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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated C-reactive protein concentration, measured by an ultrasensitive method (hsCRP), has been proved to be a risk factor for atherosclerosis progression and its complications (myocardial infarction and stroke) in otherwise healthy men and women. In patients with already diagnosed atherosclerotic disease elevated concentration of hsCRP predicts prognosis. There are multiple causes of elevated hsCRP concentration: metabolic changes (e.g. as a part of metabolic syndrome), genetic background and chronic infections. Proinflammatory effect of adipose tissue in obese individuals seems to play an important role, hsCRP levels correlate with markers of abdominal obesity. Elevated hsCRP concentrations can be lowered both pharmacologically and by a lifestyle change. This review covers current knowledge of pathophysiology of elevated hsCRP concentration and possible use of this method in clinical medicine.
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PMID:[An ultrasensitive C-reactive protein assay--a new parameter in cardiovascular risk]. 1564 58

Relatively limited contemporary information is available about the magnitude of, and factors associated with, the metabolic syndrome in adult men and women. The purpose of our observational study was to describe the prevalence and predictors of the metabolic syndrome in a sample of employed adults attending a worksite cardiovascular screening program. The study sample consisted of 871 men and women between the ages of 21 and 77 years from 6 locations of the parent company. These individuals attended an employer-sponsored cardiovascular screening and wellness program during 2003. A standardized questionnaire was administered to all study participants and a number of different coronary risk factors were measured. Approximately 27% of the study sample was classified as having the metabolic syndrome. Men, persons with a history of hypertension, heart disease, or stroke, sedentary individuals, and those with an increased heart rate and higher levels of C-reactive protein were associated with presence of the metabolic syndrome. A relatively similar risk factor profile was noted in persons without a self-reported history of prior cardiovascular disease. The results of our cross-sectional observational study suggest that the prevalence of the metabolic syndrome is considerable. A number of demographic, comorbid, and other factors are associated with this syndrome. Increased attention to the metabolic syndrome, and modification of predisposing factors, remains of considerable public health and clinical importance.
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PMID:Metabolic syndrome in a screened worksite sample: prevalence and predictors. 1566 35

Inflammatory mechanisms play a prominent role in mediating all stages of atherosclerosis, and measurement of inflammatory biomarkers provides a method for detecting individuals at future vascular risk. Evidence from observational studies indicates that the hepatic acute-phase reactant, C-reactive protein (CRP), is the strongest predictor of future myocardial infarction and stroke. The addition of CRP to standard lipid screening may improve global risk prediction among those with high as well as low cholesterol. Statins have been shown to have beneficial effects on plaque inflammation, stability and CRP levels, in addition to their lipid-lowering effects. Data from two large statin trials suggest that testing for CRP may identify many individuals without hyperlipidaemia who are at high risk for future cardiovascular events and who may benefit from statin therapy. If confirmed in ongoing large-scale prospective trials, screening for inflammation using CRP as a biomarker could prove an important adjunctive method for identifying individuals at increased risk who would benefit most from targeted preventive interventions.
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PMID:Predicting risk and treatment benefit in atherosclerosis: the role of C-reactive protein. 1568 68

N-homocysteinylated (Nepsilon-Hcy) proteins and corresponding antibodies have recently been discovered in humans and animals. Increased autoimmune response to Nepsilon-Hcy-proteins has been reported in stroke patients. The aim of the present study was to investigate whether antibodies against N-homocysteinylated albumin are associated with coronary artery disease (CAD). We studied 88 male patients aged 50 years or under with angiographically documented CAD and 100 age-matched apparently healthy men as controls. Serum levels of IgG antibodies against Nepsilon-Hcy-albumin were determined using an enzymelinked immunosorbent assay. Seropositivity to anti-Nepsilon-Hcy-albumin antibodies was 5-fold more frequent in CAD patients than in controls (52.3% vs 10.0%; p<0.0001). Plasma Hcy levels in CAD patients were also significantly higher in the former than in the latter group (medians, 13.0 microM vs 12.1 microM; p=0.026). Importantly, 41.2% of subjects with plasma total Hcy >14.5 mM were seropositive compared with 25.5% of normohomocysteinemic individuals (p=0.048). There was a weak correlation between anti-Nepsilon-Hcy-albumin antibodies and Hcy levels (r=0.16; p=0.03). By multivariate logistic regression analysis, seropositivity to anti-Nepsilon-Hcy-albumin antibodies was an independent predictor of early CAD (OR, 14.82; 95% CI, 4.47 to 49.19; p=0.00002). Interestingly, anti-Nepsilon-Hcy-albumin antibodies were associated with C-reactive protein levels (r=0.24; p=0.002). Seropositivity to anti-Nepsilon-Hcy-albumin antibodies showed no association with the MTHFR C677T polymorphism. Our results suggest that seropositivity to antibodies against Nepsilon-homocysteinylated albumin is associated with early-onset CAD. An autoimmune response to Nepsilon-Hcy-albumin may represent a novel mechanism involved in the early development of CAD.
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PMID:Antibodies to N-homocysteinylated albumin as a marker for early-onset coronary artery disease in men. 1571 53

Lipoprotein(a) [Lp(a)] levels are increased in dialysis patients, suggesting that they may play a role in the elevated atherosclerotic cardiovascular disease (ASCVD) risk in this population. Few prospective studies of Lp(a) level, apolipoprotein(a) [apo(a)] size, and ASCVD have been performed in the dialysis population. An inception cohort of 833 incident dialysis patients were followed prospectively. Baseline Lp(a) was measured by apo(a) size-independent ELISA and apo(a) size by Western blot after SDS-agarose gel electrophoresis. A combined prospective nonfatal and fatal ASCVD end point included myocardial infarction, coronary revascularization, cerebrovascular accident, carotid endarterectomy, peripheral revascularization, gangrene, or limb amputation. Survival analyses were performed with adjustment for baseline demographics, comorbid conditions, ASCVD risk factors, albumin, lipids, and C-reactive protein. Median follow-up was 27.4 mo, with 297 ASCVD events, 130 non-ASCVD deaths, and seven losses to follow-up over 1649 person-years. In multivariate Cox regression models, both high Lp(a) concentration (>/=53 nmol/L) and low molecular weight (LMW) apo(a) isoforms (</=22 Kringle-IV repeats) predicted ASCVD events (relative hazard [RH] = 1.38, P = 0.02; RH = 1.58, P < 0.0005, respectively). In models that included both Lp(a) concentration and apo(a) size, only apo(a) size remained associated with ASCVD. Among those with both LMW apo(a) and Lp(a) level >123 nmol/L, the relative hazard (RH) of ASCVD was 1.73 (P < 0.0005), compared with high molecular weight apo(a) and Lp(a) level <123 nmol/L. No interactions by age, race, gender, diabetes, or ASCVD were present. Both LMW apo(a) size and high Lp(a) level predict ASCVD risk in dialysis patients, but the association of ASCVD with LMW isoforms is stronger than the association with high Lp(a) concentration.
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PMID:High lipoprotein(a) levels and small apolipoprotein(a) size prospectively predict cardiovascular events in dialysis patients. 1587 82

Statins reduce cholesterol levels through competitive inhibition of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, the key enzyme that regulates cholesterol synthesis. The cholesterol-lowering effect of statins is also due to an increase in the uptake of cholesterol by cells as a result of intracellular cholesterol depletion and enhanced expression of low-density lipoprotein (LDL) receptors. The use of statins as lipid-lowering agents has lead to remarkable changes in the treatment and prevention of ischemic heart disease. Results of large clinical trials of patients with ischemic heart disease have demonstrated that statins reduce inflammatory markers such as C-reactive protein, an independent risk factor in the disease. Statins exhibit properties that are beyond their lipid-lowering effects. These non-lipid-lowering properties involve the inhibition of the isoprenoid pathway through decreased synthesis of many nonsteroidal isoprenoid compounds. The focus on the immunomodulatory effect of statins is the result of the positive outcome of pravastatin treatment in cardiac transplantation patients, as well as angiographic regression studies showing insignificant changes in the degree of coronary stenosis despite a large reduction in cardiac events. Statin treatment reduces the risk of ischemic stroke despite the fact that LDL cholesterol is not directly associated with the risk of stroke. This observation lead to the investigation of the role of statins in inflammation and the immune system. Recent research data demonstrated that statins inhibit the induction of the major histocompatibility (MHC) class II expression by interferon-gamma (IFN-gamma), leading to repression of MHC II-mediated T-cell activation. Furthermore, statins inhibit the expression of specific cell surface receptors on monocytes, adhesion molecules and also integrin-dependent leucocyte adhesion. While statins may stimulate the secretion of caspase-1, IL-1beta and IL-18 in peripheral mononuclear cells in response to Mycobacterium tuberculosis, they exhibit additional effects on inflammation by decreasing IL-6 synthesis in human vascular smooth muscle cells (VSMC) in vitro. The focus of this monograph is to highlight the role of statins in the modulation of the immune system and inflammatory processes.
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PMID:Modulation of the inflammatory process by statins. 1582 62

Stroke is a leading cause of death and disability worldwide. A new and exciting development in cardiovascular disease is the recognition of the role of inflammation in atherosclerosis. C-reactive protein, an acute phase reactant, appears to be a promising biomarker for cardiovascular disease, possibly more predictive than cholesterol and also may play an etiological role. C-reactive protein also appears to be predictive of stroke risk, although less so in the elderly. Although the number of studies on stroke (apart from cardiovascular disease) is limited, there is a significant graded increase in stroke risk within the low-to-high normal range of C-reactive protein. C-reactive protein is readily amenable to treatment with anti-inflammatory drugs, such as aspirin and statins. New and increasingly available high-sensitivity assays may make C-reactive protein a standard screening tool for cardiovascular disease.
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PMID:C-reactive protein, cardiovascular disease and stroke: new roles for an old biomarker. 1585 80

In different study populations, several studies have shown that modest C-reactive protein elevation, in the range of apparently healthy individuals, is a strong predictor of future vascular events. Willcox and colleagues summarize the epidemiological and clinical observations that have led to the enthusiastic suggestion that determination of serum C-reactive protein levels could also be used as an adjunct for risk assessment in primary and secondary prevention of cerebrovascular disease. Currently, high-sensitivity C-reactive protein assays as a screening test to ascertain individuals at risk of cerebrovascular disease does not provide an accurate determination of the risk of stroke likelihood, and adequate evidence that early detection improves health outcomes and that an early intervention is likely to have a beneficial impact. High-sensitivity C-reactive protein assays as a screening test, only provide inadequate evidence to be considered as an effective cerebrovascular screening test, especially in the elderly.
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PMID:Clinical application of C-reactive protein in stroke prevention: bright and dark sides of the moon. 1585 46

Acute phase proteins (APPs) have been implicated to play important roles during both acute and chronic inflammatory processes in different diseases including ischemic stroke. Though there are several studies showing the importance of APPs as inflammation markers in acute ischemic stroke (AIS), the time course of these proteins during acute phase of AIS is not well known. Thus, the aim of this study was to show the changes in plasma levels of six APPs (i.e., haptoglobin [Hp], ceruloplasmin [Cp], high-sensitive C-reactive protein [h-CRP], fibrinogen, complement 3 [C3] and complement 4 [C4]) during the first 10 days after acute stroke. The study group consisted of 34 female and 19 male patients (n = 53; mean age 65 +/- 12 years), who had first acute ischemic stroke (AIS). An age-matched control group (n = 53; 32 female and 21 male subjects, mean age 62 +/- 6 years) was also included. To evaluate the plasma levels of six APPs, the blood samples of patients with AIS were withdrawn on admission (day 1), and after 3, 5 and 10 days, whereas only one measurement was performed in the control group. In addition, several cerebrovascular risk factors were determined. The peak levels of APPs were higher in the AIS group than the control group (p < 0.0001). In serial measurements, the levels of h-CRP, Hp, C3 and C4 showed alterations during 10 days after AIS (p < 0.0001, p < 0.05, p < 0.0001, p < 0.0001, respectively). The alterations in levels of fibrinogen and Cp were not statistically significant (p > 0.05). After stroke, h-CRP, C3 and fibrinogen reached their highest values on the third day, Cp and C4 on the fifth day, and Hp on the tenth day. The plasma levels of h-CRP correlated positively with other five APPs studied (p < 0.05). These findings support the importance of inflammation processes after stroke. We suggest that the differences in levels of APPs could be used in predicting the outcome of stroke patients.
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PMID:Assessment of acute phase proteins in acute ischemic stroke. 1588 64

Increasing evidence suggests that inflammation plays an important role in the development of both cardiovascular and cerebrovascular events. Recently C-reactive protein (CRP) levels have been reported to be a prognostic factor for cerebrovascular and cardiovascular events. The main objective of the study was to evaluate the prognostic value of CRP levels in a first ever ischaemic stroke at one month. All ischaemic stroke patients who were admitted to Hospital Universiti Kebangsaan Malaysia (HUKM) between May 2002 and July 2002 were eligible for the study. CRP levels were taken within 72 hours after an acute ischaemic stroke. The functional ability was assessed using the Barthel Index (BI) after one month of stroke. During the study period 84 patients were admitted to HUKM with the diagnosis of ischaemic stroke; 49 patients were enrolled and 35 were excluded. Twenty-nine patients (59.2%) had elevated CRP levels (median 1.64+/-3.07 mg/dL, range 0.06 to 16.21 mg/dL). Elevated CRP levels were found to be a predictor of severe functional disability (BI<5) and were also associated with larger infarcts. In conclusion, elevated CRP levels are associated with poorer functional outcome and predict a larger infarct size.
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PMID:The prognostic value of C-reactive protein (CRP) levels in patients with acute ischaemic stroke. 1588 66


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