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Coronary interventions

Culprit lesion location and outcomes in patients with multivessel disease and infarct-related cardiogenic shock: a core laboratory analysis of the CULPRIT-SHOCK trial

EuroIntervention 2021;17:418-424. DOI: 10.4244/EIJ-D-20-00561

1. Sorbonne Université, ACTION Study Group, INSERM UMRS 1166, Institut de Cardiologie (AP-HP), Paris, France; 2. The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at mount Sinai, New York, NY, USA; 3. 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Wilhelminen hospital and Sigmund Freund University, Medical School, Vienna, Austria; 4. Statistician Unit, statEthic, Levallois-Perret, France; 5. ACTION Study Group, Unité de Recherche Clinique, Hôpital Lariboisière (Ap-HP), Paris, France; 6. Heart Centre Ludwigshafen, Department of Cardiology, Ludwigshafen am Rhein, Germany; 7. Heart Centre Leipzig at University of Leipzig and Leipzig Heart Institute, Leipzig, Germany

Background: Critical culprit lesion locations (CCLL) such as left main (LM) and proximal left anterior descending (LAD) are associated with worse clinical outcome in myocardial infarction without cardiogenic shock (CS).

Aims: We aimed to assess whether CCLL identify a subgroup of patients with poorer prognosis when presenting with CS.

Methods: In the CULPRIT-SHOCK trial, a core laboratory reviewed all coronary angiograms to identify CCLL. A CCLL was defined as a culprit lesion with a >70% diameter stenosis of the LM, LM equivalent (>70% diameter stenosis of both proximal LAD and proximal circumflex), proximal LAD or last remaining vessel. We evaluated the primary study endpoint of the CULPRIT-SHOCK trial according to CCLL.

Results: A total of 269 (43%) out of 626 patients eligible for this analysis had a CCLL. Death or renal replacement therapy within 30 days, death within 30 days and death within one year were significantly higher in the CCLL than in the non-CCLL group (58.4% vs 43.4%, p<0.001, 55.8% vs 39.5%, p<0.001, 61.0% vs 44.5%, p<0.001, respectively). This was consistent after adjustment for baseline and angiographic characteristics. No interaction with the randomisation group (culprit lesion-only or immediate multivessel PCI) was found.

Conclusions: CCLL is frequent in CS and independently associated with worse clinical outcomes irrespective of the revascularisation strategy. Trial registration: www.clinicaltrials.gov NCT01927549

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