C-Reactive Protein and B-Type Natriuretic Peptide Predict Hospitalization for Heart Failure and Cardiovascular Death

Background: Heart failure (HF) is an important cause of morbidity in patients with acute coronary syndromes (ACS). C-reactive protein (CRP) has been implicated in experimental models as exacerbating myocardial injury, but data regarding the clinical relationship of high-sensitivity CRP (hsCRP) and B-type natriuretic peptide (BNP) concentrations with the risk of HF after ACS are few.

Methods: PROVE IT–TIMI 22 randomized 4162 patients who had been stabilized after ACS to either intensive or moderate statin therapy. hsCRP and BNP were measured 30 days after randomization. Hospitalizations for HF and cardiovascular death occurring after day 30 were assessed for a mean follow-up of 24 months.

Results: Patients who developed HF had higher concentrations of hsCRP (3.7 mg/L vs 1.9 mg/L, P < 0.001) and BNP (59 ng/L vs 22 ng/L, P < 0.0001). HF increased in a stepwise manner with hsCRP quartile [adjusted hazard ratio (HRadj) for Q4 vs Q1, 2.5; P = 0.01] and BNP quartile (HRadj for Q4 vs Q1, 5.8; P < 0.001), with similar results obtained for HF and cardiovascular death. In a multivariable analysis, higher concentrations of hsCRP and BNP were both independently associated with HF [HRadj, 1.9 for hsCRP >2.0 mg/L (P = 0.01) and 4.2 for BNP >80 ng/L (P < 0.001)]. Patients with increases in both markers were at the greatest risk of HF, compared with patients without an increased marker concentration (HRadj, 8.3; P = 0.01). The benefit of intensive statin therapy in reducing HF was consistent among all patients, regardless of hsCRP or BNP concentration.

Conclusions: Both hsCRP and BNP measured 30 days after ACS are independently associated with the risk of HF and cardiovascular death, with the greatest risk occurring when both markers are increased.

TIMI Study Group, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115.

C-REACTIVE PROTEIN MODULATES HUMAN LUNG FIBROBLAST MIGRATION

C-reactive protein (CRP) has been classically used as a marker of inflammation. The aim of this study was to investigate the effect of CRP on migration of human fetal lung fibroblasts (HFL-1) to human plasma fibronectin (HFn). Using the blindwell chamber technique, CRP inhibited HFL-1 migration in a dose-dependent fashion (at 1 μ g/mL, inhibition: 32.5% ± 7.1%; P < .05). Western blot analysis showed that CRP inhibited the p38 mitogen-activated protein kinase (MAPK) activity in the presence of HFn. Moreover, the MAPK inhibitors SB202190 (25 μ M) and SB203580 (25 μ M) inhibited HFn-induced cell migration, suggesting an important role of p38 MAPK in HFn-induced migration. Taken together, these results suggest that the inhibitory effect of CRP is mediated by blocking MAPK. In summary, this study demonstrates that CRP directly modulates human lung fibroblasts migration. Thus, CRP may contribute to regulation of wound healing and may be endogenous antifibrotic factor acting on lung fibrosis.
Published in: Experimental Lung Research, Volume 35, Issue 1 February 2009 , pages 48 - 58



Keywords: lung fibroblast; C-reactive protein MAPK; migration

The effect of C-reactive protein on functional outcome in ischemic stroke patients.

This study was performed to evaluate the effect of C-reactive protein (CRP) measured within 24 hr after stroke onset on functional outcome in ischemic stroke patients. The medical records of 28 first-ever hemiplegic ischemic stroke patients with the lesions on the middle cerebral arterial territory were reviewed. Subjects were classified into experimental group (serum C-reactive protein >or= 0.5 mg/dL) and control group (serum CRP<0.5 mg/dL) based on the level of serum CRP measured within 24 hr after stroke onset. Serum CRP measured within 24 hr after stroke onset was significantly correlated with functional scales in ischemic stroke patients

Int J Neurosci. 2009;119(3):336-44
Ryu SR, Choi IS, Bian RX, Kim JH, Han JY, Lee SG.
Department of Physical & Rehabilitation Medicine, Research Institute of Medical Sciences, Chonnam National University Medical School & Hospital, Hak-Dong, Dong-Gu, Gwangju City, Republic of Korea.