The Official Journal of EuroPCR and the European Association of Percutaneous Coronary Interventions (EAPCI)
Culprit lesion location and outcomes in patients with multi-vessel disease and infarct-related cardiogenic shock.
A core laboratory analysis of the CULPRIT-SHOCK trial
Marie Hauguel-Moreau1; Olivier Barthélémy2; serdar Farhan3; Kurt Huber4; Stéphanie Rouanet5; Michel Zeitouni2; Paul Guedeney2; Georges Hage2; Eric Vicaut6; Uwe Zeymer7; Steffen Desch8; Holger Thiele8; Gilles Montalescot2;
1. Sorbonne Univeristé, ACTION Study Group, INSERM UMRS_1166, Institut de cardiology (AH-HP), Paris, France, France 2. Sorbonne Université, ACTION Study Group, INSERM UMRS 1166, Institut de Cardiologie (AP-HP), Paris, France 3. The Zena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at mount Sinai, New York, New York 4. 3rd Department of Medicine, Cardiology and Intensive Care Medicine, Wilhelminen hospital and Sigmund Freund University, Medical School, Vienna, Austria 5. Statistician Unit, statEthic, Levallois-Perret, France 6. ACTION Study Group, Unité de Recherche Clinique, Hôpital Lariboisière (Ap-HP), Paris, France 7. Heart Centre Ludwigshafen, Department of Cardiology, Germany 8. Heart Centre Leipzig at University of Leipzig and Leipzig Heart Institute, Leipzig, Germany
As a public service to our readership, this article - peer reviewed by the Editors of EuroIntervention - has been published immediately upon acceptance as it was received. The content of this article is the sole responsibility of the authors, and not that of the journal or its publishers.
Please note that supplementary movies are not available online at this stage. Once a paper is published in its edited and formatted form, it will be accompanied online by any supplementary movies.
To read the full content of this article, please log in to download the PDF.
Aim: 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). We aimed to assess whether CCLL identifies a subgroup of patients at poorer prognosis when presenting with CS.
Methods and results: In the CULPRIT-SHOCK trial, a core-laboratory reviewed all coronary angiograms to identify CCLL. CCLL was defined as a culprit lesion realizing a >70% diameter stenosis of LM, LM equivalent (>70% diameter stenoses 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.
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 within 1 year were significantly higher in CCLL than in 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). It was consistent after adjustment for baseline and angiographic characteristics. No interaction with the randomization group (culprit lesion-only or immediate multivessel PCI) was found.
Conclusion: CCLL is frequent in CS and independently associated with worse clinical outcome irrespective of the revascularization strategy.