A23 - Systemic Inflammatory Burden Correlates with Severity and Predicts Outcomes in Patients with Cardiogenic Shock Supported by a Percutaneous Mechanical Support Device

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Support:The development of this supplement was funded by Abiomed.

Correspondence Details:Nikolaos Diakos,

Open Access:

The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content.

Background: In-hospital mortality associated with cardiogenic shock (CS) remains as high as 50%. Inflammation plays a central role in the pathogenesis of heart failure; however, little is known about the role of inflammation as a prognostic marker or therapeutic target in CS.

Hypothesis: We sought to investigate whether systemic inflammation is associated with clinical outcomes in CS.

Methods: We retrospectively analysed clinical data, including the neutrophil-to-lymphocyte ratio (NLR), a marker of low-grade inflammation, among 111 consecutive patients with CS supported by veno-arterial extracorporeal membrane oxygenation (VA-ECMO) or Impella. Patients with sepsis were excluded from our analysis.

Results: Of the 111 patients, 55% (n=61) survived CS and either underwent device explantation (36%, n=40) or were bridged to left ventricular assist device or cardiac transplant (19%, n=21). Compared to non-survivors, survivors were younger (56 ± 2 versus 64 ± 2 years, p=0.01), had better renal function (creatinine 1.8 ± 0.1 versus 2.6 ± 0.2 mg/dl, p=0.0017), higher haemoglobin (12 ± 0.4 versus 10 ± 0.4 g/dl, p=0.006) and lower right atrial pressure (15 ± 1 versus 19 ± 1 mmHg, p=0.02) at the time of device implantation.

NLR was significantly lower in patients with earlier stages of cardiogenic shock (SCAI class C 6.5 ± 1 versus SCAI class D 10.8 ± 1, p=0.008). Compared to non-survivors, survivors had a lower NLR (7.4 ± 0.9 versus 14.4 ± 11, p<0.001). NLR was independently predictive of survival after adjusting for other covariates (OR 0.9, CI [0.83–0.98]). The discriminative power of NLR alone was similar to the MELD Xi score (AUC 0.73, p=0.0005 and AUC 0.73, p=0.018 respectively). The percentage elevation in NLR levels was higher among CS patients supported with VA-ECMO versus Impella (627.5 ± 319% versus 99.9 ± 28%, VA-ECMO versus Impella, p=0.02).

Conclusion: NLR is a simple, widely available marker of inflammatory burden and correlates with in-hospital mortality among patients with cardiogenic shock requiring percutaneous mechanical circulatory support.