ESC heart failure · 2025
Heart failure decompensation with cardiogenic shock exhibits distinct sequential inflammatory profiles.
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Brahmbhatt Darshan H, Scolari Fernando Luis, Fung Nicole L, Otsuki Madison, Lawler Patrick R, Ross Heather J, Kuzmanov Uros, Gramolini Anthony O, Luk Adriana C, Billia Filio
Аннотация
AIMS: The inflammatory profile of cardiogenic shock (CS) after myocardial infarction affects outcomes; however, little is known about the impact of inflammatory changes in CS caused by acute decompensated heart failure (ADHF-CS). We measured levels of inflammatory cytokines in patients with ADHF-CS admitted to a cardiac intensive care unit (CICU).
METHODS: We identified patients admitted to our CICU with ADHF-CS who had consented to having biospecimens stored. We identified two comparator groups of patients with HF seen as outpatients with stored biospecimens: firstly, those who had no history of decompensation and did not develop CS during follow-up after sample acquisition (stable HF), and secondly, a group of patients who developed CS during follow-up (pre-CS). All samples underwent 48-plex cytokine and white blood cell differential testing with the differences between groups analysed by comparing means.
RESULTS: Eighty-four ADHF-CS patients were identified who had samples obtained at a median of 2 [inter-quartile range (IQR) 0-7] days after CICU admission. Thirty-six pre-CS outpatients had samples taken 137 (IQR 41-258) days before admission with CS, and 338 stable HF control patients were included. Cytokine profiles differed between ADHF-CS and stable HF. Patients with CS had higher pro-inflammatory cytokine levels [including interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-8 (IL-8)] and total white cell counts than stable HF patients. Analysis of the pre-CS outpatient group suggested an intermediate stage in subacute transition to CS.
CONCLUSIONS: ADHF-CS is characterized by high levels of pro-inflammatory cytokines and total white count, compared with ambulatory HF. Decompensation from HF has two distinct inflammatory phases that may help identify outpatients at risk of CS.
METHODS: We identified patients admitted to our CICU with ADHF-CS who had consented to having biospecimens stored. We identified two comparator groups of patients with HF seen as outpatients with stored biospecimens: firstly, those who had no history of decompensation and did not develop CS during follow-up after sample acquisition (stable HF), and secondly, a group of patients who developed CS during follow-up (pre-CS). All samples underwent 48-plex cytokine and white blood cell differential testing with the differences between groups analysed by comparing means.
RESULTS: Eighty-four ADHF-CS patients were identified who had samples obtained at a median of 2 [inter-quartile range (IQR) 0-7] days after CICU admission. Thirty-six pre-CS outpatients had samples taken 137 (IQR 41-258) days before admission with CS, and 338 stable HF control patients were included. Cytokine profiles differed between ADHF-CS and stable HF. Patients with CS had higher pro-inflammatory cytokine levels [including interleukin-1 (IL-1), interleukin-6 (IL-6) and interleukin-8 (IL-8)] and total white cell counts than stable HF patients. Analysis of the pre-CS outpatient group suggested an intermediate stage in subacute transition to CS.
CONCLUSIONS: ADHF-CS is characterized by high levels of pro-inflammatory cytokines and total white count, compared with ambulatory HF. Decompensation from HF has two distinct inflammatory phases that may help identify outpatients at risk of CS.