4.6 Article

Phenotyping Cardiogenic Shock

期刊

出版社

WILEY
DOI: 10.1161/JAHA.120.020085

关键词

cardiogenic shock; clusters; heart failure; hemodynamics; machine learning; myocardial infarction; phenotypes

资金

  1. NIH RO1 [RO1HL139785-01]
  2. Abbott Laboratories Inc (Abbott Park, IL)
  3. Abiomed Inc (Danvers, MA)
  4. Boston Scientific Inc (Minneapolis, MN)
  5. Getinge Inc (Wayne, NJ)
  6. Danish Heart Foundation [16-R107-A6576]

向作者/读者索取更多资源

In this study, three distinct phenotypes of cardiogenic shock were identified and validated using machine learning, each with specific associations with clinical profiles and in-hospital mortality. These findings may lead to targeted patient enrollment in clinical trials and the development of tailored treatment strategies for subsets of patients with cardiogenic shock.
Background Cardiogenic shock (CS) is a heterogeneous syndrome with varied presentations and outcomes. We used a machine learning approach to test the hypothesis that patients with CS have distinct phenotypes at presentation, which are associated with unique clinical profiles and in-hospital mortality. Methods and Results We analyzed data from 1959 patients with CS from 2 international cohorts: CSWG (Cardiogenic Shock Working Group Registry) (myocardial infarction [CSWG-MI; n=410] and acute-on-chronic heart failure [CSWG-HF; n=480]) and the DRR (Danish Retroshock MI Registry) (n=1069). Clusters of patients with CS were identified in CSWG-MI using the consensus k means algorithm and subsequently validated in CSWG-HF and DRR. Patients in each phenotype were further categorized by their Society of Cardiovascular Angiography and Interventions staging. The machine learning algorithms revealed 3 distinct clusters in CS: non-congested (I), cardiorenal (II), and cardiometabolic (III) shock. Among the 3 cohorts (CSWG-MI versus DDR versus CSWG-HF), in-hospital mortality was 21% versus 28% versus 10%, 45% versus 40% versus 32%, and 55% versus 56% versus 52% for clusters I, II, and III, respectively. The cardiometabolic shock cluster had the highest risk of developing stage D or E shock as well as in-hospital mortality among the phenotypes, regardless of cause. Despite baseline differences, each cluster showed reproducible demographic, metabolic, and hemodynamic profiles across the 3 cohorts. Conclusions Using machine learning, we identified and validated 3 distinct CS phenotypes, with specific and reproducible associations with mortality. These phenotypes may allow for targeted patient enrollment in clinical trials and foster development of tailored treatment strategies in subsets of patients with CS.

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