Kinetics of procalcitonin, C-reactive protein and interleukin-6 in cardiogenic shock – Insights from the CardShock study. (1st January 2021)

• Record Type: Journal Article
• Authors: Kataja, Anu; Tarvasmäki, Tuukka; Lassus, Johan; Sionis, Alessandro; Mebazaa, Alexandre; Pulkki, Kari; Banaszewski, Marek; Carubelli, Valentina; Hongisto, Mari; Jankowska, Ewa; Jurkko, Raija; Jäntti, Toni; Kasztura, Monika; Parissis, John; Sabell, Tuija; Silva-Cardoso, Jose; Spinar, Jindrich; Tolppanen, Heli; Harjola, Veli-Pekka
• Is Part Of: International journal of cardiology. Volume 322(2021)
• Page Start: 191
• Page End: 196
• Publication Date: 2021-01-01
• Subjects: Cardiogenic shock -- Inflammation -- Procalcitonin -- Interleukin 6 -- C-reactive protein; Cardiology -- Periodicals; Electronic journals; 616.12
• DOI: 10.1016/j.ijcard.2020.08.069
• Languages: English
• ISSNs: 0167-5273

Abstract

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 (0−120 h ) 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. Highlights: Inflammatory marker levels are considerably elevated during the first days of CS. PCT peaks early at 24 h, while CRP continues to rise until 48 to 72 h in CS. High levels of PCT and IL-6 are strongly associated with systemic hypoperfusion in CS. High inflammatory marker levels are associated with increased mortality in CS.