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

Although the metabolic syndrome (MetS) is positively associated with high-sensitivity C-reactive protein (hsCRP), negatively associated with N-terminal pro-brain natriuretic peptide (Nt-proBNP) and inconsequently related to urine albumin/creatinine ratio (UACR) they are all associated with cardiovascular events. Therefore, we wanted to determine the influence of MetS on the predictive values of UACR, hsCRP and Nt-proBNP. On the basis of the definition of MetS by the International Diabetes Federation, a Danish population sample of 1983 apparently healthy subjects was divided into three groups: 530 subjects without any elements of MetS, 1093 subjects with some elements of MetS and 360 subjects with MetS. During the following 9.5 years the composite end point of cardiovascular death, non-fatal myocardial infarction or stroke (composite cardiovascular end point, CEP) occurred in 204 subjects. In Cox-regression analyses adjusting for age, gender and smoking, all three cardiovascular risk markers predicted CEP independently of MetS. Despite no significant interaction with MetS, high log(hsCRP) was associated with CEP primarily in subjects without any elements of MetS (hazard ratio (HR)=4.5 (1.5-14.0), P<0.01), log(Nt-proBNP) primarily in subjects with some elements of MetS (HR=3.0 (1.6-5.6), P<0.01), and logUACR independently of elements of MetS. Pre-specified gender-adjusted (men/women) cutoff values of hsCRP > or = 6.0/7.3 mg l(-1) predicted CEP in subjects without elements of MetS with positive and predictive values of 11.5 and 98%, respectively. UACR > or = 0.73/1.06 mg mmol(-1) predicted CEP in subjects with MetS with positive and predictive values of 23.5 and 93%, respectively. In apparently healthy subjects, high hsCRP was associated with CEP primarily in subjects without MetS, high Nt-proBNP in subjects with elements of MetS and UACR independently of MetS.
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PMID:Impact of the metabolic syndrome on the predictive values of new risk markers in the general population. 1852 12

More than 40% of patients hospitalized with heart failure have preserved left ventricular ejection fraction (HF-PLVEF) and are at high risk for cardiovascular (CV) events. The purpose of this study was to determine the value of N-terminal pro-brain natriuretic peptide (NT-proBNP) and brain natriuretic peptide (BNP) in predicting CV outcomes in patients with HF-PLVEF. Participants with an ejection fraction >40% in the prospective CHARM Echocardiographic Substudy were included in this analysis. Plasma NT-proBNP levels were measured, and 2 cut-offs were selected prospectively at 300 pg/ml and 600 pg/ml. BNP cut-off was set at 100 pg/ml. Clinical characteristics were recorded, and systolic and diastolic function were evaluated by echocardiography. The primary substudy outcome was the composite of CV mortality, hospitalization for heart failure, and myocardial infarction or stroke. A total of 181 patients were included, and there were 17 primary CV events (9.4%) during a median follow-up time of 524 days. In a model including clinical characteristics, echocardiographic measures, and BNP or NT-proBNP, the composite CV event outcome was best predicted by NT-proBNP >300 pg/ml (hazard ratio 5.8, 95% confidence intervals [CI] 1.3 to 26.4, p = 0.02) and moderate or severe diastolic dysfunction on echocardiography. When NT-proBNP >600 pg/ml was used in the model, it was the sole independent predictor of primary CV events (hazard ratio 8.0, 95% CI 2.6 to 24.8, p = 0.0003) as was BNP >100 pg/ml (hazard ratio 3.1, 95% CI 1.2 to 8.2, p = 0.02) in the BNP model. In conclusion, both elevated NT-proBNP and BNP are strong independent predictors of clinical events in patients with HF-PLVEF.
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PMID:Usefulness of N-terminal pro-brain natriuretic Peptide and brain natriuretic peptide to predict cardiovascular outcomes in patients with heart failure and preserved left ventricular ejection fraction. 1877 98

The study aim was to determine whether urine albumin/creatinine ratio (UACR), high-sensitivity C-reactive protein (hsCRP) or N-terminal pro-brain natriuretic peptide (Nt-proBNP) added to risk prediction based on HeartScore and history of diabetes or cardiovascular disease. A Danish population sample of 2460 individuals was divided in three groups: 472 subjects receiving cardiovascular medication or having history of diabetes, prior myocardial infarction or stroke, 559 high-risk subjects with a 10-year risk of cardiovascular death above 5% as estimated by HeartScore, and 1429 low-moderate risk subjects with estimated risk below 5%. During the following 9.5 years the composite end point of cardiovascular death, non-fatal myocardial infarction or stroke (CEP) occurred in 204 subjects. CEP was predicted in all three groups by UACR (HRs: 2.1, 2.1 and 2.3 per 10-fold increase, all P<0.001) or by hsCRP (HRs: 1.9, 1.9 and 1.7 per 10-fold increase, all P<0.05), but not by Nt-proBNP (HRs: 1.1, 2.6 and 3.7 per 10-fold increase, last two P<0.001) (P<0.05 for interaction). In the low-moderate risk group, pre-specified gender adjusted (men/women) cutoff values of UACR> or =0.73/1.06 mg mmol(-1) or hsCRP> or =6.0/7.3 mg l(-1) identified a subgroup of 16% who experienced one-third of the CEPs. In the patient group, combined absence of high UACR and high Nt-proBNP> or =110/164 pg ml(-1) (men/women) identified a subgroup of 52% who experienced only 15% of the CEPs. Additional use of UACR and hsCRP in subjects with low-moderate risk and UACR and Nt-proBNP in subjects with known diabetes of cardiovascular disease changed HeartScore risk classification significantly in 19% of the population.
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PMID:New risk markers may change the HeartScore risk classification significantly in one-fifth of the population. 1878 34

Accelerated atherosclerosis can lead to an increased prevalence of coronary artery disease, heart failure, brain stroke and peripheral arterial disease. Thus, subjects with chronic renal failure are exposed to increased morbidity and mortality from cardiovascular events. A strong and pervasive link exists between kidney failure and cardiac disease. A variety of individual biomarkers have been evaluated and several have been found to successfully predict the outcome in patients with kidney disease. These include markers of myocardial necrosis, such as cardiac troponin T and I, markers of heart failure, such as B-type of natriuretic peptide and its associated inactive N-terminal fragment, markers of systemic inflammation--C-reactive protein, and an endogenous inhibitor of nitric oxide synthase-asymmetric dimethyl arginin. Increased concentrations of C-reactive protein, B-type of natriuretic peptide, asymmetric dimethyl arginine, and troponin predict a high risk of cardiovascular mortality as well as a mortality due to other causes in patients with chronic renal failure or end stage renal disease (Tab. 1, Ref. 33). Full Text (Free, PDF) www.bmj.sk.
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PMID:Cardiac biomarkers and chronic renal diseases. 1883 40

We tested the hypothesis that plasma brain natriuretic peptide (BNP) levels are elevated in patients with acute cerebrovascular diseases (CVD) independent of heart disease, and reflect CVD severity. After careful evaluations for heart disease, the study included 79 consecutive patients with CVD without any evidence of heart disease admitted within 48 h after onset (71+/-10 years), and 26 control subjects without CVD (CT, 67+/-12 years). Ischemic stroke subtypes were defined by the TOAST classification. Large-artery atherosclerosis (LAA, n=27), small-artery occlusion (SAO, n=27), and intracerebral hemorrhage (ICH, n=25) were included. The plasma BNP levels were measured at admission and 1 month later. Stroke severity and brain infarct volume were evaluated. There were no significant differences in the clinical profiles including echocardiographic parameters among the groups. The plasma BNP level (pg/mL) upon admission was higher in LAA (70.6+/-53.9) than in SAO (38.2+/-28.4) and CT (28.5+/-19.9) (both p<0.05). The level in ICH (47.3+/-28.6) was not significantly different from that in CT. The BNP level in ischemic stroke was positively correlated with the NIH Stroke Scale (NIHSS) (rho=0.42, p<0.05) and infarct volume (r=0.34, p<0.05). Brain infarct volume and NIHSS were independent contributors to the plasma BNP level in ischemic stroke. One month later, the BNP level was significantly decreased and was similar in all CVD groups. The plasma BNP level transiently increased in patients with LAA independently of heart disease, and reflected infarct volume and the severity of acute ischemic stroke.
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PMID:Elevated plasma brain natriuretic peptide levels independent of heart disease in acute ischemic stroke: correlation with stroke severity. 1897 47

Although the presence of abnormal late gadolinium enhancement (LGE) in cardiac amyloidosis has been well established, its prognostic implication and utility to identify cardiac involvement in patients with systemic amyloidosis is unknown. The aim of this study was to assess the diagnostic and prognostic significance of cardiovascular magnetic resonance imaging in patients with amyloid light-chain amyloidosis but unknown cardiac involvement. Cardiovascular magnetic resonance imaging with LGE was performed in 28 patients with systemic amyloidosis. The presence of cardiac amyloidosis was determined by separate clinical evaluation. The performance of LGE for the prediction of cardiac amyloidosis and prognostic implications of LGE were determined. LGE was observed in 19 patients (68%). The sensitivity, specificity, positive predictive value, and negative predictive value of LGE for the identification of clinical cardiac involvement were 86%, 86%, 95%, and 67%, respectively. During a median follow-up period of 29 months, there were 5 deaths (82% survival). LGE itself did not predict survival (p = 0.62). LGE volume was positively correlated with serum level of B-type natriuretic peptide (BNP; R = 0.64, p < or =0.001), and in multivariate analysis, LGE volume proved the strongest independent predictor of BNP. BNP was correlated with New York Heart Association class (p = 0.03). Reduced right ventricular end-diastolic volume (p <0.01) and stroke volume (p = 0.02) were associated with mortality. In conclusion, in patients with systemic amyloidosis, LGE is highly sensitive and specific for the identification of cardiac involvement but does not predict survival. LGE is strongly correlated with heart failure severity as assessed by BNP.
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PMID:Diagnostic and prognostic utility of cardiovascular magnetic resonance imaging in light-chain cardiac amyloidosis. 1919 18

We tested the hypothesis that, in adults with essential hypertension, plasma levels of midregional proatrial natriuretic peptide (MR-proANP) are associated with target organ damage. MR-proANP is a newly described stable fragment of N-terminal proatrial natriuretic peptide. Participants included 1,919 adults with hypertension identified from the community (1,037 African-Americans, 65 +/- 9 years of age, 72% women; 882 non-Hispanic whites, 61 +/- 9 years of age, 55% women). We measured MR-proANP by an immunoluminometric assay. Measurements of target organ damage included the ankle-brachial index (ABI), urinary albumin-creatinine ratio (UACR), and left ventricular (LV) mass (available only in African-Americans). Generalized estimating equations were used to assess whether plasma MR-proANP was associated with measurements of target organ damage, independent of potential confounding variables. In African-Americans, higher MR-proANP was significantly associated with lower ABI (p <0.0001), higher UACR (p <0.0001), and greater LV mass (indexed to height to the power of 2.7, p <0.0001). After adjustment for age, gender, body mass index, systolic blood pressure, estimated glomerular filtration rate, smoking history, diabetes mellitus, total and high-density lipoprotein cholesterols, medication (blood pressure lowering, statin, and aspirin) use, and previous myocardial infarction or stroke, higher MR-proANP levels remained significantly associated with lower ABI (p = 0.01), higher UACR (p = 0.0007), and greater LV mass index (p <0.0001). In non-Hispanic whites, higher MR-proANP levels were significantly associated with lower ABI (p = 0.002) and greater UACR (p = 0.001), but not after adjustment for the covariates listed earlier. In conclusion, plasma MR-proANP may be a marker of target organ damage in the setting of hypertension, especially in African-Americans.
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PMID:Relation of plasma midregional proatrial natriuretic peptide to target organ damage in adults with systemic hypertension. 1940 68

Acute-phase levels of B-type natriuretic peptide (BNP) and the N-terminal fragment of the BNP prohormone (NT-pro-BNP) have been associated with mortality when measured in patients with an acute ischemic stroke; however, data regarding the longer-term value of NT-pro-BNP for long-term prognostication after ischemic stroke are limited. Two hundred sixteen patients (mean age 67 +/- 13 years) with acute ischemic stroke were seen 6 months after index admission at which time a structured evaluation including measurement of plasma NT-pro-BNP was performed. Patients were followed for 45 months, with all-cause mortality as the clinical end point. Median NT-pro-BNP concentration for the entire group was 147 pg/ml (10th to 90th percentiles 37 to 869). At follow-up 45 patients (21%) had died. NT-pro-BNP concentrations were significantly higher in decedents (308 pg/ml, 10th to 90th percentiles 74 to 2,279) than in the 171 survivors (132 pg/ml, 10th to 90th percentiles 35 to 570, p <0.001). Patients with NT-pro-BNP < or =147 pg/ml had a significantly improved survival rate on univariate analysis (p <0.001). In multivariate analysis after adjustment for age, stroke severity, heart and renal failures, levels of NT-pro-BNP were an independent predictor of mortality >6 months after stroke (adjusted hazard ratio 1.5, 95% confidence interval 1.1 to 1.9, p = 0.005). In conclusion, NT-pro-BNP concentrations measured during the stable phase after acute ischemic stroke are strongly predictive of long-term mortality.
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PMID:Usefulness of natriuretic peptide testing for long-term risk assessment following acute ischemic stroke. 1957 62

Echocardiographically determined inappropriateness of left ventricular mass (LVM) is an independent risk factor for cardiovascular events. Although LV hypertrophy is associated with an increase in the plasma brain natriuretic peptide level and decreased LV diastolic filling, it is unknown whether the inappropriateness of LVM affects them. We studied 77 untreated hypertensive patients (49 men, 28 women, aged 59+/-12 years). The plasma brain natriuretic peptide level was measured, in addition to routine echo Doppler indexes of LV geometry and function. The appropriateness of LVM to cardiac workload was evaluated by the ratio of the observed LVM to the value predicted for individual sex, stroke work and height(2.7) (oLVM/pLVM). Multivariate analysis showed that the plasma brain natriuretic peptide level increased with LVM index but decreased when oLVM/pLVM increased. The ratio of the peak early diastolic flow velocity of mitral flow to the peak early diastolic velocity of mitral annulus (E/E') correlated not only with oLVM/pLVM but also with the LVM index (r=0.30, P<0.05; r=0.37, P<0.05, respectively). However, when a multiple stepwise regression analysis was carried out, only LVM index was determined to be a significant correlate of the E/E' ratio, indicating that the inappropriateness of LVM does not affect the E/E' ratio in hypertensive patients. Brain natriuretic peptide levels are influenced not only by the extent of LV hypertrophy but also by the inappropriateness of hypertrophy in untreated hypertensive patients. Diastolic filling is mostly affected by the extent of LV hypertrophy and not by the appropriateness of hypertrophy.
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PMID:Inappropriateness of ventricular hypertrophy is important as a determinant of BNP but not of diastolic filling in untreated hypertensive patients. 1966 18

Taurine neuroinhibitory features have suggested its potential for neuroprotection. The aim of the present study was to assess whether it prevents or counteracts brain ischemia and reperfusion-induced cell injury. Rat brain cortical slices were subjected to oxygen/glucose deprivation and reperfusion. Tissue damage was assessed by measuring the release of glutamate and lactate dehydrogenase (LDH) during reperfusion and by determining final tissue water gain, taken as an index of cell swelling. When added during the reperfusion period taurine did not significantly affect oxygen/glucose deprivation-induced LDH and glutamate release, while it antagonised tissue water gain in a concentration-dependent manner (IC(50)=46.5 microM). The latter effect was antagonised by 50% when a taurine transport inhibitor, 2-(guanidino)ethanesulphonic acid (GES), or a GABA(A) receptor antagonist, bicuculline, was added together with taurine, while it was completely abolished when both GES and bicuculline or the volume-sensitive outwardly rectifying (VSOR) Cl(-) channel blocker, 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), was used. On the contrary, when present throughout the entire experiment, taurine significantly reduced oxygen/glucose deprivation-induced LDH and glutamate release with a maximal effect (45% reduction) between 5 and 20 mM. Taurine antagonised also tissue water gain according to a "U-shaped" concentration-response curve, which was significant within the range of 0.01-1.0 mM concentration. This effect was partially counteracted by GES as well as by bicuculline and fully reverted by NPPB. In conclusion, since brain edema is a major contributing factor to morbidity and mortality in stroke, the present findings give the rational basis for assessing taurine efficacy in reducing brain edema in vivo.
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PMID:Protection by taurine of rat brain cortical slices against oxygen glucose deprivation- and reoxygenation-induced damage. 1969 42


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