C-Reactive Protein as a Risk Marker for Post-Infarct Heart Failure over a Multi-Year Period

Inflammatory activation during acute ST-elevation myocardial infarction (STEMI) can contribute to post-infarct heart failure (HF). This study aimed to determine prognostic value of high-sensitivity C-reactive protein concentration (CRP) for HF over a long-term follow-up in 204 patients with a first STEMI undergoing guideline-based therapies including percutaneous coronary intervention. CRP was measured at admission, 24 h (CRP(24)), discharge (CRP(DC)), and one month (CRP(1M)) after index hospitalization for STEMI. Within a median period of 5.6 years post-index hospitalization for STEMI, hospitalization for HF (HFH) which is a primary endpoint, occurred in 24 patients (11.8%, HF+ group). During the study, 8.3% of HF+ patients died vs. 1.7% of patients without HFH (HF- group) (p = 0.047). CRP(24), CRP(DC), and CRP(1M) were significantly higher in HF+ compared to HF- group. The median CRP(1M) in HF+ group was 2.57 mg/L indicating low-grade systemic inflammation, in contrast to 1.54 mg/L in HF- group. CRP(1M) ≥ 2 mg/L occurred in 58.3% of HF+ vs. 42.8% of HF- group (p = 0.01). Kaplan–Meier analysis showed decreased probability of survival free from HFH in patients with CRP(24) (p < 0.001), CRP(DC) (p < 0.001), and CRP(1M) (p = 0.03) in quartile IV compared to lower quartiles. In multivariable analysis, CRP(DC) significantly improved prediction of HFH over a multi-year period post-STEMI. Persistent elevation in CRP post STEMI aids in risk stratification for long-term HF and suggests that ongoing cardiac and low-grade systemic inflammation promote HF development despite guideline-based therapies.