Are platelets a 'forgotten' source of sepsis-induced myocardial depressing factor(s)?

Alexandre Mebazaa

doi:10.1186/cc6220

Abstract

The mechanism of sepsis-induced cardiac failure was initially thought to be related to the presence of 'myocardial depressant' substances that directly alter heart function. Exosomes released by platelets and identified in the plasma are suggested to, at least partially, explain myocardial depression in sepsis. This hypothesis needs to be evaluated by clinical studies.

Highlights

The clue for the sepsis-induced cardiac dysfunction in patients with septic shock came from Parker and colleagues’ study in 1984 [2]
Using simultaneous radionuclide cardiac imaging and thermodilution cardiac output studies on patients with septic shock, they showed a ‘paradox’: all patients had a high cardiac output and maintained a stroke volume index associated with a depressed left ventricular ejection fraction < 0.45
Survivors had a left ventricular ejection fraction that remained low for 4 days and rose to normal values within 7–10 days [2]

Summary

Introduction

The clue for the sepsis-induced cardiac dysfunction in patients with septic shock came from Parker and colleagues’ study in 1984 [2]. Using simultaneous radionuclide cardiac imaging and thermodilution cardiac output studies on patients with septic shock, they showed a ‘paradox’: all patients had a high cardiac output and maintained a stroke volume index associated with a depressed left ventricular ejection fraction < 0.45. It is agreed that systolic function deteriorates in the early phase of septic shock in humans, as confirmed by echocardiographic studies.

Results

Conclusion