Abstract
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 (CRP24), discharge (CRPDC), and one month (CRP1M) 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). CRP24, CRPDC, and CRP1M were significantly higher in HF+ compared to HF- group. The median CRP1M in HF+ group was 2.57 mg/L indicating low-grade systemic inflammation, in contrast to 1.54 mg/L in HF- group. CRP1M ≥ 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 CRP24 (p < 0.001), CRPDC (p < 0.001), and CRP1M (p = 0.03) in quartile IV compared to lower quartiles. In multivariable analysis, CRPDC 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.
Highlights
Heart failure (HF) remains a significant complication post myocardial infarction (MI) and is associated with high cardiovascular mortality [1,2,3,4]
Despite guideline-based therapies which lead to decreased mortality of patients with acute ST-segment elevation myocardial infarction (STEMI), HF occurs in up to 30% of STEMI patients depending on the time point of assessment, diagnostic criteria for HF, and therapeutic approach for STEMI [1,2,3,4,5]
In our previous studies of patients with acute STEMI treated with percutaneous coronary intervention (PCI) we found that elevated C-reactive protein (CRP) predicts left ventricular (LV) systolic dysfunction (LVSD) and left ventricular remodeling (LVR), and points to an increased risk of HF in patients with post-infarct LVSD [5,10,11]
Summary
Heart failure (HF) remains a significant complication post myocardial infarction (MI) and is associated with high cardiovascular mortality [1,2,3,4]. Enhanced inflammatory response leads to further cardiac injury and progressive left ventricular (LV) dysfunction and remodeling (LVR) which can contribute to HF development [5,9,10,11,12,13]. Cardiac inflammation in response to MI may trigger systemic inflammation that accelerates atherosclerosis progression, endothelial dysfunction, and vascular remodeling. This can promote HF development [9,14,15,16]. Higher IL-6 was associated with increased risk of post-infarct
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