Inflammatory burden in acute heart failure: association of hsCRP with cardiac structure and function, lung ultrasound findings, and survival
Z Hassan Juma, F Soeskov Davidovski, C Espersen, J I M H Borchsenius, L M Adam, A Stanchev, K Grundtvig Skaarup, M Flarup Dons, M Sengeloev, K Feldballe Bernholm, J Christensen, A M Reimer Jensen, L Steen Duus, M Christian Hoejbjerg Lassen, T Biering-SoerensenAbstract
Background
Systemic inflammation is increasingly recognized as a key contributor to acute heart failure (AHF) and is associated with adverse outcomes. However, its relationship with objective imaging markers of cardiac dysfunction and pulmonary congestion in AHF remains incompletely understood.
Purpose
This study examined associations between systemic inflammation assessed by high-sensitivity C-reactive protein (hsCRP), echocardiographic and lung ultrasound (LUS) findings, and adverse outcomes in hospitalised AHF patients.
Methods
In this prospective, two-center observational cohort, adults hospitalized with AHF between 2022 and 2024 were consecutively enrolled; patients with active infection were excluded. Active infection was defined as antibiotic treatment during hospitalization or documented infection, identified through systematic review of medical records and medication lists. Transthoracic echocardiography, 8-zone LUS, and laboratory testing were performed at enrolment and repeated at 1-3-month follow-up. Patients were stratified into tertiles of hsCRP, and trends across tertiles were evaluated. Associations between hsCRP and echocardiographic parameters were assessed using multivariable linear regression models. Clinical outcomes, including all-cause mortality, were analysed using multivariable Cox proportional hazards regression.
Results
Among 350 patients (mean age 77.5 ± 11.8 years; 54% female), hsCRP tertiles were defined as ≤5.20 mg/L (T1), 5.20-14.78 mg/L (T2), and >14.78 mg/L (T3). Increasing hsCRP tertiles were associated with longer hospital stay and higher in-hospital mortality (p-trend=0.013 and p<0.001, respectively). Higher hsCRP tertiles were associated with impaired cardiac function, including lower left ventricular ejection fraction (LVEF) across tertiles (40%, 34%, and 35%; p-trend=0.033), and progressively worse global longitudinal strain (GLS) (10.4%, 9.7%, and 8.9%; p-trend=0.013), resulting in more prevalent impaired LVEF (≤40%) and GLS (<16%) in higher hsCRP tertiles. Pulmonary congestion was more prevalent across hsCRP tertiles, reflected by increasing median B-line counts (3, 5, and 6; p-trend=0.048) (Figure 1). At follow-up, echocardiographic parameters were similar across baseline hsCRP tertiles and residual congestion was low. During a median follow-up of 365 days (IQR 106-671), all-cause mortality increased stepwise across tertiles (16%, 31%, and 42%; p<0.001), and hsCRP remained independently associated with mortality after multivariable adjustment per 1 mg/L increase (HR 1.19, 95% CI 1.04-1.36; p=0.009) (Table 1).
Conclusion
In patients hospitalised with AHF, elevated hsCRP was associated with worse cardiac function, greater pulmonary congestion, and increased mortality, supporting its role as an integrated marker of disease severity.Clinical profile and outcomes by hsCRPCox models of mortality by hsCRP