1Universitäres Herz- und Gefäßzentrum Hamburg Klinik für Kardiologie Hamburg, Deutschland; 2Universitätsklinikum Hamburg-Eppendorf Klinik für Kardiologie Hamburg, Deutschland; 3Universitäres Herz- und Gefäßzentrum Hamburg Allgemeine und Interventionelle Kardiologie Hamburg, Deutschland; 4Universitätsklinikum Hamburg-Eppendorf Klinik für Intensivmedizin Hamburg, Deutschland
Background: Acute heart failure (AHF) is a serious condition associated with a 30-day-mortality of approximately 4-11%. Furthermore, AHF is associated with unfavourable mid- and long-term outcomes. Cardiovascular causes of AHF range from acute myocardial infarction and myocarditis to arrhythmia-induced cardiomyopathy. Increased inflammation has been reported in AHF and may be associated with adverse outcomes including progression to chronic heart failure. It is unclear to what extent inflammation in AHF is caused by underlying cardiovascular and systemic disease processes and to acute infections. Aims of this study were to describe the prevalence of infection and of inflammation without infection in AHF, to investigate profiles of circulating biomarkers and to evaluate their respective associations with relevant outcomes in AHF.
Methods: Consecutive patients with AHF treated in a tertiary care centre between 2019 and 2021 were enrolled in an on-going single centre, prospective cohort study and retrospectively analysed. Inclusion criteria were NT-proBNP ≥ 300pg/ml and a recent (within the last 5 days) new-onset or severe worsening of heart failure (HF) symptoms. Presence of inflammation was defined by high-sensitive C-reactive protein (hsCRP) > 1mg/l. Infection was differentiated by application of the following definitions:
1) Suspected infection: Fever and/or putrid cough and/or dysuria and/or flank pain and/or gastrointestinal symptoms and/or abdominal pain and/or wound infection in the past 3 days.
2) Confirmed infection: Positive blood/urine cultures at admission and/or antibiotics before or at admission and/or infiltration on chest x-ray and/or other imaging findings indicating infection at admission.
Multivariable cox and logistic regression models adjusted for age, sex, left ventricular ejection fraction at baseline and NYHA functional heart failure class at baseline were applied. Evaluated clinical outcomes were HF progression, defined as increase in SCAI stage.
Results: Overall, a total of 174 patients were analysed (33.% (n = 58) women, median age 75 years (SD 12.34)). Pre-existing HF was found 138 (81%) patients. De-novo AHF was present in 31 (18%) patients. Median LV-EF at baseline was 36% and median NT-proBNP was 7245pg/ml. Causes of HF were ischemic (51.9%, n = 81), dilated (14.7%, n = 23) and valvular (13.5%, n = 21). Inflammation was found in 79 (45.4%) patients. A confirmed infection was found in 32 (18%), a suspected infection was found in 22 (13%) patients. Higher hsCRP concentrations were associated with higher NT-proBNP (p = 0.0021) (Figure 1), high-sensitive Troponin-I (p = 0.00857) and Proadrenomedullin (proADM) (p = 0.0074) concentrations. Elevated hsCRP was associated with a higher risk of progression to cardiogenic shock (HR 1.175 (95% CI) per 1mg/dl; p = 0.024), irrespective of the presence or absence of an infection. We will analyse and report results from 300 patients in April 2024.
Conclusions: In this preliminary analysis of patients presenting with acute heart failure, elevated concentration of hsCRP were associated with development of cardiogenic shock, independent of the presence of an infection. Increased concentrations of hsCRP are associated with markers for myocardial injury (troponin), cardiac strain (BNP), and vascular leakage (proADM). Our data support the concept that systemic inflammation contributes to cardiac dysfunction in acute heart failure.