C-Reactive Protein Is a Potent Predictor of Mortality Independently of and in Combination With Troponin T in Acute Coronary Syndromes: A TIMI 11A Substudy

Morrow, David A.; Rifai, Nader; Antman, Elliott M.; Weiner, Debra L.; McCabe, Carolyn H.; Cannon, Christopher P.; Braunwald, Eugene

doi:10.1016/s0735-1097(98)00136-3

Cited by 716 publications

(413 citation statements)

References 37 publications

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“…The present study confirms previous observations that levels of CRP and MPO are elevated during ACS, 4,6,7,9 suggesting the participation of these proteins in the pathophysiologic process. After 2.4 y of follow-up, these markers significantly decreased with the stabilization of the disease.…”

Section: Discussionsupporting

confidence: 92%

“…1 -3 Much data exist on the prognostic capacity of C-reactive protein (CRP) determined in patients with acute coronary syndrome (ACS). 4 Some, but not all, studies have demonstrated an association between CRP levels and increased mortality. 5 -8 A novel inflammatory marker, myeloperoxidase, released by neutrophils activation, has also shown potential for risk stratification in ACS patients.…”

Section: Introductionmentioning

confidence: 99%

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Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

Borges¹,

Borges²,

Stella³

et al. 2009

Clinical Cardiology

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Background: C-reactive protein (CRP) and myeloperoxidase (MPO) are involved in the pathogenesis of atherosclerosis, mainly during periods of instabilization. This study aims to test the hypothesis that patients with acute coronary syndrome (ACS) maintain a persistent inflammatory state, and that this is associated with long-term mortality. Hypothesis: We hypothesized that serum C-reactive protein and myeloperoxidase collected at the index event and later, could add to the prognostic information in patients with ACS. Methods: In a prospective cohort of 115 consecutive patients with ACS, myeloperoxidase and C-reactive protein were measured at admission and 2 y later. Patients were followed-up for the occurrence of cardiac death and other major cardiac events. Results: Levels of CRP decreased from 26±34 mg/L in the acute phase to 6±8 mg/L in the chronic phase (p<0.001), and MPO levels decreased from 86±43 pM to 27±32 pM (p<0.001). After 29±12 mo, 27% patients died, 39% had new episode of ACS, and 30% underwent revascularization procedures. Initial CRP levels above 10 mg/L were associated with higher long-term mortality (hazard ratio [HR]

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

Borges¹,

Borges²,

Stella³

et al. 2009

Clinical Cardiology

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“…High-sensitivity C-reactive protein (CRP), a marker of inflammation, has been identified as an independent predictor of adverse cardiac events in healthy populations and in patients with stable coronary artery disease or ACS (6)(7)(8)(9)(10)(11). Although it is clear that inflammation plays a role in atherosclerotic complications (12), the relationship between CRP and troponin release following PCI has not been clarified.…”

mentioning

confidence: 99%

Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention

Hubáček

Basran

Shrive

et al. 2009

Canadian Journal of Cardiology

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“…14 Elevated C-reactive protein (CRP) levels have been shown to be associated with ACS. 15,16 CRP levels reflect the intensity of an inflammatory process involving macrophages, T and B cells, immunoglobulin (Ig) G deposition, and M-CSF production. CRP has a proinflammatory effect on endothelial cells and VSMCs.…”

mentioning

confidence: 99%

Activated Monocytes Induce Smooth Muscle Cell Death

et al. 2002

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Background — Plaque disruption is the inciting event for coronary thrombosis and acute coronary syndromes. Multiple factors influence plaque rupture, including the loss of vascular smooth muscle cells (VSMCs). We hypothesized that monocytes/macrophages (MMs) activated by macrophage colony-stimulating factor (M-CSF) are responsible for VSMC death. Methods and Results — VSMC apoptosis was markedly increased in the presence of both M-CSF and MMs (58.8±3.3%) compared with VSMCs plus M-CSF without MMs (15.7±1.5%, P ≤0.00005), VSMCs plus MMs without M-CSF (22.7±3.7%, P ≤0.0001), or control VSMCs alone (13.2±2.1%, P ≤0.0001). MM cell contact was required for M-CSF–stimulated killing of VSMCs, and MMs displayed an M-CSF concentration-dependent killing effect. Abciximab binds Mac-1 (CD11b/CD18) on MMs. When added to VSMCs exposed to MMs and M-CSF, abciximab (7 μg/mL) significantly reduced VSMC apoptosis (19.1±2.2%, P ≤0.0003). Therapeutic doses of tirofiban (0.35 μg/mL) and eptifibatide (5 μg/mL), which inhibit platelet glycoprotein (GP) IIb/IIIa but not Mac-1, did not block activated MM-induced VSMC apoptosis (65.0±3.4% and 51.3±2.5%, respectively). A recombinant anti–CD-18 antibody had an effect similar to that of abciximab (16.5±0.4%). Conclusions — These data suggest that monocytes and physiological concentrations of M-CSF trigger VSMC apoptosis. Abciximab and specific inhibitors of the Mac-1 receptor can antagonize this process.

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C-Reactive Protein Is a Potent Predictor of Mortality Independently of and in Combination With Troponin T in Acute Coronary Syndromes: A TIMI 11A Substudy

Cited by 716 publications

References 37 publications

Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

Serial Analyses of C‐Reactive Protein and Myeloperoxidase in Acute Coronary Syndrome

Prognostic implications of C-reactive protein and troponin following percutaneous coronary intervention

Activated Monocytes Induce Smooth Muscle Cell Death

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