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      The Impact of Ischemic Time on the Predictive Value of High-Sensitivity C-Reactive Protein in ST-Segment Elevation Myocardial Infarction Patients Treated by Primary Percutaneous Coronary Intervention

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      , MD 1 , , MD 1 , , , MD 1 , , MD 1 , , MD 1 , , MD 2 , , MD 3 , Other Korean Working Group in Myocardial Infarction Investigators

      Korean Circulation Journal

      The Korean Society of Cardiology

      C-reactive protein, Myocardial infarction, Myocardial reperfusion

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          Abstract

          Background and Objectives

          The high-sensitivity C-reactive protein (hs-CRP), a marker of inflammation, has been known to be elevated in patients with coronary artery disease. However, there is controversy about the predictive value of hs-CRP after acute myocardial infarction (MI). Therefore, we evaluated the impact of ischemic time on the predictive value of hs-CRP in ST-segment elevation myocardial infarction (STEMI) patients who were treated by primary percutaneous coronary intervention (PCI).

          Subjects and Methods

          We enrolled 5123 STEMI patients treated by primary PCI from the Korean Working Group in Myocardial Infarction and divided enrolled patients into four groups by symptom-to-balloon time (SBT) and level of hs-CRP (Group I: SBT <6 hours and hs-CRP <3 mg/L, Group II: SBT <6 hours and hs-CRP ≥3 mg/L, Group III: SBT ≥6 hours and hs-CRP <3 mg/L, and Group IV: SBT ≥6 hours and hs-CRP ≥3 mg/L). To evaluate the impact of ischemic time on the predictive value of hs-CRP in STEMI patients, we compared the cumulative cardiac event-free survival rate between these four groups.

          Results

          The sum of the cumulative incidence of all-cause mortality and recurrence of MI was higher in Group IV than in the other groups. However, there was no significant difference among Group I, Group II, and Group III. The Cox-regression analyses showed that an elevated level of hs-CRP (≥3 mg/L) was an independent predictor of long-term cardiovascular outcomes only among late-presenting STEMI patients (p=0.017, hazard ratio=2.462).

          Conclusion

          For STEMI patients with a long ischemic time (≥6 hours), an elevated level of hs-CRP is a poor prognostic factor of long-term cardiovascular outcomes.

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          Most cited references19

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          Genetically elevated C-reactive protein and ischemic vascular disease.

          Elevated levels of C-reactive protein (CRP) are associated with increased risks of ischemic heart disease and ischemic cerebrovascular disease. We tested whether this is a causal association. We studied 10,276 persons from a general population cohort, including 1786 in whom ischemic heart disease developed and 741 in whom ischemic cerebrovascular disease developed. We examined another 31,992 persons from a cross-sectional general population study, of whom 2521 had ischemic heart disease and 1483 had ischemic cerebrovascular disease. Finally, we compared 2238 patients with ischemic heart disease with 4474 control subjects and 612 patients with ischemic cerebrovascular disease with 1224 control subjects. We measured levels of high-sensitivity CRP and conducted genotyping for four CRP polymorphisms and two apolipoprotein E polymorphisms. The risk of ischemic heart disease and ischemic cerebrovascular disease was increased by a factor of 1.6 and 1.3, respectively, in persons who had CRP levels above 3 mg per liter, as compared with persons who had CRP levels below 1 mg per liter. Genotype combinations of the four CRP polymorphisms were associated with an increase in CRP levels of up to 64%, resulting in a theoretically predicted increased risk of up to 32% for ischemic heart disease and up to 25% for ischemic cerebrovascular disease. However, these genotype combinations were not associated with an increased risk of ischemic vascular disease. In contrast, apolipoprotein E genotypes were associated with both elevated cholesterol levels and an increased risk of ischemic heart disease. Polymorphisms in the CRP gene are associated with marked increases in CRP levels and thus with a theoretically predicted increase in the risk of ischemic vascular disease. However, these polymorphisms are not in themselves associated with an increased risk of ischemic vascular disease. 2008 Massachusetts Medical Society
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            Targeting C-reactive protein for the treatment of cardiovascular disease.

            Complement-mediated inflammation exacerbates the tissue injury of ischaemic necrosis in heart attacks and strokes, the most common causes of death in developed countries. Large infarct size increases immediate morbidity and mortality and, in survivors of the acute event, larger non-functional scars adversely affect long-term prognosis. There is thus an important unmet medical need for new cardioprotective and neuroprotective treatments. We have previously shown that human C-reactive protein (CRP), the classical acute-phase protein that binds to ligands exposed in damaged tissue and then activates complement, increases myocardial and cerebral infarct size in rats subjected to coronary or cerebral artery ligation, respectively. Rat CRP does not activate rat complement, whereas human CRP activates both rat and human complement. Administration of human CRP to rats is thus an excellent model for the actions of endogenous human CRP. Here we report the design, synthesis and efficacy of 1,6-bis(phosphocholine)-hexane as a specific small-molecule inhibitor of CRP. Five molecules of this palindromic compound are bound by two pentameric CRP molecules, crosslinking and occluding the ligand-binding B-face of CRP and blocking its functions. Administration of 1,6-bis(phosphocholine)-hexane to rats undergoing acute myocardial infarction abrogated the increase in infarct size and cardiac dysfunction produced by injection of human CRP. Therapeutic inhibition of CRP is thus a promising new approach to cardioprotection in acute myocardial infarction, and may also provide neuroprotection in stroke. Potential wider applications include other inflammatory, infective and tissue-damaging conditions characterized by increased CRP production, in which binding of CRP to exposed ligands in damaged cells may lead to complement-mediated exacerbation of tissue injury.
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              Hemostatic factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group.

              Increased levels of certain hemostatic factors may play a part in the development of acute coronary syndromes and may be associated with an increased risk of coronary events in patients with angina pectoris. We conducted a prospective multicenter study of 3043 patients with angina pectoris who underwent coronary angiography and were followed for two years. Base-line measurements included the concentrations of selected hemostatic factors indicative of a thrombophilic state or endothelial injury. The results were analyzed in relation to the subsequent incidence of myocardial infarction or sudden coronary death. After adjustment for the extent of coronary artery disease and other risk factors, an increased incidence of myocardial infarction or sudden death was associated with higher base-line concentrations of fibrinogen (mean +/- SD, 3.28 +/- 0.74 g per liter in patients who subsequently had coronary events, as compared with 3.00 +/- 0.71 g per liter in those who did not; P = 0.01), von Willebrand factor antigen (138 +/- 49 percent vs. 125 +/- 49 percent, P = 0.05), and tissue plasminogen activator (t-PA) antigen (11.9 +/- 4.7 ng per milliliter vs. 10.0 +/- 4.2 ng per milliliter, P = 0.02). The concentration of C-reactive protein was also directly correlated with the incidence of coronary events (P = 0.05), except when we adjusted for the fibrinogen concentration. In patients with high serum cholesterol levels, the risk of coronary events rose with increasing levels of fibrinogen and C-reactive protein, but the risk remained low even given high serum cholesterol levels in the presence of low fibrinogen concentrations. In patients with angina pectoris, the levels of fibrinogen, von Willebrand factor antigen, and t-PA antigen are independent predictors of subsequent acute coronary syndromes. In addition, low fibrinogen concentrations characterize patients at low risk for coronary events despite increased serum cholesterol levels. Our data are consistent with a pathogenetic role of impaired fibrinolysis, endothelial-cell injury, and inflammatory activity in the progression of coronary artery disease.
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                Author and article information

                Journal
                Korean Circ J
                Korean Circ J
                KCJ
                Korean Circulation Journal
                The Korean Society of Cardiology
                1738-5520
                1738-5555
                October 2013
                30 October 2013
                : 43
                : 10
                : 664-673
                Affiliations
                [1 ]Division of Cardiology, Department of Internal Medicine, Gwangju Veterans Hospital, Gwangju, Korea.
                [2 ]Department of Cardiovascular Medicine, Kyung Hee University College of Medicine, Seoul, Korea.
                [3 ]Department of Cardiovascular Medicine, Chonnam National College of Medicine, Gwangju, Korea.
                Author notes
                Correspondence: Wan Kim, MD, Division of Cardiology, Department of Internal Medicine, Gwangju Veterans Hospital, 99 Cheomdanwolbong-ro, Gwangsan-gu, Gwangju 506-705, Korea. Tel: 82-62-602-6100, Fax: 82-62-602-6931, kvhwkim@ 123456chol.com
                Article
                10.4070/kcj.2013.43.10.664
                3831012
                45646af8-7e6e-4e05-9e6f-ba4ba9485302
                Copyright © 2013 The Korean Society of Cardiology

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Original Article

                Cardiovascular Medicine

                c-reactive protein, myocardial infarction, myocardial reperfusion

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