related to left-sided heart disease (LHD) suggesting a link between these two entities. We hypothesized that both are characterized by endothelial dysfunction and increased adhesion molecule expression. SCD patients and normal volunteers underwent a screening questionnaire, echocardiogram, and blood donation for preparation of platelet-poor plasma. PAH was defined as a tricuspid regurgitant jet (TRJ) velocity > or =2.5 m/sec and/or the presence of isolated right ventricular hypertrophy or decreased systolic function. LHD was defined as either left-sided systolic/diastolic dysfunction or significant valvular disease. Plasma vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), P- and E-selectin, nitric oxide (NO(x)), erythropoietin, and vascular endothelial growth factor (VEGF) levels were assayed by enzyme-linked immunoassay. Forty-three percent of sickle cell anemia (HbSS) and 28% of hemoglobin SC disease (HbSC) disease patients had PAH. Additionally, 10-15% of SCD patients had LHD. VCAM-1 levels were significantly increased in HbSS patients compared with HbSC patients and normal volunteers. VCAM-1 and P-selectin levels correlated positively with TRJ velocity in HbSS patients (r = 0.45, P = 0.03, r = 0.2, P = 0.05, respectively). ICAM-1, E-selectin, NO(x), erythropoietin, and VEGF levels were similar across subject groups. PH is common in SCD and, at times, due to LHD. Increased VCAM-1 and P-selectin expression was associated with TRJ elevation regardless of etiology suggesting a similar effect on endothelial gene expression and possibly providing a pathologic link between PAH and PH related to LHD in SCD.
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PMID:Pulmonary arterial hypertension and left-sided heart disease in sickle cell disease: clinical characteristics and association with soluble adhesion molecule expression. 1838 29

The reversibility of pulmonary arterial hypertension (PAH) in children with congenital heart disease (CHD) is strongly associated with the degree of intimal proliferation, vessel narrowing, and number of circulating endothelial cells (CECs). Circulating endothelial cells may arise from either endothelial damage or accelerated turnover during vessel remodeling, but nothing is known about endothelial microparticles (EMPs) and other biomarkers reflecting endothelial alterations. This study aimed to document endothelial markers further according to the irreversibility of PAH secondary to CHD. The study investigated soluble markers of endothelial damage or activation (thrombomodulin, soluble endothelial protein C receptor, and soluble E-selectin), inflammation (interleukin-6), and angiogenic cytokine levels [vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)] in 26 patients with CHD, 16 with reversible PAH (median age, 2 years) and 10 with irreversible PAH (median age, 9 years). Endothelial activation/apoptosis was evaluated by measuring EMP levels. Plasma procoagulant activity also was measured. The results show that the levels of soluble markers indicating endothelial activation were not predictors of PAH irreversibility. Lower levels of PlGF were observed in reversible compared with irreversible PAH but were not associated with the CEC level, the mean pulmonary artery pressure (mPAP), or age. No significant difference in procoagulant activity or EMP level was found between irreversible and reversible PAH. Among a large panel of biomarkers reflecting endothelial activation, regeneration, and injury, the high CEC levels previously described proved to be the only marker allowing discrimination between reversible and irreversible PAH secondary to CHD.
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PMID:Comparison of endothelial biomarkers according to reversibility of pulmonary hypertension secondary to congenital heart disease. 2019 55