Abstract
The initial bundle of cares strongly affects haemodynamics and outcomes in acute decompensated heart failure cardiogenic shock (ADHF-CS). We sought to characterize whether 24h haemodynamic profiling provides superior prognostic information as compared with admission assessment and which haemodynamic parameters best predict in-hospital death. All patients with ADHF-CS and with available admission and 24h invasive haemodynamic assessment from two academic institutions were considered for this study. The primary endpoint was in-hospital death. Regression analyses were run to identify relevant predictors of study outcome. We included 127 ADHF-CS patients [65 (inter-quartile range 52-72) years, 25.2% female]. Overall, in-hospital mortality occurred in 26.8%. Non-survivors were older, with greater CS severity. Among admission variables, age [odds ratio (OR)=1.06; 95% confidence interval (CI): 1.02-1.11; Padj=0.005] and CPIRAP (OR=0.62 for 0.1 increment; 95% CI: 0.39-0.95; Padj=0.034) were found significantly associated with in-hospital death. Among 24h haemodynamic univariate predictors of in-hospital death, pulmonary elastance (PaE) was the strongest (area under the curve of 0.77; 95% CI: 0.68-0.86). PaE (OR=5.98; 95% CI: 2.29-17.48; Padj<0.001), pulmonary artery pulsatility index (PAPi, OR=0.77; 95% CI: 0.62-0.92; Padj=0.013) and age (OR=1.06; 95% CI: 1.02-1.11; Padj=0.010) were independently associated with in-hospital death. Best cut-off for PaE was 0.85mmHg/mL and for PAPi was 2.95; cohort phenotyping based on these PaE and PAPi thresholds further increased in-hospital death risk stratification; patients with 24h high PaE and low PAPi exhibited the highest in-hospital mortality (56.2%). Pulmonary artery elastance has been found to be the most powerful 24h haemodynamic predictor of in-hospital death in patients with ADHF-CS. Age, 24h PaE, and PAPi are independently associated with hospital mortality. PaE captures ventricular (RV) afterload mismatch and PAPi provides a metric of RV adaptation, thus their combination generates four distinct haemodynamic phenotypes, enhancing in-hospital death risk stratification.
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