Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to evaluate the influence of ACE in various biological media (blood, sputum, and lung tissue) on the clinical manifestations and morphofunctional cardiac variables in 137 patients with chronic obstructive pulmonary disease (COPD), of whom 17% had mild, 70% had medium, and 13% had severe degree of the disease according to Federal program, 1999. Seventy percent of the patients had stage II pulmonary hypertension according to Paleyev, 1986, while the number of patients with stage I and III was 14 and 16%, respectively. Circulatory insufficiency was mild (NYHA I to II) in 124 patients, and medium (NYHA III) in 13 patients only. The results of the study demonstrate that COPD exacerbation is accompanied by an increase in ACE activity, mostly in the lung tissue, induced sputum (IS), and, to a lesser degree, in blood serum; ISA CE activity is almost the same as that in the lung tissue. The study established a direct correlation between IS ACE activity and the level of C-reactive protein, an inflammatory process activity marker, and a reverse correlation between IS ACE activity and respiratory function variables, the latter characterizing bronchial obstruction. The study shows a strong direct correlation between IS ACE activity and the degree of right ventricular (RV) and left ventricular (LV) hypertrophy, as well as diastolic function disturbances according to RV isovolumetric relaxation time and LV early diastolic filling delay time. There is a strong reverse correlation between IS ACE activity and the disbalance of the ratio of blood flow velocities during early and late diastolic ventricular filling. The study found no significant correlations between ACE activity and the variables of ventricular systolic function. The study demonstrates a significant role of ACE activity changes in the progression of obstruction, inflammation, and myocardial remodeling.
...
PMID:[Angiotensin converting enzyme activity in the clinical course and forming of cor pulmonale in patients with chronic obstructive pulmonary diseases]. 1675 52

C-reactive protein (CRP) plays a role in the pathogenesis of cardiovascular disease. It is a marker and predictor of cardiovascular disease. CRP possesses numerous cardiovascular effects (clotting, generation of oxygen radicals, increase in the expression of adhesion molecules and plasminogen activator inhibitor-1, plaque destabilization) that could result in cardiovascular disease. This review describes the effects of various cardiovascular drugs on the levels of CRP in health and disease. Cyclooxygenase inhibitors (aspirin, rofecoxib, celecoxib), platelet aggregation inhibitors (clopidogrel, abciximab), lipid lowering agents (statins, ezetimibe, fenofibrate, niacin, diets), beta-adrenoreceptor antagonists and antioxidants (vitamin E), as well as angiotensin converting enzyme (ACE) inhibitors (ramipril, captopril, fosinopril), reduce serum levels of CRP; while enalapril and trandolapril have not been shown to have the same effect. Angiotensin receptor blockers (ARBs) (valsartan, irbesartan, olmesartan, telmisartan) markedly reduce serum levels of CRP. The findings with other ARBs (losartan and candesartan) were inconsistent. Antidiabetic agents (rosiglitazone and pioglitazone) reduce CRP levels, while insulin is ineffective. Calcium channel antagonists have variable effects on CRP levels. Hydrochlorothiazide and oral estrogen do not affect CRP. The CRP-lowering effect of statins is more pronounced than their lipid lowering effect and is not dependent on their hypolipemic activity. The effect of atorvastatin on CRP seems to be dose-dependent. CRP-lowering effect of statins is likely to contribute to the favorable outcome of statin therapy. The data suggest that lipid lowering agents, ACE inhibitors, ARBs, antidiabetic agents, antiinflammatory and antiplatelet agents, vitamin E, and beta-adrenoreceptor antagonists lower serum or plasma levels of CRP, while vitamin C, oral estrogen and hydrochlorothiazide do not affect CRP levels.
...
PMID:C-reactive protein (CRP)-lowering agents. 1693 32

Coronary artery ectasia (CAE) is well-recognized, angiographic finding of abnormal coronary dilatation, and detected in 0.3-5.3% of angiographic studies. The gold standard for diagnosis this type of aneurysm is coronary angiography, which provides information about the size, sample, location and number of aneurysms. Despite growing prevalence in recent years, controversy still exists as to the pathogenetic mechanisms that underlie this entity. An increased incidence of CAE has been reported in several disorders. Examples include atherosclerotic vascular disease, heterozygous familial hypercholesterolemia, usage of substances including herbicide spray, acetylcholinesterase inhibitors and nitrates, previous arterial balloon angioplasty, polyarteritis nodosa and Kawasaki syndrome. In addition, possible factors contributing to CAE are imbalance between matrix metalloproteinase and tissue inhibitor of metalloproteinase, angiotensin converting enzyme genotype, elevated homocysteine levels, cocaine user, smoking, vascular trauma, nitrate use and diabetes. Emerging investigations have pinpointed inflammation as a central process in all stages of atherosclerosis. This inflammatory process culminates in acute thrombotic complications and clinical events, which is involved in different clinical settings of atherosclerotic diseases. Recent data have also showed that CAE is associated with inflammatory response presented as elevated inflammatory cytokines and C-reactive protein. Accordingly, more complete understanding of the pro- and anti-inflammatory circuits that operate during CAE in particular may foster the development of novel therapeutic approaches.
...
PMID:Is any link between inflammation and coronary artery ectasia? 1722 19

The purpose of the study was to evaluate the clinico-diagnostic importance of the degree of inflammation and endothelial dysfunction in patients with chronic heart failure (CHF) receiving either standard therapy including ACE inhibitors or the same therapy plus aspirin. One hundred twenty CHF patients aged 45 to 74 were examined. The patients were studied clinically; laboratory tests included measurement of the cerum levels of cytokines with solid-phase immune enzyme assay and serum C-reactive protein (CRP) levels with photometric turbidimetric technique; the vasoregulating function and antithrombogenic activity of vascular wall were evaluated. Improvement in the clinical condition of II to III functional class patients receiving standard therapy was associated with a decrease in pro-inflammatory cytokine and CRP serum levels, as well as a tendency towards improvement in the vasoregulating function and a decrease in the antithrombogenic endothelial activity, mostly due to vascular wall fibrinolytic activity. Standard therapy combined with aspirin led to less prominent changes in the patients' conditions; a simultaneous decrease in the levels of all the cytokines under study was not noted; the vasoregulating activity of the vascular endothelium decreased. The data obtained may be used as additional criteria to objectively evaluate the severity of the condition of CHF patients and to control the effectiveness of the therapy.
...
PMID:[The degree of inflammation and endothelial dysfunction in treatment of chronic heart failure in patients with coronary artery disease]. 1729 77

Myocardial ischemia provoked in the laboratory during mental stress (MSI) in patients with stable coronary artery disease (CAD) predicts subsequent clinical events. The pathophysiology of MSI differs from that of exercise ischemia, and the mechanisms tying MSI to poor prognosis are not known. C-reactive protein (CRP) is a risk marker for cardiovascular events in patients with CAD, but little is known regarding the relationship of CRP to MSI. The purpose of this study was to examine the association of CRP to risk of MSI in CAD patients. Eighty-three patients with stable CAD underwent simultaneous single-photon emission computed tomography (SPECT) imaging with technetium-99m tetrofosmin myocardial perfusion imaging (MPI) and transthoracic echocardiography (TTE), at rest and during MS induced by laboratory mental stress. Serum CRP levels were measured 24 h after MS. MSI was defined by the presence of a new perfusion defect on SPECT and/or new regional wall motion abnormality on TTE during MS. Of the 83 patients, 30 (36%) developed MSI. There was no difference in gender, sex, BMI, histories of diabetes, hypertension, smoking, lipid profile, medications used (including statins, beta-blockers, ACE inhibitors, and aspirin), or hemodynamic response during MS between those with and without MSI. In univariate logistic regression analysis, each unit (1 mg/L) increase in CRP level was associated with 20% higher risk of MSI (OR 1.2, 95% CI 1.01-1.39, P=.04). This relationship remained in multivariate models. These data suggest that levels of CRP may be a risk marker for MSI in patients with CAD.
...
PMID:C-reactive protein and vulnerability to mental stress-induced myocardial ischemia. 1738 Jan 91

Elevated C-reactive protein (CRP) levels have been associated with increased cardiovascular risk in hypertensive adults. The aim of this study was to determine whether plasma CRP level is more predictive of left ventricular hypertrophy (LVH) than is ambulatory blood pressure (BP) in hypertensive children. Baseline and 12-month follow-up measures of BP, body mass index (BMI), low-density lipoprotein/high density lipoprotein cholesterol, left ventricular mass (LVM), and CRP data collected from 48 newly diagnosed, untreated hypertensive children were analyzed. CRP was measured by a highly sensitive nephelometric method. Left ventricular mass index (LVMI) was calculated as LVM/height2.7, and LVH was defined as LVMI>38.6 g/m2.7 being the cut-point for the 95th percentile found in healthy children. Average systolic BP (SBP), diastolic BP (DBP), SBP index, and DBP index were calculated. All patients received hydrochlorothiazide therapy in combination with angiotensin converting enzyme inhibitor treatment. Five patients also had angiotensin receptor blocker therapy to reach the target BP (<95th percentile corrected for age and gender). In a multiple regression analysis, LMVI was correlated with CRP, BMI, SBP, and SBP index. CRP alone explained 77% of the variance of LVMI, whereas BMI, SBP, and SBP index explained only 1.3, 0.3, and 0.4% of the variance, respectively. CRP was also the most significant correlate of follow-up LVH. In conclusion, elevated CRP level is significantly associated with LVH in children with essential hypertension. BP reduction with renin-angiotensin system blocker and hydrochlorothiazide therapy reduces LVH while lowering CRP level.
...
PMID:C-reactive protein and incident left ventricular hypertrophy in essential hypertension. 1756 29

High tissue matrix metalloproteinase (MMP) activity has been reported to be associated with atherosclerosis and plaque rupture. The aim of this study was to elucidate the diagnostic value of serum MMP-1 in carotid stenosis and its dynamic change after stenting. We measured high-sensitivity C-reactive protein (hs-CRP) and MMP-1 in 37 patients with carotid stenosis (>or= 50%) and 84 controls. In 30 patients who underwent stenting, MMP-1 and hs-CRP were assessed immediately after stenting. We found that patients with carotid stenosis exhibited significantly higher MMP-1 compared with controls, but there was no difference in hs-CRP. Moreover, MMP-1 was elevated immediately after stenting. In multivariate analyses, MMP-1 was negatively correlated with statin and angiotensin converting enzyme inhibitor/angiotensin-II receptor blocker use in controls. In conclusion, higher levels and rapid surge after stenting in patients with carotid stenosis indicate that MMP-1 is an important composition of plaques, and suggest its potential role in the assessment of plaque burden and stability of carotid stenosis.
...
PMID:High serum level of matrix metalloproteinase-1 and its rapid surge after intervention in patients with significant carotid atherosclerosis. 1821 85

Current thinking supports the notion that several inflammatory proteins intervene with endothelium and haemostatic factors leading to plaque formation and rupture. Of these, C-reactive protein (CRP), monocyte/macrophage colony-stimulating factor (MCSF) and interleukin-6 (IL-6) promote atherogenesis by inducing monocyte-macrophage activation, foam cell formation, platelet activation, tissue factor expression, release of other procoagulant cytokines or downregulation of atheroprotective cytokines such as interleukin 10 and transforming growth factor b-1 (TGFb-1). CRP, MSCF and IL-6 are interrelated and have been found in increased blood concentrations in CAD. Increased levels of CRP and IL-6 predict a higher cardiovascular event rate in the general population and in addition to high MCSF or low TGFb-1 predict adverse outcome in CAD patients independently of traditional risk factors. Moreover, in CAD patients, the predictive value of MCSF is additive and beyond that of CRP suggesting the need of a "multimarker approach" in assessing cardiovascular risk. Accumulating evidence supports the utility of non-invasive markers of subclinical atherosclerosis, namely carotid intimal media thickness, flow mediated dilatation of the brachial artery, augmentation index or pulse wave velocity, in the prediction of cardiovascular risk particularly in primary prevention settings. The combination of these non-invasive tests has been shown to improve their prognostic accuracy compared to each other alone. Although several therapeutic strategies like vaccination against antigens promoting atherogenesis, cyclooxygenase inhibitors, statins, and ACE inhibitors may reduce the levels of these inflammatory markers and improve the non-invasive markers of subclinical atherosclerosis, the impact on cardiovascular risk resulting from these changes is unknown. The combination of an established inflammatory marker such as CRP or a vascular marker such as IMT with novel biochemical and vascular markers of cardiovascular disease may offer additive prognostic information for adverse outcome.
...
PMID:Inflammatory and non-invasive vascular markers: the multimarker approach for risk stratification in coronary artery disease. 1837 39

Genetic polymorphisms may be linked to inter-individual differences in erythropoietin (EPO) resistance. We investigated the -511C/T polymorphism of the IL-1B gene and the I/D polymorphism of the ACE gene for any association with EPO resistance index (ERI) in maintenance hemodialysis patients (n=167). Because EPO responsiveness is multi-factorial, we also included other possible influences (age, sex, time on dialysis, ACE inhibitor or angiotensin receptor blocker use, ferritin, transferrin saturation, intact PTH, high sensitivity C-reactive protein, albumin, Kt/V, and presence of diabetes mellitus) on ERI in our analyses. Multiple regression analysis showed significant association of the IL-1B-511CC and ACE DD polymorphisms with ERI (P=0.038 and P=0.004 in the recessive model, respectively). The combination (C) of alleles of two loci showed that C1 (I-T) was significantly associated with ERI in the co-dominant and recessive models (P=0.005 and P=0.0001, respectively). Subjects who did not carry C1 showed significantly decreased ERI (10.10+/-5.15 IU/kg weight/g hemoglobin) compared to other study subjects (C1/C1 and C1/-; 12.97+/-4.90 and 15.12+/-7.43 IU/kg weight/g hemoglobin, respectively). Our study indicates that the IL-1B-511C/T and ACE I/D polymorphisms may be useful genetic markers of EPO requirement in hemodialysis patients. These findings might also provide a new perspective on therapeutic approaches to the treatment of end stage renal disease patients with anemia.
...
PMID:Polymorphisms in two genes, IL-1B and ACE, are associated with erythropoietin resistance in Korean patients on maintenance hemodialysis. 1844 54

Aim of the study was to investigate peculiarities of effects of rosuvastatin on the state of oxidative stress and endogenous inflammation in patients with extensive atherosclerosis. Patients with extensive atherosclerosis included into the study (n=46, mean age 56.5 +/- 2.2 years) were distributed to 2 equivalent according to clinico-instrumental data groups. To patients of group 1 (n=24) standard therapy was prescribed (antiaggregants, ACE inhibitors, b-adrenoblockers, and nitrates when indicated), patients of group 2 (n=22) in addition to standard therapy took rosuvastatin (10 mg/day). Investigations included measurement of parameters of serum lipid profile, content of thiol groups of blood serum proteins, activity of enzyme glutathione peroxidase, in vivo oxidation of whole blood serum and HDL, concentration of 3-nitrotirosine, high sensitivity C-reactive protein and interleukin-6, activity of type 2IIA secretory phospholipase A2. It was found that level of 3-nitrotirosine and activity of secretory phospholipase A2 together with high sensitivity C-reactive protein appear to be effective markers of systemic oxidative stress and endogenous inflammation in patients with extensive atherosclerosis. Treatment with rosuvastatin in moderate doses significantly suppressed activity of endogenous inflammation and oxidative stress by way of activation of antioxidant system of plasma, decrease of oxidation of fractions of lipoproteins, suppression of " nitrotirosine " stress, as well as partial inhibition of efficacy of action of secretory phospholipase A2, lowering of content of C-reactive protein and interleukin-6.
...
PMID:[Molecular mechanisms of effects of rosuvastatin on systemic oxidative stress and endogenous inflammation in patients with atherosclerosis]. 1878 9


<< Previous 1 2 3 4 5 6 7 Next >>

---