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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the association between a persistent elevation of C-reactive protein (CRP) level and the presence or severity of ischemic heart disease (IHD) in patients with continuous ambulatory peritoneal dialysis (CAPD). Seventy-three patients, who were over 40 years old, underwent dipyridamole thallium single photon emission computed tomography (SPECT), and followed-up for more than 1 year were enrolled. We measured stored plasma for CRP every 3 months. Elevation of CRP was defined as greater than or equal to 5 mg/L and persistent elevation of CRP as elevated CRP levels that lasted longer than 6 months. Serum albumin, cholesterol, lipoprotein(a), and plasma fibrinogen were measured at 3 months after the start of CAPD. Twenty-six patients showed an elevation of CRP for more than 6 months during the follow-up period. Twenty-eight patients showed positive findings on thallium SPECT. Coronary angiography showed significant stenosis (narrowing of the diameter more than 50%) in 23 of the 25 patients studied. Seventeen (65%) of 26 patients who had an elevated CRP level for longer than 6 months had positive thallium SPECT. The presence of diabetes, albumin, fibrinogen, and the presence of a persistent elevation of CRP were different between the patients with positive (n = 28) or negative thallium SPECT (n = 45). A multivariate logistic regression analysis showed that a persistent elevation of CRP is the only predictor of positive thallium SPECT (P = 0.002). There was a tendency of association, although it was not statistically significant, between the persistence of CRP elevation and the severity of IHD (P = 0.066). Three of 9 patients who had a persistent elevation of CRP and a negative thallium SPECT had a history of cerebral infarction or peripheral vascular disease. Therefore, 77% (20/26) of an elevated CRP level that lasted longer than 6 months can be explained by the presence of IHD or other atherosclerotic vascular disease. In conclusion, a persistent elevation of CRP level in patients with CAPD was strongly associated with IHD. For patients who have a persistent elevation of CRP without an apparent cause, we recommend a workup for IHD or other atherosclerotic cardiovascular disease.
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PMID:Persistent elevation of C-reactive protein and ischemic heart disease in patients with continuous ambulatory peritoneal dialysis. 1184 Mar 75

Interventions to modify cardiovascular risk factors have the greatest benefit in individuals at greatest risk of a cardiovascular event, not necessarily those with the most extreme levels of any particular risk factor. Patients with vascular disease are readily identified, but risk calculation in those without disease provides a way of integrating several risk factors to identify individuals at greatest risk. Equations have been derived from different epidemiological studies (Framingham, PROCAM, etc.) to estimate the risk of different clinical end-points [coronary heart disease (CHD) or cardiovascular disease (CVD)]. Some algorithms have been adapted to produce risk charts' or 'tables'; others have been modified to incorporate additional risk factors. Current UK guidelines all endorse calculation of CHD risk using the Framingham algorithm. This predicts risk well for some North European populations but less reliably in low-risk populations. It does not incorporate some risk factors, including serum triglycerides, family history, C-reactive protein, or homocysteine. Risk calculation should not be used in those with evidence of vascular disease, genetic hyperlipidaemia or a strong family history of CHD, and should be interpreted with caution in non-Caucasians. Measurement of high-density lipoprotein (HDL)-cholesterol is essential for accurate risk calculation. This has significant cost and workload implications for the laboratory. The way a laboratory reports results should be designed in such a way as to facilitate simple and accurate risk calculation.
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PMID:HDL-cholesterol and cardiac disease: which table to use? 1185 84

The concept of risk assessment and reduction, introduced initially by the Framingham Heart Study and refined in other models, forms the cornerstone of preventive cardiology. Risk factor assessment determines the therapeutic strategy, because the intensity of preventive intervention is tailored to the patient's risk of coronary heart disease. The conventional risk factors for coronary heart disease include elevated serum total cholesterol and LDL cholesterol, low HDL cholesterol, elevated blood pressure, cigarette smoking, diabetes, vascular disease, menopausal status (women only), and age. Aggressive risk factor reduction, formerly used exclusively in secondary prevention, may be pivotal to optimal patient management in high-risk primary prevention. A number of noninvasive imaging modalities have the potential to measure and to monitor atherosclerosis in asymptomatic individuals and include exercise ECG testing, electron beam computed tomography, magnetic resonance coronary angiography, positron emission tomography, ankle-brachial index, and B-mode ultrasound. Novel serum markers, including C-reactive protein and homocysteine, have the ability to gauge risk in the individual patient. Systemic therapy for risk reduction in primary prevention may be preferable to local therapy (eg, angioplasty and bypass) and may more effectively prevent acute coronary events than these more invasive approaches.
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PMID:New tools for coronary risk assessment: what are their advantages and limitations? 1185 32

We have assessed the prevalence of heparin-platelet factor 4 antibodies in a group of 100 patients on chronic intermittent hemodialysis with repeated exposure to heparin in order to establish the clinical significance of an immunological response to heparin. Heparin-induced platelet reactivity was studied in a subgroup of 86 patients. Routine laboratory parameters such as plasma C-reactive protein, albumin and immunoglobulins were included. Clinical endpoints were thrombosis in blood access, change of blood access, other thromboembolic events, bleeding complications, falling platelet count, and ischemic vascular disease or death within 1 year of blood sampling. Blood access thrombosis was a frequent complication (26%), often leading to change of dialysis blood access (21%). Antibodies were detected in 3-6% of hemodialysis patients and antibody levels correlated to blood access thrombosis and change of access (p<0.05). An unexpected finding was that of increased heparin-induced platelet reactivity in 36% of the control group of 24 uremic patients prior to dialysis or exposure to heparin. The findings suggest that antibodies to heparin-platelet factor 4 may contribute to hypercoagulability during hemodialysis, leading to thrombotic complications in affected patients.
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PMID:The presence of heparin-platelet factor 4 antibodies as a marker of hypercoagulability during hemodialysis. 1191 67

Multiple factors contribute to the development of chronic allograft nephropathy (CAN) in renal transplant recipients, and atherogenesis is considered to be an important pathologic process contributing to the development of this disease. There is growing acknowledgment of the role of inflammation in the pathogenesis of atherosclerosis, and markers of inflammation, such as C-reactive protein (CRP), have been shown to predict atherosclerotic vascular disease in the general and end-stage renal disease populations. In this pilot study, we hypothesized that elevations in pretransplant concentrations of CRP predict an increased incidence of CAN after renal transplantation. This case-control study compared pretransplant CRP levels in patients with allograft dysfunction and biopsy-proven CAN (n = 15) with a control group of transplant recipients with normal allograft function (n = 43). The median concentration of serum CRP was significantly higher in the CAN versus the control patients (13.1 +/- 3.9 mg/L versus 3.5 +/- 2.5 mg/L; P = 0.01). This difference was sustained when restricting to patients who did not experience acute rejection. When dividing the patients into tertiles based on CRP concentration, the adjusted risk of CAN increased more than threefold with each increment in CRP by tertile (adjusted odds ratio, 3.16; P = 0.03). The findings of our pilot study show an association between pretransplant elevations of CRP and CAN in end-stage renal disease patients who go on to receive a renal transplant. Cohort studies in larger groups of transplant patients are needed to confirm a causal pathway between pretransplant inflammation, atherogenesis, and CAN.
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PMID:Pretransplant serum C-reactive protein and the risk of chronic allograft nephropathy in renal transplant recipients: a pilot case-control study. 1197 55

Because cardiovascular disease (CVD) is the most important cause of death in women in the United States, it is imperative that the main risk factors for CVD in women be identified and modified. The risk factors that have the strongest impact on the incidence of CVD in women are not necessarily the same as those for men. The risk for women increases at menopause, most likely because of the decrease in levels of circulating estrogen. The classic risk factor for CVD is altered lipid levels. In middle-aged women, elevated low-density lipoprotein cholesterol levels are somewhat less important relative to lowered levels of high-density lipoprotein cholesterol and elevated triglyceride levels as independent risk factors. The metabolic syndrome, which encompasses a range of conditions known to be CVD risk factors, also has a greater impact on the incidence of CVD in women than in men. Various emerging risk factors appear to be important indicators for vascular disease in women, including C-reactive protein, homocysteine, and lipoprotein(a) levels. Many of these risk factors are affected by hormone replacement therapy, which may diminish CVD risk in postmenopausal women. Because of the complex origin of CVD, it is important to target the full array of risk factors for modification, rather than focusing on a single factor or treatment to the exclusion of other important markers.
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PMID:Risk factors for coronary artery disease in women. 1208 1

Obesity is increasing in prevalence worldwide and in all age groups. In nonpregnant individuals, obesity is associated with dyslipidemia; hyperinsulinemia; vascular dysfunction; and, more recently, low-grade chronic inflammation. However, whether such effects are sustained during pregnancy has been sparsely investigated but is important to establish, given the association of maternal obesity with numerous adverse metabolic and vascular consequences. We consecutively recruited 47 healthy women in the third trimester of pregnancy and divided the participants into 2 groups, lean [n = 24; median body mass index (BMI), 22.1 kg/m(2)] and obese (n = 23; median BMI, 31.0 kg/m(2)) around the median first trimester BMI. The age, parity, and smoking history were comparable in both groups. A detailed panel of metabolic and inflammatory parameters was measured and an in vivo assessment of endothelial-dependent and -independent microvascular function made using laser doppler imaging. Although low-density lipoprotein cholesterol and glycosylated hemoglobin were similar, fasting triglyceride concentrations were higher [2.70 (interquartile range, 2.3-3.21) vs. 2.20 (IQ range, 2.0-2.6) mmol/liter, P = 0.02] and high-density lipoprotein concentrations were lower [1.55 (IQ range, 1.1-1.7) vs. 1.72 (IQ range, 1.4-2.0) mmol/liter, P = 0.02] in the obese group. Leptin [55.6 (range, 45-64.4) ng/ml vs. 23.8 (range, 13.2-35.2) ng/ml, P < 0.0001] and fasting insulin [14.5 (range, 11.4-27.3) vs. 6.5 (range, 4.6-9.7) mU/liter, P < 0.0001] levels were more than double. Similarly, levels of inflammatory parameters, IL-6 [3.15 (range, 2.4-3.5) vs. 2.1 (range, 1.73-2.85) pg/ml, P = 0.003], and sensitive C-reactive protein [4.45 (range, 2.9-6.6) vs. 2.25 (range, 0.92-3.65) mg/ml, P = 0.0015] were also substantially elevated. Both endothelial-dependent and -independent vasodilatory responses were significantly reduced in the obese group (P = 0.0003 and P = 0.02, respectively, ANOVA) and systolic blood pressure was higher (P = 0.01). Metabolic factors, C-reactive protein (r = 0.289, P = 0.049), and insulin (r = 0.339, P = 0.02) were related inversely to endothelial-dependent function. These comprehensive data demonstrate that, as in nonpregnant obese individuals, obesity in pregnancy is associated not only with marked hyperinsulinemia (without necessarily glucose dysregulation) and dyslipidemia but also impaired endothelial function, higher blood pressure, and inflammatory up-regulation. Such a spectrum of risk factors may contribute to maternal complications in obese women and, as a result, influence fetal programming of adult vascular disease. Clearly, these data provide further rationale to examine the potential benefits of preconceptual weight loss and antenatal exercise.
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PMID:Maternal obesity is associated with dysregulation of metabolic, vascular, and inflammatory pathways. 1221 76

Calcification complications are frequent among long-term dialysis patients. However, the prognostic implication of cardiac valve calcification in this population is not known. This study aimed to determine if cardiac valve calcification predicts mortality in long-term dialysis patients. Baseline echocardiography was performed in 192 patients (mean +/- SD age, 55 +/- 12 yr) on continuous ambulatory peritoneal dialysis (mean +/- SD duration of dialysis, 39 +/- 31 mo) to screen for calcification of the aortic valve, mitral valve, or both. Valvular calcification was present in 62 patients. During the mean follow-up of 17.9 mo (range, 0.6 to 33.9 mo), 46 deaths (50% of cardiovascular causes) were observed. Overall 1-yr survival was 70% and 93% for patients with and without valvular calcification (P < 0.0001, log-rank test). Cardiovascular mortality was 22% and 3% for patients with and without valvular calcification (P < 0.0001). Multivariable Cox regression analysis showed that cardiac valve calcification was predictive of an increased all-cause mortality (hazard ratio [HR], 2.50; 95% CI, 1.32 to 4.76; P = 0.005) and cardiovascular death (HR 5.39; 95% CI, 2.16 to 13.48; P = 0.0003) independent of age, male gender, dialysis duration, C-reactive protein, diabetes, and atherosclerotic vascular disease. Eighty-nine percent of patients with both valvular calcification and atherosclerotic vascular disease, 23% of patients with valvular calcification only, 21% of patients with atherosclerotic vascular disease only, and 13% of patients with neither complication died at 1-yr (P < 0.0005). The cardiovascular death rate was 85% for patients with both complications, 13% for patients with valvular calcification only, 14% for patients with atherosclerotic vascular disease only, and 5% for those with neither complication (P < 0.0005). The number of calcified valves was associated with all-cause mortality (P < 0.0005) and cardiovascular death (P < 0.0005). One-year all-cause mortality was 57% for patients with both aortic and mitral valves calcified, 40% for those with either valve calcified, and 15% for those with neither valve calcified. In conclusion, cardiac valve calcification is a powerful predictor for mortality and cardiovascular deaths in long-term dialysis patients. Valvular calcification by itself has similar prognostic importance as the presence of atherosclerotic vascular disease. Its coexistence with other atherosclerotic complications indicates more severe disease and has the worst outcome.
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PMID:Cardiac valve calcification as an important predictor for all-cause mortality and cardiovascular mortality in long-term peritoneal dialysis patients: a prospective study. 1250 48

Malnutrition in end-stage renal disease (ESRD) is characterized by hypoalbuminemia, decreased serum creatinine and prealbumin, and decreased subjective global assessment (SGA) scores. Markers of malnutrition predict mortality and correlate closely with inflammatory markers, including serum cytokines and acute phase proteins. After multiple regression analysis, markers of inflammation become stronger predictors of mortality than nutritional markers, suggesting that malnutrition is a result of inflammation. The etiology of inflammation is variable and includes vascular access infection, bioincompatible dialyzers, back filtration of nonsterile dialysate, periodontal disease, urinary tract infections, and other pyogenic infections. Renal failure also may serve to promote inflammation through protein carbonylation. Differences in care patterns of ESRD patients and genetics may contribute to inflammation as evidenced by lower levels of C-reactive protein (CRP) in Asian populations. Inflammation results in loss of muscle mass and hypoalbuminemia as a consequence of its decreased synthesis and increased catabolism. Vascular disease occurs partly because of changes in lipoprotein structure and function, including oxidation of low-density lipoprotein (LDL) and modification of high-density lipoprotein (HDL) by serum amyloid A (SAA) and loss of apolipoprotein A-I. Leukocyte adhesion is promoted by changes in endothelial structure and function, whereas plasma proteins associated with cardiovascular disease (fibrinogen, lipoprotein[a]; SAA) are increased. Consequences of inflammation in ESRD patients include muscle wasting, erythropoetin resistance, and vascular disease. Whereas improvements in nutrition can increase serum albumin and creatinine levels, identification and removal of the underlying cause of inflammation should be one treatment goal.
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PMID:Inflammation in ESRD: causes and potential consequences. 1267 42

A growing body of evidence supports the hypothesis that C-reactive protein (CRP) is a marker of inflammation in coronary artery disease. The purpose of the present study was to test the hypothesis that CRP correlates with macrophage accumulation during the initial stages of coronary vascular disease. Adult male pigs were fed a normal chow (NF) or a high-fat high-cholesterol (HF) diet for 20 wk. After 20 wk, blood was collected for analyses of interleukin-6 (IL-6), CRP, and lipids. After blood collection, the pigs were euthanized and the right coronary arteries (RCA) were harvested and fixed in neutral buffered formalin. Paraffin-embedded sections of RCA were stained immunohistochemically for CRP, scavenger receptor A (SRA), and monocyte chemoattractant protein-1 (MCP-1). All cholesterol fractions were elevated in the HF vs. the NF group (P < 0.05). There was little or no positive staining for CRP, SRA, or MCP-1 in the RCA of NF pigs, but there was extensive staining in lipidladen macrophage foam cells in the HF pigs. Double staining revealed colocalization of CRP with SRA and CRP with MCP-1 in foam cells. Serum IL-6 was below the assay detection limit in all pigs. Serum CRP correlated directly with plasma total cholesterol (R = 0.727, P = 0.041) and accumulation of SRA-positive macrophages (R = 0.938, P < 0.001) in RCA of HF pigs. We conclude that serum CRP correlates with macrophage accumulation and coronary artery disease in hypercholesterolemic pigs.
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PMID:C-reactive protein correlates with macrophage accumulation in coronary arteries of hypercholesterolemic pigs. 1275 76


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