Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased levels of von Willebrand factor (vWf) and C-reactive protein (CRP) predict cardiovascular mortality in selected populations. It is uncertain whether vWf and CRP predict mortality in a general population and whether vWf and CRP predict mortality through similar pathways. This study investigated the association of vWf and CRP with cardiovascular and all-cause mortality among diabetic and nondiabetic subjects. An age-, sex-, and glucose tolerance-stratified sample (n=631) of a population-based cohort aged 50 to 75 years was followed prospectively for 5 years. After 5 years of follow-up, 58 subjects had died (24 of cardiovascular causes). vWf (>1.56 IU/mL) and CRP (>2.84 mg/L) levels in the upper tertile were associated with, respectively, a 3- and 2-fold increase in cardiovascular mortality after adjustment for age, sex, and glucose tolerance status. Analyses in nondiabetic and diabetic subjects separately gave similar results. After further adjustment for hypertension, levels of HDL cholesterol and triglyceride, smoking habits, ischemic heart disease, and peripheral arterial disease, the relative risks (RRs) were 3.0 (95% CI 1.2 to 7.9) for vWf and 1.4 (95% CI 0.6 to 3.5) for CRP. When both vWf and CRP were included in the latter multivariate analysis, the RRs were 3.0 (95% CI 1.1 to 7.9) for vWf and 1.3 (95% CI 0.5 to 3.4) for CRP. The association between vWf and risk of cardiovascular mortality was independent of blood group (O versus non-O) and, moreover, similar among subjects with different blood groups. Repeating the analyses for all-cause mortality gave similar results for CRP. For vWf, the RR was 2.0 (95% CI 1.1 to 3.5) after adjustment for all other risk factors. Increased levels of vWf are independently associated with cardiovascular and all-cause mortality in both diabetic and nondiabetic subjects. The association between increased levels of CRP and cardiovascular mortality was partly explained by other risk factors. Mutual adjustment of vWf and CRP did not markedly change the results, favoring the hypothesis that vWf and CRP predict mortality through different pathways.
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PMID:von Willebrand factor, C-reactive protein, and 5-year mortality in diabetic and nondiabetic subjects: the Hoorn Study. 1059 89

In recent years it has been established that inflammation is a key mechanism in the pathogenesis of atherosclerosis and in coronary artery disease progression. Inflammation is a host response to a wide variety of tissue injuries. A persistent or continually repeated insult will lead to chronic inflammation which may result in tissue destruction and/or loss of normal organ function. Atherosclerosis and other pathologies involving inflammation are associated with increased levels of cytokines, which in turn raise acute-phase proteins levels in blood (acute inflammation markers, i.e. fibrinogen and C-reactive protein). It has been shown recently that concentrations of these proteins are higher in individuals at increased risk of developing cardiac events in the years to come. This is true both in apparently healthy men and women and in ischaemic heart disease patients. CRP is currently the inflammatory marker which appears to have captured the investigators' attention around the globe. In this report we review the current data on the relationship between atherosclerosis and inflammation, with special attention to cytokines and acute phase reactants. The use of acute phase reactants as prognostic risk markers in ischaemic heart disease is also discussed.
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PMID:[Ischemic cardiopathy: inflammation markers and the cardiovascular risk]. 1061 9

We found a novel G-->C change at nucleotide 1059 within exon 2 of the CRP gene encoding the C-reactive protein. The CRP 1059G/C polymorphism could be detected by digestion with endonuclease MaeIII. The frequency of the CRP 1059C allele was 0.109 in Caucasians, but it was absent from Canadian Oji-Cree. Because of the importance of the CRP gene product in inflammation and its recent association with ischemic heart disease syndromes, this polymorphism may be useful in the association studies of atherosclerosis and its related phenotypes.
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PMID:Human C-reactive protein (CRP) 1059G/C polymorphism. 1072 74

The endothelium plays a crucial role in the process of atherosclerotic disease by its regulatory functions on the vasculature, such as control of vasomotor tone, local hemostasis and proliferative processes. Dysfunction of endothelial vasoreactivity contributes to reduced myocardial blood supply and, therefore, might promote myocardial ischemia. To control vasomotor tone, the endothelium releases a variety of substances such as prostacyclin, hyperpolarizing factor, endothelin and, most importantly, nitric oxide (NO). Endothelium-dependent vasodilation is impaired in patients with environmental or genetic risk factors for atherosclerotic disease, such as hypercholesterolemia, mainly due to increased oxidative stress produced by superoxide anions, which rapidly inactivate nitric oxide. Experimentally, an imbalance between nitric oxide and superoxide anions towards reduced nitric oxide bioavailability enhances migration of monocytes into the vessel wall and proliferation of smooth muscle cells. These oxidative processes, resembling a chronic inflammatory process, extending to the vessel wall, contribute to plaque architecture, e.g., by destabilization of fibrous caps. Indeed, long-term follow-up of patients with endothelial dysfunction demonstrated that impaired endothelium-dependent vasodilation is associated with increased cardiovascular event rates. Recent clinical data supported the role of endothelial dysfunction in patients with acute coronary syndrome and demonstrated a relation with elevated C-reactive protein levels, an unspecific marker of inflammation. Taken together, assessment of coronary endothelial vasoreactivity may serve as an index integrating the overall stress imposed by risk factors on the arterial wall and provides pivotal information, both as a diagnostic and prognostic tool in patients at risk for coronary heart disease.
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PMID:Atherosclerosis-associated endothelial dysfunction. 1115 99

About half of the patients presenting with myocardial infarction do not have the classic risk factors. This finding has stimulated a search for other factors that may be responsible and, when present, may help to predict which patients are at greatest risk for myocardial infarction and other cardiovascular events. With improved understanding of the pathogenesis of ischemic heart disease, new insights into potential markers of underlying atherosclerosis and cardiovascular risk have been gained. In recent years, data have accumulated demonstrating that certain markers of inflammation--both systemic and local--play a key role in the development of atherosclerosis. Specifically, elevated levels of one systemic marker of inflammation, C-reactive protein, are associated with an increased risk of cardiovascular disease events. Moreover, potentially important associations have been established between elevated markers of inflammation, such as C-reactive protein and increased efficacy of established therapies; and, in particular, lipid-lowering therapy with the hepatic hydroxymethylglutaryl coenzyme A reductase inhibitor pravastatin. This article discusses the pathogenesis of atherosclerosis, the role of endothelial dysfunction and plaque rupture, and evidence for the role of inflammation and reviews how therapy might reduce vascular inflammation.
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PMID:Inflammation and coronary heart disease: an overview. 1117 13

Mortality rates attributable to cerebrovascular and ischemic heart disease increase among older adults during the winter. Prothrombotic changes in the hemostatic system related to seasonal factors, such as ambient temperature changes, and winter acute respiratory tract infections, may contribute to this excess seasonal mortality. A prospective nested case-control study was conducted to assess the impact of winter acute respiratory tract infections on fibrinogen, factor VII, factor VIIa, D-dimer, prothrombin fragment 1.2, PAI-1, soluble P-selectin and C-reactive protein (CRP) in older adults. The change in laboratory parameters from baseline (fall) to the time of infection in both middle-aged and elderly individuals was compared with matched non-infected controls. In older adult participants with winter acute respiratory tract infections, significant increases occurred in fibrinogen and C-reactive protein, but not in any other markers. The mean fibrinogen increased 1.52 g/L (38%) and the mean CRP increased 37 mg/L (370%) over baseline (both p <0.001). In a multivariate analysis, both infection and season were associated with the increase in fibrinogen, but only infection was associated with the CRP increase. Old age magnified the increase in CRP but not in fibrinogen. Winter acute respiratory tract infections induce an exaggerated inflammatory response in older adults. The associated increase in fibrinogen, an independent risk factor for ischemic heart disease, may be partly responsible for the excess winter vascular mortality.
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PMID:Prothrombotic changes in hemostatic parameters and C-reactive protein in the elderly with winter acute respiratory tract infections. 1124 41

Plasma levels of C-reactive protein (CRP, a marker of the reactant plasma protein component of the inflammatory response) and of fibrin D-dimer (a marker of cross-linked fibrin turnover) have each been associated in recent studies with the risk of future ischemic heart disease (IHD). Previous experimental studies have shown that fibrin degradation products, including D-dimer, have effects on inflammatory processes and acute-phase protein responses. In the Speedwell Prospective Study, we therefore measured CRP and D-dimer levels in stored plasma samples from 1690 men aged 49 to 67 years who were followed-up for incident IHD for an average of 75+/-4 months (mean+/-SD) and studied their associations with each other, with baseline and incident IHD, and with IHD risk factors. CRP and D-dimer levels were each associated with age, plasma fibrinogen, smoking habit, and baseline evidence of IHD. CRP was associated with D-dimer (r=0.21, P<0.00001). On univariate analyses, both CRP and D-dimer were associated with incident IHD. The incidence of IHD increased with CRP independently of the level of D-dimer (P=0.0002) and also increased with D-dimer independently of the level of CRP (P=0.048). In multivariate analyses, inclusion of D-dimer and conventional risk factors reduced the strength of the association between CRP and incident IHD; likewise, inclusion of CRP and conventional risk factors reduced the strength of the association between D-dimer and incident IHD. We conclude that although these respective markers of inflammation and fibrin turnover show modest association with each other in middle-aged men, they may have additive associations with risk of incident IHD. Further larger studies are required to test this hypothesis.
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PMID:C-reactive protein, fibrin D-dimer, and incident ischemic heart disease in the Speedwell study: are inflammation and fibrin turnover linked in pathogenesis? 1130 79

C-reactive protein (CRP), the prototypic acute phase reactant and a sensitive marker of inflammation, consistently predicts new coronary events, including myocardial infarction and death, in patients with ischemic heart disease. The data are very consistent with regard to the long-term outcome, but in many studies are also significant for in-hospital events. The predictive value of CRP is, in the majority of the studies, independent of and additive to that of the troponins. Moreover recent data suggest that CRP may be a reliable marker of the risk of restenosis after percutaneous coronary interventions and that its levels can be modulated by statins. Taken together, all these data suggest that CRP, probably with different cut-offs, should be used as a marker of risk and as a guide to therapy in patients hospitalized for acute coronary syndromes and in outpatients suffering from ischemic heart disease.
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PMID:Clinical use of C-reactive protein for the prognostic stratification of patients with ischemic heart disease. 1130 27

Risk stratification of patients with acute coronary syndromes (ACS) is pivotal for correct allocation of health resources and for maximizing the benefit of available treatment modalities. However, clinical and electrocardiographic indicators of high risk lack sufficient sensitivity for the detection of major cardiac events. The complementary information provided by the measurement of different biomarkers is believed to be very useful. Specifically, elevations of cardiac troponin I (cTnI) and T (cTnT) are strongly associated with a high-risk profile both at short- and long-term. This has been definitely demonstrated in many studies as well as in cumulative meta-analysis. The role of different biomarkers, such as those reflecting activation of hemostasis and the presence of inflammation, is however less defined. At the moment, no study has prospectively evaluated these biomarkers in the whole spectrum of unselected patients with ACS. It is also unclear whether these biomarkers add independent prognostic value to the clinical and electrocardiographic indicators of adverse outcome and whether they offer additional information when compared to each other. The Early Prognostic Value of Biochemical Markers of Myocardial Damage, Activation of Hemostatic Mechanism and Inflammation in Acute Ischemic Syndromes (EMAI) study has been prospectively designed to solve these issues. In this study, we have evaluated the prognostic value of cTnI and cTnT, D-dimer, prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT) and C-reactive protein (CRP) in patients with ACS at the time of admission. We have enrolled in 31 Italian Coronary Care Units 1971 patients with rest anginal pain within 12 h from admission and electrocardiographic evidence of myocardial ischemia. Of these, 730 patients resulted to have ST-segment elevation myocardial infarction eligible for a reperfusion strategy and 1241, an acute coronary syndrome without persisting ST-segment elevation. Primary outcome measure of the study is the composite of death and non-fatal MI within 30 days from admission, which has occurred in 8.9% of the study population.
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PMID:Cardiac markers and risk stratification: an integrated approach. 1155 47

C-reactive protein (CRP) is the prototype acute phase reactant and therefore a marker of systemic inflammation. In the last decades, accumulating data have demonstrated the role of inflammation in the pathogenesis of ischemic heart disease. High CRP levels, measured by high-sensitivity methods, on admission have a short-term negative prognostic value and are associated with a worse outcome. In epidemiological studies, minor elevations of CRP are associated with future risk of myocardial infarction, stroke and peripheral vascular disease. This increased risk is independent of other biochemical and clinical risk factors, and the association between high CRP and an abnormal cholesterol ratio significantly increases the risk in the individual patient. Finally, the observation of an increased level of CRP may be of clinical utility in primary prevention, because these subjects favourably benefit from statin therapy.
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PMID:C-reactive protein and primary prevention of ischemic heart disease. 1155 52


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