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      Preprocedural C-Reactive Protein Predicts Outcomes after Primary Percutaneous Coronary Intervention in Patients with ST-elevation Myocardial Infarction a systematic meta-analysis

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          Abstract

          Risk assessment in patients with acute coronary syndromes (ACS) is critical in order to provide adequate treatment. We performed a systematic meta-analysis to assess the predictive role of serum C-reactive protein (CRP) in patients with ST-segment elevation myocardial infarction (STEMI), treated with primary percutaneous coronary intervention (PPCI). We included 7 studies, out of 1,033 studies, with a total of 6,993 patients with STEMI undergoing PPCI, which were divided in the high or low CRP group, according to the validated cut-off values provided by the corresponding CRP assay. High CRP values were associated with increased in-hospital and follow-up all-cause mortality, in-hospital and follow-up major adverse cardiac events (MACE), and recurrent myocardial infarction (MI). The pre-procedural CRP predicted in-hospital target vessel revascularization (TVR), but was not associated with acute/subacute and follow-up in-stent restenosis (ISR), and follow-up TVR. Thus, pre-procedural serum CRP could be a valuable predictor of global cardiovascular risk, rather than a predictor of stent-related complications in patients with STEMI undergoing PPCI. This biomarker might have the potential to improve the management of these high-risk patients.

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          Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials.

          Ellen Keeley, Judith Boura, Cindy Grines (2003)
          Many trials have been done to compare primary percutaneous transluminal coronary angioplasty (PTCA) with thrombolytic therapy for acute ST-segment elevation myocardial infarction (AMI). Our aim was to look at the combined results of these trials and to ascertain which reperfusion therapy is most effective. We did a search of published work and identified 23 trials, which together randomly assigned 7739 thrombolytic-eligible patients with ST-segment elevation AMI to primary PTCA (n=3872) or thrombolytic therapy (n=3867). Streptokinase was used in eight trials (n=1837), and fibrin-specific agents in 15 (n=5902). Most patients who received thrombolytic therapy (76%, n=2939) received a fibrin-specific agent. Stents were used in 12 trials, and platelet glycoprotein IIb/IIIa inhibitors were used in eight. We identified short-term and long-term clinical outcomes of death, non-fatal reinfarction, and stroke, and did subgroup analyses to assess the effect of type of thrombolytic agent used and the strategy of emergent hospital transfer for primary PTCA. All analyses were done with and without inclusion of the SHOCK trial data. Primary PTCA was better than thrombolytic therapy at reducing overall short-term death (7% [n=270] vs 9% [360]; p=0.0002), death excluding the SHOCK trial data (5% [199] vs 7% [276]; p=0.0003), non-fatal reinfarction (3% [80] vs 7% [222]; p<0.0001), stroke (1% [30] vs 2% [64]; p=0.0004), and the combined endpoint of death, non-fatal reinfarction, and stroke (8% [253] vs 14% [442]; p<0.0001). The results seen with primary PTCA remained better than those seen with thrombolytic therapy during long-term follow-up, and were independent of both the type of thrombolytic agent used, and whether or not the patient was transferred for primary PTCA. Primary PTCA is more effective than thrombolytic therapy for the treatment of ST-segment elevation AMI.
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            C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992.

            W. Koenig, M Sund, M. Fröhlich … (1999)
            Inflammatory reactions in coronary plaques play an important role in the pathogenesis of acute atherothrombotic events; inflammation elsewhere is also associated with both atherogenesis generally and its thrombotic complications. Recent studies indicate that systemic markers of inflammation can identify subjects at high risk of coronary events. We used a sensitive immunoradiometric assay to examine the association of serum C-reactive protein (CRP) with the incidence of first major coronary heart disease (CHD) event in 936 men 45 to 64 years of age. The subjects, who were sampled at random from the general population, participated in the first MONICA Augsburg survey (1984 to 1985) and were followed for 8 years. There was a positive and statistically significant unadjusted relationship, which was linear on the log-hazards scale, between CRP values and the incidence of CHD events (n=53). The hazard rate ratio (HRR) of CHD events associated with a 1-SD increase in log-CRP level was 1.67 (95% CI, 1.29 to 2. 17). After adjustment for age, the HRR was 1.60 (95% CI, 1.23 to 2. 08). Adjusting further for smoking behavior, the only variable selected from a variety of potential confounders by a forward stepping process with a 5% change in the relative risk of CRP as the selection criterion, yielded an HRR of 1.50 (95% CI, 1.14 to 1.97). These results confirm the prognostic relevance of CRP, a sensitive systemic marker of inflammation, to the risk of CHD in a large, randomly selected cohort of initially healthy middle-aged men. They suggest that low-grade inflammation is involved in pathogenesis of atherosclerosis, especially its thrombo-occlusive complications.
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              Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease.

              Steven E Nissen, E. Murat Tuzcu, Paul Schoenhagen … (2005)
              Recent trials have demonstrated better outcomes with intensive than with moderate statin treatment. Intensive treatment produced greater reductions in both low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP), suggesting a relationship between these two biomarkers and disease progression. We performed intravascular ultrasonography in 502 patients with angiographically documented coronary disease. Patients were randomly assigned to receive moderate treatment (40 mg of pravastatin orally per day) or intensive treatment (80 mg of atorvastatin orally per day). Ultrasonography was repeated after 18 months to measure the progression of atherosclerosis. Lipoprotein and CRP levels were measured at baseline and follow-up. In the group as a whole, the mean LDL cholesterol level was reduced from 150.2 mg per deciliter (3.88 mmol per liter) at baseline to 94.5 mg per deciliter (2.44 mmol per liter) at 18 months (P<0.001), and the geometric mean CRP level decreased from 2.9 to 2.3 mg per liter (P<0.001). The correlation between the reduction in LDL cholesterol levels and that in CRP levels was weak but significant in the group as a whole (r=0.13, P=0.005), but not in either treatment group alone. In univariate analyses, the percent change in the levels of LDL cholesterol, CRP, apolipoprotein B-100, and non-high-density lipoprotein cholesterol were related to the rate of progression of atherosclerosis. After adjustment for the reduction in these lipid levels, the decrease in CRP levels was independently and significantly correlated with the rate of progression. Patients with reductions in both LDL cholesterol and CRP that were greater than the median had significantly slower rates of progression than patients with reductions in both biomarkers that were less than the median (P=0.001). For patients with coronary artery disease, the reduced rate of progression of atherosclerosis associated with intensive statin treatment, as compared with moderate statin treatment, is significantly related to greater reductions in the levels of both atherogenic lipoproteins and CRP. Copyright 2005 Massachusetts Medical Society.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 27 January 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 41530
                Affiliations
                [1 ]University Hospital Essen, Medical Faculty, West German Heart and Vascular Center, Department of Cardiology and Vascular Diseases , Hufelandstr. 55, 45147 Essen, Germany
                [2 ]University of Medicine and Pharmacy Carol Davila - University and Emergency Hospital, Cardiac Research Unit , Splaiul Independentei 169, 050098 Bucharest, Romania
                Author notes
                Article
                Publisher Item ID: srep41530
                DOI: 10.1038/srep41530
                PMC ID: 5270244
                PubMed ID: 28128312
                SO-VID: f7c66f42-37ee-4197-b510-fb3b48de88ed
                Copyright © Copyright © 2017, The Author(s)
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 12 October 2016
                Date accepted : 19 December 2016
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