Infections after myocardial infarction and cardiogenic shock and their reflection by inflammation parameters

Objective

Cardiogenic shock shows a high incidence of infections. The preceding myocardial trauma and shock as well as bacterial infection may trigger an inflammatory response. We investigated whether different inflammation parameters can alternatively be related to myocardial trauma/shock versus infection.

Patients

Fifteen patients (10 males/five females), mean age 69 ± 10.5 years and mean APACHE III score 83.36 ± 14.1, were enrolled in this prospective study. Cause of ICU admission was cardiogenic shock due to myocardial infarction (MI). Inclusion criteria were need of mechanical ventilation and vasopressor support. All patients developed respiratory tract infections and were treated with antibiotics.

Methods

Measurements started on day 1 after MI and were performed daily until day 10. Polymorphonuclear leukocyte (PMN) functions were measured in fresh whole blood: PMN migration was measured with a membrane filter method under FMLP stimulation; ROS release with luminol-enhanced chemiluminescence under PMA stimulation. Blood levels of PMN elastase, PMN blood count, sL-selectin, IL-6, IL-10, PCT, CRP, neopterin; and the infarction-related and shock-related parameters Troponin T and lactate were measured with routine methods. Changes in the parameters over time were determined with linear regression of log y.

Results

Among the parameters, three groups of reactivity emerged. Parameters of group I developed maximum reactions on days 1, 2 or 3 after MI, and values decreased significantly over the observation period. This group included PMN elastase, IL-6, PCT, Troponin T and lactate. Group II parameters developed maxima respectively minima on days 3, 4 and 5. This group included PMN-ROS release and neopterin (maxima), and PMN blood count and migration (minima). Parameters of group III showed maximum values on days 2 or 3, but no significant decrease (CRP and IL-10), or no distinct changes at all (sL-selectin). Infections appeared on day X = 3.92 ± 1.25 standard deviation after MI. Thus, top values of group II parameters coincided with the onset of infection, while in group I high values followed immediately MI and shock.

Conclusion

PMN-elastase, IL-6 and PCT parallel Troponin T and lactate can thus be considered to be triggered by myocardial trauma and shock. They are no indicators of infection. Blood PMN numbers, migration and ROS release as well as neopterin reached minimum/maximum values around the clinical manifestation of infection, suggesting associations with infections. Their decrease/ increase may indicate the onset of infections.