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
Ted Rogers Centre for Heart Research, Peter Munk Cardiac Centre, University Health Network, Toronto, Ontario, Canada.
Division of Cardiology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.
ESC Heart Fail. 2025 Jun;12(3):2077-2086. doi: 10.1002/ehf2.15217. Epub 2025 Feb 9.
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).
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.
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.
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.
心肌梗死后心源性休克(CS)的炎症特征会影响预后;然而,对于急性失代偿性心力衰竭所致心源性休克(ADHF-CS)中炎症变化的影响知之甚少。我们测量了入住心脏重症监护病房(CICU)的ADHF-CS患者的炎症细胞因子水平。
我们确定了入住我院CICU且同意储存生物标本的ADHF-CS患者。我们确定了两组作为对照的门诊心力衰竭患者,他们也储存了生物标本:第一组是那些没有失代偿病史且在样本采集后的随访期间未发生CS的患者(稳定型心力衰竭),第二组是在随访期间发生CS的患者(CS前期)。所有样本均进行了48种细胞因子和白细胞分类检测,并通过比较均值分析组间差异。
共确定了84例ADHF-CS患者,他们在入住CICU后中位2天[四分位数间距(IQR)0 - 7天]采集了样本。36例CS前期门诊患者在发生CS入院前137天(IQR 41 - 258天)采集了样本,并纳入了338例稳定型心力衰竭对照患者。ADHF-CS组和稳定型心力衰竭组的细胞因子谱不同。CS患者的促炎细胞因子水平[包括白细胞介素-1(IL-(1)、白细胞介素-6(IL-6)和白细胞介素-8(IL-8)]及白细胞总数均高于稳定型心力衰竭患者。对CS前期门诊患者组的分析表明,这是亚急性转变为CS的中间阶段。
与门诊心力衰竭患者相比,ADHF-CS的特征是促炎细胞因子水平和白细胞总数较高。心力衰竭失代偿有两个不同的炎症阶段,这可能有助于识别有CS风险的门诊患者。