Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monocyte chemoattractant protein-1 (MCP-1) plays a fundamental role in monocyte recruitment and has been implicated in atherosclerosis. The present study tested the hypothesis that increased levels of MCP-1 are associated with an increased risk for restenosis post stent implantation. The plasma MCP-1 antigen levels were measured pre-stenting, and at 24 and 48 h and 6 months post stenting in 41 patients with stable exertional angina (SEA) who had undergone successful stent implantation. Nineteen patients with chest pain syndrome were selected as a control group. Initial plasma MCP-1 antigen levels (mean +/- SE, pg/ml) in the patients with SEA were significantly higher than those in the control group (852.3+/-51.4 vs 418.2+/-26.7, p<0.001). The patients with SEA were divided into 2 groups based on follow-up angiographic findings: 17 patients with restenosis (R group); 24 patients without restenosis (N group). The lesion was significantly longer in the R group than in the N group (p<0.03). Plasma MCP-1 antigen levels at pre-stenting were not significantly different between the 2 groups (820.6+/-69.1 in the R group vs 874.7+/-73.8 in the N group). Serial changes of plasma MCP-1 levels were plotted as percent changes from the initial levels (mean +/- SE, %) and were significantly higher in the R group than in the N group at 48 h and at 6 months post stent implantation (104.6+/-4.8 vs 89.2+/-3.4, p<0.01, 109.6+/-11.2 vs 98.5+/-5.0, p<0.05). The study concludes that MCP-1 production at stented coronary arterial sites is associated with an increased risk for restenosis post stent implantation.
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PMID:Plasma monocyte chemoattractant protein-1 antigen levels and the risk of restenosis after coronary stent implantation. 1131 19

TNF-alpha as a pleiotropic, proinflammatory cytokine seems to play a role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). TNF-alpha is binding to two cell surface receptors and its serum activity is modified by soluble forms of these receptors: sTNF-R I and sTNF-R II. The aim of this study was to assess serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II in patients (pts) with CAD. We examined serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II by ELISA in: 45 pts with stable exertional angina (group I); 32 pts with unstable angina (group II) within 6, 24, and 48 h after the chest pain; and 23 pts before and 6, 24, and 48 h after PTCA (group III). The control group (group C) consisted of 20 healthy subjects. We evaluated: clinical state of patients and results of some diagnostic examinations (lipids, ECG, echocardiography, coronary angiography). Mean serum concentrations of TNF-alpha were significantly higher in pts ith CAD (group I: 18.25 +/- 5.5 pg/ml; group II: 17.24 +/- 4.0 pg/ml; group III: 18.70 +/- 0.6 pg/ml; p < 0.001) than in healthy pts (8.31 +/- 1.4 pg/ml). In turn mean serum concentrations of sTNF-R I were significantly higher both in group I (1399.6 +/- 536.3 pg/ml; p < 0.05) and III (1544.0 +/- 391.4 pg/ml; p < 0.01) than in control group (1093.9 +/- 456.9 pg/ml). There were not differences in mean serum concentrations of sTNF-R II. We found no differences between mean serum concentrations of TNF-alpha, sTNF-R I and sTNF-R II either after the chest pain (group II); or before and after PTCA (group III). In group I mean TNF-alpha correlated with serum triglycerides and HDL-cholesterol (r = 0.412 and r = -0.424; p < 0.01); sTNF-R I correlated with LDL-cholesterol (r = -0.309; p < 0.05); and sTNF-R II correlated with total cholesterol and LDL-cholesterol (r = 0.311 and r = 0.316; p < 0.05). The serum concentrations of TNF-alpha are increased in patients with CAD, but this does not reflect the clinical state of patients. In pts with stable angina these increased levels of TNF-alpha may be accompanied with higher concentrations of sTNF-R I--it seems to be the compensatory mechanism in long-term atherosclerosis. Lipid disturbances may influence the cytokines metabolism in pts with CAD.
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PMID:[Tumor necrosis factor alpha and its soluble receptors in serum of patients with coronary artery disease]. 1157 24

Background: Cytokines may play a role in the pathogenesis of atherosclerosis and coronary artery disease (CAD). Methods: We examined serum concentrations of selected pro- (TNFalpha, IL-2) and anti-inflammatory (IL-10) cytokines, and soluble forms of TNF receptors (sTNFR 1 and sTNFR 2) by ELISA in 45 patients with stable exertional angina (group 1), 32 patients with unstable angina (group 2), and 20 healthy subjects (group C). Results: Serum concentrations of both TNFalpha (group 1, 18.3; group 2, 17.2 pg/ml; P<0.001) and IL-10 (group 1, 46.1; group 2, 41.5 pg/ml; P<0.05) were significantly higher in patients with CAD than in group C (8.3 and 14.3 pg/ml, respectively). sTNFR 1 serum level was higher in group 1 (1399.6; P<0.05) than in healthy volunteers (1093.9 pg/ml). In turn, the serum level of IL-2 was significantly higher in unstable patients than it was in groups 1 and C (89.4, 59.8 and 52.8 pg/ml, respectively). In group 1, both TNFalpha and IL-2 correlated with serum lipids. Conclusions: Patients with CAD, irrespective of the form of the disease, have higher serum levels of pro- and anti-inflammatory cytokines than control subjects. Increased concentrations of IL-2 in unstable angina may suggest additional immunologic activation. The pro-inflammatory cytokine levels seem to be related to lipid disturbances.
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PMID:Selected cytokines and soluble forms of cytokine receptors in coronary artery disease. 1189 69

Adipose tissue is a secretory organ producing a variety of bioactive substances, such as adiponectin. Adiponectin has antiatherogenic properties while plasminogen activator inhibitor type 1 (PAI-1) is closely involved in the development of atherosclerosis. The relationship between adiponectin and PAI-1 in patients with coronary artery disease (CAD) has not been clarified. This study examined plasma levels of adiponectin and PAI-1 in 64 patients with stable exertional angina (SEA) and 65 patients with the chest pain syndrome (CPS). Plasma log-adiponectin levels were significantly lower in patients with SEA (0.62+/-0.08 micro g/dL) compared to those with CPS (0.86+/-0.05 micro g/dL) (p<0.0001). The plasma levels of log-PAI-1 were significantly higher in patients with SEA (1.23+/-0.18 ng/mL) compared to those with CPS (1.15+/-0.22 ng/mL) (p<0.05). Plasma log-adiponectin levels correlated negatively with diabetes mellitus (DM), body mass index (BMI), log-PAI-1 (r=-0.284, p<0.001), triglyceride (TG), and remnant-like particles cholesterol (RLP-C), and positively with high-density lipoprotein cholesterol (HDL-C) levels. Plasma levels of log-PAI-1 correlated positively with DM, BMI,TG and RLP-C levels, and negatively with HDL-C levels. Multiple logistic regression analysis identified sex, angina pectoris, and PAI-1 as independent determinants of hyperadiponectinemia (p<0.05). Adiponectin is inversely related to PAI-1. DM, BMI,TG, HDL-C, and RLP-C are common mediators between adiponectin and PAI-1, and treatment for common mediators may prevent the development of CAD by reducing PAI-1 and increasing adiponectin levels.
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PMID:Adiponectin is inversely related to plasminogen activator inhibitor type 1 in patients with stable exertional angina. 1511 65

With the purpose of investigating peculiarities of psychogenically induced myocardial infarction (PIMI) 82 patients with primary myocardial infarction (MI) were chosen as the subjects of the given controlled study and divided into two groups. The main group consisted of 33 patients, the rest 49 formed the control group. The study showed that coronary atherosclerosis was more pronounced in the patients of the main group, among whom cases of exertional angina in past history were more frequent, and who had more pronounced coronary calcinosis compared to the patients of the control group. At the same time, the clinical course of MI in such patients is relatively benign, but it is more often complicated by early postinfarction angina. All this suggests that the pathogenesis of PIMI differs from that of "classic" MI. In particular, PIMI may be associated with the involvement of more distant parts of coronary vessels. Patients with PIMI seem to need to be regarded as having high risk of repeated coronary disasters.
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PMID:[Characteristics of the pathogenesis, manifestations and clinical course of psychogenically induced myocardial infarctions]. 1580 28

We reviewed the literature related to the effects of high-dose zinc in arteriosclerosis-induced angina pectoris. Lipid peroxidation and LDL oxidation are believed to be critical for arteriosclerosis, and consequently angina pectoris. Administration of biologically available zinc was a beneficial treatment in a significant percentage of patients with severely symptomatic, inoperable atherosclerotic disease. In these patients, there was no difference in zinc concentration between patients with and without atherosclerosis in whole blood, erythocytes or hair, but there was a major difference between normal aorta and diseased aortas (40.6 ppm zinc in normal aorta vs. 23.2 ppm zinc in atherosclerotic aorta, 40.6 ppm zinc in normal aorta vs. 19.4 ppm zinc in atherosclerotic aneurysm aorta, and no difference between normal and aneurysm aorta), although copper was low in aneurysm aorta. Medication with high-dose zinc sulfate to raise zinc serum concentrations from 95 to 177 microg/dl resulted in objective improvement in 12 of 16 of these patients, including a patient that also had Raynaud's disease. Long term environmental exposure to zinc resulted in a 40% reduction in the incidence of angina of effort compared to people not exposed to environmental zinc (P<0.01) and a 40% reduction in the incidence of probable ischemia in exercise (P<0.001). Lead had no effect while cadmium exposure resulted in more than tripling the incidence of angina of effort (P<0.001). The antioxidative action of zinc prevents oxidation of LDL cholesterol and consequently stops the main mechanism of atherogenesis. Zinc blocks calcium and its several actions on atherogenesis. Increased amounts of cytotoxic cytokines such as TNF-alpha, IL-beta and IL-8, often produced in the elderly, are blocked by high-dose zinc. We hypothesize that higher serum concentrations of LDL cholesterol resulting from administration of 300 mg of zinc per day is caused by a release of low density cholesterol from cardiovascular tissues, beneficially flushing it into the serum where it is readily observed, thus decreasing arteriosclerosis, increasing circulation, terminating angina pectoris and restoring more youthful cardiac function. Although prevention of cholesterol-induced arteriosclerosis by zinc is predicted from findings related to oxidative stress and lipid peroxidation, removal of LDL might be attributable to action of ionic zinc on ICAM inhibition. In stark contrast to current practice, high-dose zinc should be considered as basic in the strategy of prophylaxis and therapy of the atherosclerosis process to terminate angina pectoris and restore youthful cardiac function.
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PMID:High-dose zinc to terminate angina pectoris: a review and hypothesis for action by ICAM inhibition. 1608 66

We examined 4 groups of patients younger than 70 years with atherosclerosis of coronary and/or cerebral arteries. In 98 patients the disease began as acute myocardial infarction, 65 patient from the very beginning suffered from angina of effort, 33 had ischemic cerebral stroke, and in 26 dyscirculatory encephalopathy was diagnosed. Among patients with ischemic heart disease (IHD) and cerebrovascular damages (CVD) 87 and 89%, respectively, had dyslipidemia (DLP). Disorders of lipid composition of the blood with pronounced hypercholesterolemia prevailed in patients with IHD and elevated level of triglycerides or selective decrease of antiatherogenic fraction of lipoproteides - in patients with CVD (especially in patients with stroke). When treatment is prescribed to patients with IHD and CVD at the background of DLP it is necessary to take into consideration DLP variants in order to obtain most effective action of statins and fibrates.
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PMID:[About dyslipidemic states characteristic for various forms of ischemic heart disease and cerebrovascular damages]. 1826 Sep 3

The aim of the work--the study of risk factors and detection of prevailing clinical form of diabetic foot infections (DFI) in dependence on type diabetes mellitus (DM). 157 patients with DM and DFI (25 type 1 DM cases and 132 type 2 DM cases) and 689 DM patients without DFI (282 type 1 DM cases and 407 type 2 DM cases) were examined. DFI cases differed from both type DM without DFI in greater number of complications. Associated with decompensated DM amputations and developing ulcerations were been mentioned in history in about a quarter of both type DM patients. DFI risk factors in type 1 DM appeared to be a combination of sensor and autonomic neuropathy (OR: 6.58; 95% CI: 2.74-14.9; a < 0.05), preprpoliferative retinopathy (RP) (OR: 4.62; 95% CI: 1.98-10.7; a < 0.05), in type 2 DM: macroangiopathy of lower extremities (OR: 4.59; 95% CI 2.98-7.1; a < 0.05), obesity (OR: 4.65; 95% CI 2.42-8.9; a < 0.05), concomitant exertional angina (OR 3.3; 95% CI 2.2-5.1; a < 0.05), a proteinuric stage of nephropathy (OR: 2.6; 95% CI: 1.74-3.9; a < 0.05), prominent sensor neuropathy (OR: 2.3; 95% CI 1.3-4.2; a < 0.05), preprpoliferative RP (OR: 2.1; 95% CI 1.41-3.13; a < 0.05). In type 1 DM and DFI neuropathic form of DFI prevailed (88%), in type 2 DM--neuroischemic form of DFI (66%). Ischemic form of DFI was determined in type 2 DM only (6%). In type 2 DM cases with DFI there was revealed a high rate of risk factors of atherosclerosis.
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PMID:[The risk factors and clinical forms of diabetic foot infections in dependence on the type of diabetes mellitus]. 1875 47

Atheroma calcification is a common feature of advanced atherosclerosis, however with the advent of CT scanning it has become possible to detect extensive coronary calcification in the absence of flow-limiting lesions. While this phenomenon is known in renal disease, it also exists in some patients with exertional angina. Vascular pathology suggests biomineralisation associated with development of osteoblast-like cells in the arterial wall. While some conventional risk factors are shared with atheroma formation, others such as ethnicity and medications appear more specific to extensive calcification and may mirror those for osteoporosis. Similarly an atherogenic diet can predispose to both conditions while some elements promote or inhibit coronary calcification but not atheroma formation. The immune and endocrine systems contribute to both conditions but not necessarily in the same way, with vitamins D and K more related to calcification than atheroma formation. Finally, statins significantly lower low density lipoprotein (LDL) cholesterol and reduce atheroma formation but are largely powerless against extensive calcification. Although investigations into the exact cause of extensive coronary calcification are in their infancy, early results suggest that it is sufficiently different in nature from atheroma formation to be considered as a separate condition. Further research would yield a greater understanding, which would aid management and the development of specific biomarkers to reduce the cost and radiation risk of CT scanning.
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PMID:Extensive coronary calcification: a clinically unrecognised condition. 2018 Jul 69

Presented herein is a clinical case report concerning a 59-year-old male patient suffering from multifocal atherosclerosis after endured repeat acute ischaemic attacks in various arterial basins of the brain. Analysing his case history revealed functional class II-IV angina of effort. Ultrasonographic and angiographic findings showed a haemodynamically significant plaque in the ostium of the left internal carotid artery, hypoplasia of the right vertebral artery, a haemodynamically meaningful narrowing of the left vertebral artery, subtotal stenosis of the anterior interventricular branch and pronounced alterations in the right vertebral artery. The first stage of surgery consisted in stenting of the left internal carotid artery and anterior interventricular branch, followed by the second stage consisting in the stenting of the left vertebral artery with an angiographically good outcome. The check-up CT of the brain and 24-hour ECG monitoring showed no negative dynamics. In July 2005, the patient was subjected to craniocerebral microarterial shunting on the right. No relapses of AIAs have so far been observed.
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PMID:[Landmark of the internal carotid artery stenting, anterior interventricular branch of the left coronary artery and vertebral artery in a patient with multifocal atherosclerosis]. 2063 29


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