Salman and colleagues retrospectively analysed patients with sepsis and reported an incidence of AF of 31% [15]. With respect to the incidence of new-onset Ku-0059436 AF in septic shock, Seguin and colleagues included a subgroup of 23 patients and observed new-onset AF in 30%, which is slightly lower when compared with our finding of 46% [5]. One reason for this difference might be our restrictive definition of septic shock, in particular the requirement of vasopressor therapy with norepinephrine for more than five hours with a dosage more than 0.1 ��g/kg/min.In the present study, septic shock patients with new-onset AF were older, more frequently revealed a history of hypertension and developed a higher maximal SOFA score during ICU stay in comparison to septic shock patients with maintained SR.

Age and a history of hypertension have been identified in previous studies as risk factors for the development of AF in non-selected ICU patients [5,7]. The higher SOFA score in septic shock patients with new-onset AF indicates that presumably there is an association between severity of illness and the development of AF.A variety of further factors including pre-existing heart failure, ischemic heart disease, valvular disease, electrolyte disturbances and use of catecholamines have been addressed as potential co-factors or causes for the development of new-onset AF in critically ill patients [5-7]. In the current study, only a small number of patients developing new-onset AF revealed pre-existing heart failure, ischemic heart disease or valvular disease.

Furthermore, we did not find apparent electrolyte disturbances when new-onset AF occurred. Also, regarding the treatment with catecholamines there was no significant difference between septic shock patients with new-onset AF in comparison to those with maintained SR. The present data do not support the hypothesis that one of these factors plays a mayor role in the development of AF in critically ill patients.The pathophysiological mechanism underlying the development of AF in critically ill patients and in particular in septic shock is not known. However, there is increasing evidence that the systemic inflammatory response per se is a predominant trigger of AF in critically ill patients. The occurrence of AF after cardiac surgery has been shown to be closely related to the complement CRP activation on the postoperative day two or three [16].

Also, in the non-operative setting, a series of studies has now demonstrated an association of elevated CRP levels with the development and maintenance of AF [17-19]. Chung and colleagues found two-fold higher CRP levels in patients with AF than in control subjects. Furthermore, patients with persistent AF had higher CRP levels than Anacetrapib those with paroxysmal AF, suggesting that inflammation plays an important role in the maintenance of AF [17].