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

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Query: EC:4.1.1.6 (CAD)
4,420 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 30 cases of cervical incompetence in pregnancy morphological and infectious factors of the amnial membranes were examined with regard to a predictive function versus premature rupture of membranes (PROM). The sonographically visible chorioamniotic dissociation (CAD, cut-off-value greater than or equal to 3 mm) and the C-reactive protein (CRP, cut-off-value greater than or equal to 6 mg/l) showed an sufficient predictive force. The combination of CAD and CRP could predict all cases of PROM. In addition, it could be shown that ascending infections are not only cause of PROM but also of morphological changes of the cervix and the amnial membranes in cervical incompetence. So therapy of an incompetent cervix should include competent vaginal sanitation. An immunological model of premature cervical ripening and damage of the membranes by proteases, kinins and prostaglandins started by phagocytosis activity is discussed.
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PMID:[Chorioamniotic dissociation and C-reactive protein as predictors of early premature amniotic rupture]. 219 24

Lp(a) is an independent risk factor for recurrent atherosclerotic heart disease in men and women after menopause. Excess levels of Lp(a) are seen in both males and females, more common in Africans, African Americans, and Asian populations than in whites. Since the standard lipid profile does not report Lp(a), it has to be ordered separately. Screening for Lp(a) should be considered under the following circumstances: (a) patient or family history of premature atherosclerotic heart disease, (b) familial history of hyperlipidemia, (c) established atherosclerotic heart disease with a normal routine lipid profile, (d) hyperlipidemia refractory to therapy, and (e) history of recurrent arterial stenosis. Treatment options are (a) a new extended-release form of niacin 3 to 4 g daily (although most effective in lowering Lp(a) and in reducing atherosclerotic heart disease mortality rates, its use may be limited because of side effects); (b) estrogen replacement after menopause, (however, concomitant progesterone therapy dilutes the effectiveness of estrogens); (c) lowering LDL with statins (generally effective in atherosclerotic heart disease but has no effect on Lp(a) levels), (d) aspirin and antibiotics (may be effective when C-reactive protein levels are high); and (e) folic acid (reduces homocysteine levels). The general measures that halt the progression of CAD should always be adhered to, namely, maintaining normal weight, a daily exercise program, blood pressure control, a low-cholesterol-forming diet, and daily aspirin.
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PMID:Lp(a) lipoprotein--an independent risk factor for coronary heart disease after menopause. 1115 87

Low-grade inflammatory activity is associated with an increased risk for ischaemic coronary events. sPLA(2) (secretory non-pancreatic type II phospholipase A(2)) serum activity is increased in chronic inflammatory diseases and may also contribute to atherogenesis. Since the endothelium is a major target for inflammatory cytokines, we hypothesized that elevated serum activity of sPLA(2) is associated with an impaired vasodilator function in patients with documented CAD (coronary artery disease). Endothelium-dependent (acetylcholine, 10-50 microg/min) and endothelium-independent (sodium nitroprusside, 2-8 microg/min) FBF (forearm blood flow) responses were measured by venous occlusion plethysmography in 50 male patients with angiographically documented CAD. sPLA(2) serum activity was inversely correlated with acetylcholine-induced FBF responses ( r =-0.36; P <0.05). In addition, there was a significant correlation between sPLA(2) and CRP (C-reactive protein; r =0.33, P <0.02). In contrast, FBF responses to sodium nitroprusside did not correlate with sPLA(2) serum activity. In order to identify independent predictors of an impaired endothelium-dependent vasodilator function in patients with CAD, a multivariate analysis was performed including the inflammatory serum markers as well as classical risk factors of CAD. This analysis demonstrated that both sPLA(2) ( P <0.05) and CRP serum levels ( P <0.05) were the only significant independent predictors of an impaired acetylcholine-induced FBF response. In conclusion, elevated sPLA(2) serum activity is associated with a significant impairment in systemic endothelial vasodilator function in patients with CAD. The identification of sPLA(2) as a novel independent predictor for endothelial dysfunction provides another important clue to link a systemic marker of inflammation with coronary atherosclerotic disease.
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PMID:Elevated secretory non-pancreatic type II phospholipase A2 serum activity is associated with impaired endothelial vasodilator function in patients with coronary artery disease. 1474 Oct 42

Patients with rheumatoid arthritis (RA) have a two to five times increased risk of developing premature cardiovascular disease that shortens life expectancy by 5-10 years. Traditional risk factors known to promote and accelerate the progression of atherosclerotic lesions however, are often absent in patients with RA. Many similarities have emerged between the paradigm of inflammation in the pathogenesis of atherosclerosis and the well-established mechanisms of inflammation in the pathogenesis of RA. Hence it is intriguing to speculate that inflammation in RA is not confined to the joints but also present in the vessel wall. Indeed, low-grade inflammation and endothelial dysfunction play pivotal roles in the initiation, progression and propagation of the atherosclerotic process. While the healthy endothelium prevents adhesion of mononuclear cells, the defence mechanisms cease under the influence of cardiovascular risk factors and inflammation and they express adhesion molecules (selectins, vascular adhesion molecule-([VCAM-]1, intercellular adhesion molecule-[ICAM-]1) that promote the adherence of monocytes. This expression is induced by pro-inflammatory cytokines such as interleukin-(IL-)1beta and tumor necrosis factor-(TNF-)alpha, by C-reactive protein (CRP), and CD40/CD40 ligand interactions. As all of these factors are present at increased levels in the systemic circulation in RA, it appears possible that they might impact the endothelium as well. Further similarities include proteolytic enzymes such as matrix metalloproteinases (MMPs) that play a role in joint destruction as well as in destabilization and rupture of vulnerable atherosclerotic plaques. In addition, coagulation factors such as increased levels of tissue factor (TF), van Willebrand factor (vWF) and plasminogen activator inhibitor-(PAI-)1 are important in both, RA and CAD. Endothelial dysfunction has shown to correlate with cardiovascular prognosis in several studies, which indicates its clinical relevance. Endothelial function measurement is performed in the coronary or peripheral circulation (by venous occlusion plethysmography or flow-mediated dilation). Recent studies have demonstrated impaired endothelial function in patients with RA, already at early stages of the disease. Similar results are found in patients with systemic lupus erythematosus (SLE), indicating that inflammation per se may impair altering vascular function. This and more evidence supports the notion that inflammation plays a pivotal role in vascular dysfunction and may by these mechanisms explain at least part of the excess morbidity and mortality observed in RA and SLE. In light of the growing evidence of increased cardiovascular morbidity and mortality mostly independent of traditional risk factors, treatment strategies in RA should not only aim at relieving symptoms and inhibiting joint destruction but should have a beneficial effect on the vasculature to reduce cardiovascular events. Indeed, an improvement in endothelial function in RA was recently demonstrated by anti-TNF-alpha therapy and statins. Whether and to what degree the effects of anti-inflammatory strategies to improve endothelial function, which although clinically well established is still a surrogate, translate into clinical benefit for our patients with rheumatologic diseases needs to be determined in large-scale clinical trials some of which are now already under way.
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PMID:[Rheumatoid arthritis, inflammation, and atherosclerosis]. 1559 72

Carotid atherosclerotic plaque remodelling and increased risk of symptomatic plaque rupture seem to be partially mediated by matrix metalloproteinases (MMPs). In this study, we have investigated whether different MMPs are related to carotid atherosclerosis or to recent ischaemic brain disease. Eighty-four consecutive patients undergoing carotid endarterectomy for symptomatic and asymptomatic disease were studied. Plaques were analysed by ultrasound and later by morphology. Plasma MMP-2, MMP-8 and MMP-9 levels were quantified by ELISA. MMP expression and activity in carotid plaques was analysed by Western blotting and in situ zymography. Results were analysed with respect to plaque stability, morphology, symptomatic disease, presence of vascular risk factors and plasma markers of acute inflammation as high sensitivity C-reactive protein (hsCRP), fibrinogen, D-dimer and white blood cell counts. Patients with hypoechogenic plaques on ultrasound had more plasma MMP-8 (p = 0.04) and increased MMP activity as assessed by in situ zymography. Asymptomatic patients with plaque progression had more active intraplaque MMP-8 than asymptomatic patients without plaque progression. Presence of recent intraplaque haemorrhage or past history of CAD was related to increased activity of MMPs as assessed by in situ zymography (p < 0.01, CI 95% 0.8-1.0). Plasma MMP-8 and MMP-9, but not MMP-2 levels, decrease with time after ischaemic stroke. Patients with hypertension had more intraplaque active MMP-9 than normotensive (p = 0.03, CI 95% 0.7-1.0). Hypoechogenic carotid plaques had increased MMP activity and asymptomatic patients with plaque progression show increase intraplaque MMP-8 levels.
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PMID:Intraplaque MMP-8 levels are increased in asymptomatic patients with carotid plaque progression on ultrasound. 1625 88

Systemic factors and blood flow velocity related to atherosclerosis have been examined mainly separately or by in vitro studies. The aim of our study was to investigate the association between local coronary blood flow (corrected TIMI frame count, CTFC) and systemic atherosclerosis-related inflammatory parameters such as soluble intercellular adhesion molecule-1 (sICAM-1), interleukin-6 (Il-6), high sensitivity C-reactive protein (hsCRP) and von Willebrand factor (vWF) in humans. We enrolled the following groups of ischemic heart disease (IHD) patients: patients with coronary stenosis and stable (CAD, n = 96) or unstable angina (ACS, n = 27), patients with documented myocardial ischemia and normal coronary angiogram (NEG, n = 68). Patient groups showed only marginal differences in CTFC or sICAM-1 levels. In contrast, when IHD patients were studied individually, general positive correlation was found between CTFC and sICAM-1 level (r = 0.33; in NEG r = 0.25; in CAD r = 0.37; in ACS r = 0.61), being the strongest in ACS. The relation was independent from age, gender, BMI, smoking, hypertension, diabetes, previous myocardial infarction, family history of IHD, medication, hsCRP, IL-6 and vWF levels. (odds ratio, OR = 6.4; CI 95%: 2.43-16.84; p < 0.05). Nevertheless, correlation between CTFC and IL-6, hsCRP, vWF levels was not found. These results indicate inverse correlation between coronary blood flow and adhesion molecule production independently from conventional cardiovascular risk factors and inflammatory markers.
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PMID:Inverse correlation between coronary blood flow velocity and sICAM-1 level observed in ischemic heart disease patients. 1629 92

Diabetes increases the risk of coronary artery disease. We examined the effects of lifestyle modification on key contributing factors to atherogenesis, including oxidative stress, inflammation and cell adhesion. Diabetic men (N=13) were placed on a high-fiber, low-fat diet in a 3-week residential program where food was provided ad libitum and daily aerobic exercise was performed. In each subject, pre- and post-intervention fasting blood was drawn for circulating levels of serum lipids, glucose and insulin, oxidative stress marker 8-isoprostaglandin F2alpha (8-iso-PGF2alpha), the inflammatory protein C-reactive protein (CRP), and soluble intracellular adhesion molecule (sICAM)-1 and sE-selectin as indicators of endothelial activation. Using subject sera and human aortic endothelial cell (HAEC) culture systems, serum-induced monocyte adhesion, ICAM-1, vascular cell adhesion molecule-1 (VCAM-1) and cell surface abundance, and monocyte chemotactic protein-1 (MCP-1) production were determined. Nitric oxide (NO), superoxide, and hydrogen peroxide production were measured in vitro by fluorometric detection. After 3 weeks, significant reductions (p<0.05) in BMI, all serum lipids including total cholesterol (pre: 188.9+/-10.1 mg/dL versus post: 146.3+/-3.8 mg/dL) and low-density lipoprotein (103.1+/-10.2 mg/dL versus 76.4+/-4.3 mg/dL), fasting serum glucose (157.5+/-10.1 mg/dL versus 126.7+/-8.7 mg/dL), insulin (33.8+/-4.0 microU/ml versus 23.8+/-3.4 microU/ml), homeostasis model assessment for insulin resistance, 8-iso-PGF2alpha, CRP, sICAM-1, and sE-selectin were noted. In vitro, serum-stimulated monocyte adhesion, cellular ICAM-1 and VCAM-1 expression (p<0.05), and fluorometric detection of superoxide and hydrogen peroxide production decreased, while a concomitant increase in NO production was noted (all p<0.01). A combination of diet and exercise ameliorates oxidative stress, inflammation, and monocyte-endothelial interaction. Intensive lifestyle modification may improve novel CAD risk factors in men with diabetes.
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PMID:Effect of a diet and exercise intervention on oxidative stress, inflammation and monocyte adhesion in diabetic men. 1661 95

The commonly used laboratory markers of coronary involvement in subjects with acute coronary syndrome (ACS) are not yet myocardial ischemia-specific and show a late irreversible involvement of the myocardium. A laboratory test has been searched for in order to distinguish persons with myocardial ischemia and typical CAD symptoms to CAD-free individuals. Reg-Ialpha is the product of Reg-I gene which plays a significant role in myocardial regeneration. 38 individuals with suspicion of acute coronary syndrome were tested on admission, after 2 and 6 hours. In all of them cardiac troponin I, myoglobin, C-reactive protein (CRP) and Reg-I alpha were analysed. Our findings did not support the hypothesis that measurement of Reg-Ia maybe the useful marker of myocardial stress.
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PMID:Reg-Ialpha in the diagnosis of acute coronary syndrome--a pilot study. 1693 8

Systemic inflammation is associated with sympathetic cardiac activation and decreased HRV (heart rate variability) in subjects at high risk of CAD (coronary artery disease). In the present study, we examined the influence of systemic inflammation, measured by CRP (C-reactive protein), on vagal HR (heart rate) control during behavioural relaxation in patients with CAD. It was hypothesized that CRP would be associated with decreased vagal HR modulation. Consecutive patients were screened 2 weeks prior to elective PTCA (percutaneous transluminal coronary angioplasty). The study was comprised of 29 subjects who represented the first and fourth quartiles of the CRP distribution: Low (0.47+/-0.07 microg/ml)- and High (8.19+/-1.95 microg/ml)-CRP groups respectively. Vagal HR control was quantified as RR high-frequency spectral power (0.15 to 0.40 Hz), and was assessed in log-transformed absolute units (logHF power). Near-IR particle immunoassay was used to determine high-sensitivity CRP concentration. Assessment entailed 5 min of silent reading and self-guided behavioural relaxation. RR logHF power was decreased in the High-CRP group across both assessment procedures (P=0.032). Behavioural relaxation increased RR logHF power for both the Low- and High-CRP groups (P=0.033). Hierarchical linear regression determined that CRP accounted for 18.9% of the variance in RR logHF power during behavioural relaxation (P=0.03), independent of baseline RR interval, cardiac medication, respiratory logHF power and body mass index. In conclusion, patients with CAD had augmented vagal HR control with behavioural relaxation, but this effect was moderated by the severity of CRP. Therefore it may be advisable to assess systemic inflammation in interventions aimed at improving neurocardiac regulation in patients with CAD.
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PMID:C-reactive protein modulates vagal heart rate control in patients with coronary artery disease. 1713 77

Oxidant stress is widely believed to participate in cardiovascular disease pathogenesis. However, progress in defining appropriate systemic antioxidant targeted therapies has been hindered by uncertainty in defining clinically relevant systemic oxidant stress measures. In a case control study, 50 subjects with CAD (>50% stenosis in one or more major coronary vessels) and 54 without CAD (<30% stenosis in all major coronary vessels) were tested. Plasma was isolated and stored under conditions designed to prevent artificial lipid peroxidation. Systemic levels of multiple (n=9) specific fatty acid oxidation products including individual hydroxyoctadecadienoic acids (HODEs), hydroxyeicosatetraenoic acids (HETEs), and F(2)-isoprostanes were simultaneously measured by high-performance liquid chromatography (HPLC) with on-line tandem mass spectrometry, along with traditional risk factors and C-reactive protein (CRP) levels. Of the markers monitored, only 9-HETE and F(2)-isoprostanes, both products of free radical-mediated arachidonic acid oxidation, were significantly elevated in patients with angiographically defined CAD (9-HETE, 8.7 +/- 4 vs 6.8 +/- 4 micromol/mol arachidonate, P = 0.011; and F(2)-isoprostanes, 9.4 +/- 5 vs 6.2 +/- 3 micromol/mol arachidonate, P < 0.001). In multivariable analyses with simultaneous adjustment for Framingham risk score and C-reactive protein, 9-HETE (4th quartile OR = 4.8, 95% CI=1.3 to 17.1; P = 0.016) and F(2)-isoprostanes (4th quartile OR=9.7, 95% CI=2.56 to 36.9; P < 0.001) remained strong and independent predictors of CAD risk. Systemic levels of 9-HETE and F(2)-isoprostanes are independently associated with angiographic evidence of CAD and appear superior to other specific oxidation products of arachidonic and linoleic acids as predictors of the presence of angiographically evident coronary artery disease.
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PMID:Systemic elevations of free radical oxidation products of arachidonic acid are associated with angiographic evidence of coronary artery disease. 1714 56


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