Anu Kataja1, Tuukka Tarvasmäki2, Johan Lassus2, Alessandro Sionis3, Alexandre Mebazaa4, Kari Pulkki5, Marek Banaszewski6, Valentina Carubelli7, Mari Hongisto8, Ewa Jankowska9, Raija Jurkko2, Toni Jäntti2, Monika Kasztura10, John Parissis11, Tuija Sabell2, Jose Silva-Cardoso12, Jindrich Spinar13, Heli Tolppanen2, Veli-Pekka Harjola8. 1. Emergency Medicine, University of Helsinki and Department of Emergency Medicine and Services, Helsinki University Hospital, Helsinki, Finland. Electronic address: anu.kataja@helsinki.fi. 2. Cardiology, University of Helsinki and Heart and Lung Center, Helsinki University Hospital, Helsinki, Finland. 3. Acute and Intensive Cardiac Care Unit, Cardiology Department, Hospital de la Santa Creu i Sant Pau, IIB Sant Pau, CIBER-CV, Universitat Autonoma de Barcelona, Spain. 4. INSERM U942, APHP, Hôpitaux Universitaires Saint Louis Lariboisière and University Paris Diderot, Paris, France. 5. Department of Clinical Chemistry, University of Turku and Turku University Hospital, Turku, Finland. 6. Intensive Cardiac Therapy Clinic, Institute of Cardiology, Warsaw, Poland. 7. Cardiology, Department of Medical and Surgical Specialties, Radiological Sciences, and Public Health, University and Civil Hospital of Brescia, Brescia, Italy. 8. Emergency Medicine, University of Helsinki and Department of Emergency Medicine and Services, Helsinki University Hospital, Helsinki, Finland. 9. Department of Heart Diseases, Wroclaw Medical University and Center for Heart Diseases, University Hospital in Wroclaw, Poland. 10. Department of Food Hygiene and Consumer Health Protection, Faculty of Veterinary Medicine, Wroclaw, Poland. 11. Heart Failure and ER, Attikon University Hospital, University of Athens, Athens, Greece. 12. São João University Hospital Center, Department of Cardiology and CINTESIS - Center for Health Technology and Services Research, Faculty of Medicine, University of Porto, Portugal. 13. Internal Cardiology Department, University Hospital St. Ann and Medical Faculty, Brno, Czech Republic.
Abstract
BACKGROUND: Inflammatory responses play an important role in the pathophysiology of cardiogenic shock (CS). The aim of this study was to investigate the kinetics of procalcitonin (PCT), C-reactive protein (CRP), and interleukin-6 (IL-6) in CS and to assess their relation to clinical presentation, other biochemical variables, and prognosis. METHODS: Levels of PCT, CRP and IL-6 were analyzed in serial plasma samples (0-120h) from 183 patients in the CardShock study. The study population was dichotomized by PCTmax ≥ and < 0.5 μg/L, and IL-6 and CRPmax above/below median. RESULTS: PCT peaked already at 24 h [median PCTmax 0.71 μg/L (IQR 0.24-3.4)], whereas CRP peaked later between 48 and 72 h [median CRPmax 137 mg/L (59-247)]. PCT levels were significantly higher among non-survivors compared with survivors from 12 h on, as were CRP levels from 24 h on (p < 0.001). PCTmax ≥ 0.5 μg/L (60% of patients) was associated with clinical signs of systemic hypoperfusion, cardiac and renal dysfunction, acidosis, and higher levels of blood lactate, IL-6, growth-differentiation factor 15 (GDF-15), and CRPmax. Similarly, IL-6 > median was associated with clinical signs and biochemical findings of systemic hypoperfusion. PCTmax ≥ 0.5 μg/L and IL-6 > median were associated with increased 90-day mortality (50% vs. 30% and 57% vs. 22%, respectively; p < 0.01 for both), while CRPmax showed no prognostic significance. The association of inflammatory markers with clinical infections was modest. CONCLUSIONS: Inflammatory markers are highly related to signs of systemic hypoperfusion in CS. Moreover, high PCT and IL-6 levels are associated with poor prognosis.
BACKGROUND: Inflammatory responses play an important role in the pathophysiology of cardiogenic shock (CS). The aim of this study was to investigate the kinetics of procalcitonin (PCT), C-reactive protein (CRP), and interleukin-6 (IL-6) in CS and to assess their relation to clinical presentation, other biochemical variables, and prognosis. METHODS: Levels of PCT, CRP and IL-6 were analyzed in serial plasma samples (0-120h) from 183 patients in the CardShock study. The study population was dichotomized by PCTmax ≥ and < 0.5 μg/L, and IL-6 and CRPmax above/below median. RESULTS: PCT peaked already at 24 h [median PCTmax 0.71 μg/L (IQR 0.24-3.4)], whereas CRP peaked later between 48 and 72 h [median CRPmax 137 mg/L (59-247)]. PCT levels were significantly higher among non-survivors compared with survivors from 12 h on, as were CRP levels from 24 h on (p < 0.001). PCTmax ≥ 0.5 μg/L (60% of patients) was associated with clinical signs of systemic hypoperfusion, cardiac and renal dysfunction, acidosis, and higher levels of blood lactate, IL-6, growth-differentiation factor 15 (GDF-15), and CRPmax. Similarly, IL-6 > median was associated with clinical signs and biochemical findings of systemic hypoperfusion. PCTmax ≥ 0.5 μg/L and IL-6 > median were associated with increased 90-day mortality (50% vs. 30% and 57% vs. 22%, respectively; p < 0.01 for both), while CRPmax showed no prognostic significance. The association of inflammatory markers with clinical infections was modest. CONCLUSIONS: Inflammatory markers are highly related to signs of systemic hypoperfusion in CS. Moreover, high PCT and IL-6 levels are associated with poor prognosis.
Authors: Adrien Picod; Louis Morisson; Charles de Roquetaillade; Malha Sadoune; Alexandre Mebazaa; Etienne Gayat; Beth A Davison; Gad Cotter; Benjamin Glenn Chousterman Journal: Front Immunol Date: 2022-05-12 Impact factor: 8.786
Authors: Quentin de Roux; Marie Renaudier; Wulfran Bougouin; Johanna Boccara; Vincent Fihman; Raphaël Lepeule; Chamsedine Cherait; Antonio Fiore; François Hemery; Jean-Winoc Decousser; Olivier Langeron; Nicolas Mongardon Journal: Crit Care Date: 2021-07-08 Impact factor: 9.097