Key result
Elevated CRP is linked to lower survival in patients with PAH.
Why the study?
Although CRP is a known marker of inflammation and cardiovascular risk predictor, its potential role in predicting outcomes in PAH and CTEPH required prospective investigation.
Do plasma C-reactive protein (CRP) levels predict outcomes and response to therapy in patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH)?
Cohort
Do plasma C-reactive protein (CRP) levels predict outcomes and response to therapy in patients with pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH)?
p-value: p=0.02
Elevated C-reactive protein levels correlate with disease severity and predict poorer survival in patients with pulmonary arterial hypertension, and decrease following successful pulmonary endarterectomy in CTEPH.
CRP may aid PAH risk stratification; leaves open if anti-inflammatory therapies improve survival.
OBJECTIVES: Our aim was to investigate in a prospective study a potential role of C-reactive protein (CRP) in predicting the outcome in pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). BACKGROUND: CRP is a well-known marker of inflammation and tissue damage, widely recognized as a risk predictor of cardiovascular and coronary heart diseases. METHODS: Plasma levels of CRP have been measured in consecutive patients diagnosed with PAH and CTEPH, at the time of right heart catheterization. RESULTS: Circulating CRP levels were increased in CTEPH and PAH patients compared with those in control subjects (4.9 mg l(-1), 95% confidence interval [CI]: 3.9 to 6.2 mg l(-1); 4.4 mg l(-1), 95% CI: 3.5 to 5.4 mg l(-1); and 2.3 mg l(-1), 95% CI: 1.9 to 2.7 mg l(-1), respectively; p < 0.0001). In PAH patients, CRP levels correlated with New York Heart Association functional class (r = 0.23), right atrial pressure (r = 0.25), and 6-min walking distance (r = -0.19) and were significantly higher in nonsurvivors than in survivors (p = 0.003). All PAH, idiopathic PAH, and patients naive for disease-specific medication with CRP levels >5.0 mg l(-1) had a significantly lower survival rate (p = 0.02, p = 0.009, and p < 0.05, respectively). In CTEPH patients, circulating CRP levels significantly decreased 12 months after pulmonary endarterectomy (n = 23, 4.0 mg l(-1), 95% CI: 2.8 to 5.8 mg l(-1), to 1.6 mg l(-1), 95% CI: 2.2 to 3.0 mg l(-1); p = 0.004). PAH patients normalizing their CRP levels under treatment (n = 29), assigned as responders, had a significantly higher survival rate (p < 0.05). The proportion of patients treated with a parenteral prostacyclin-analogue was significantly higher among the responders than the nonresponders (55% vs. 17%, p = 0.002). CONCLUSIONS: This is the first evidence of a role of an inflammatory marker, such as CRP, in predicting outcome and response to therapy in PAH.
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Quarck et al. (2009) conducted a cohort in Pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). C-reactive protein (CRP) vs. Control subjects / CRP ≤5.0 mg/L was evaluated on Survival rate (p=0.02). Elevated C-reactive protein levels (>5.0 mg/L) were associated with a significantly lower survival rate in patients with pulmonary arterial hypertension (p=0.02).
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