Abstract
Patients with cardiogenic shock (CS) display systemic inflammation and a high rate of infections, suggesting important immune disturbances. To explore the immune response to CS, we prospectively measured, in 24 consecutive CS patients, differential white blood cell (WBC) counts and the cytokines IL-1β, IL-5, IL-6, IL-10, TNFα, IFNγ, MCP-1 and eotaxin (CCL11), at Day 1 (T1), day 3 (T2) and day 6-8 (T3). Secondary infections and their influence on cytokines and WBCs were determined. CS induced early (T1) neutrophilia and elevated levels of IL-6, IL-10 and MCP-1, correlating with shock severity. The eosinophil chemoattractant eotaxin was elevated at T1 and decreased thereafter, and a progressive rise of blood eosinophils was noted over time. Patients with the most severe shock had reduced lymphocytes and monocytes at T2 and T3. Sixty-two percent of patients developed an infection, which did not alter the profile of immune response, except from higher IL-6 levels at T2. Therefore, CS elicits an acute pro-inflammatory response, followed by a delayed increase in blood eosinophils, consistent with the development of a tissue repair response, as well as depletion of immune cells in the most severely affected patients, which might predispose to secondary infections.
Highlights
Patients with cardiogenic shock (CS) display systemic inflammation and a high rate of infections, suggesting important immune disturbances
Cardiogenic shock (CS) defines a state of systemic hypoperfusion leading to end-organ dysfunction related to cardiac pump failure primarily caused by acute myocardial infarction, and with mortality rates in the range of 27–51% according to recent reviews[1]
In the past 20 years, several investigators reported on an increase in the plasma levels of CRP11 and inflammatory cytokines, primarily IL-6 and TNFα in CS patients[4,7,8], the intensity of this response being correlated with the severity of CS4
Summary
Patients with cardiogenic shock (CS) display systemic inflammation and a high rate of infections, suggesting important immune disturbances. To explore the immune response to CS, we prospectively measured, in 24 consecutive CS patients, differential white blood cell (WBC) counts and the cytokines IL-1β, IL-5, IL-6, IL-10, TNFα, IFNγ, MCP-1 and eotaxin (CCL11), at Day 1 (T1), day 3 (T2) and day 6-8 (T3). Secondary infections and their influence on cytokines and WBCs were determined. A significant proportion of CS patients develop secondary infectious complications[5,6], which could reflect a state of impaired antimicrobial defenses These characteristics suggest the hypothesis that a state of disordered immunity stands at the foreground of the pathophysiology of CS and could represent a potential therapeutic target in this condition. We sought to explore in more detail the immune response to CS, by performing sequential measurements during the first week of hospitalization of a panel of cytokines, of differential counts of WBCs, and of the infectious complications in a series of 24 patients hospitalized for CS
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