Septic Participation in Cardiogenic Shock

Abstract

We have detected extremely low titers of IgM EndoCAb in CS suggesting endotoxin exposure. However, only inflammatory biomarkers were related to ICU mortality.

Cardiogenic shock elicits acute inflammation, delayed eosinophilia, and depletion of immune cells in most severe cases

“…Moreover, many patients surviving the acute low cardiac output syndrome associated with CS display a profile of vasodilatory shock, with low systemic vascular resistance 2 and normal or increased cardiac output 12 , consistent with the development of a systemic inflammatory response syndrome. Although the precise mechanisms responsible for triggering such inflammation in CS remain undefined, they may include innate immune activation in response to the release of damage associated molecular patterns (DAMPs or alarmins) by injured cells in ischemic tissues [13][14][15] , or the translocation of pathogen-associated molecular patterns (PAMPs), such as endotoxin, from the ischemic intestine 16 . Heart rate (bpm) 84 ( 23) 92 ( 24) 87 ( 26) 89 (16) Systolic BP (mm Hg) 89 ( 15) 98 ( 14) 100 ( 14)* 112 (39)* Diastolic BP (mm Hg) 54 ( 12) 58 ( 13) 57 ( 7) 58 (15) Mean BP (mm Hg) 63 ( 8) 70 ( 12 www.nature.com/scientificreports www.nature.com/scientificreports/ blood pressure, and positive correlation with norepinephrine treatment and NT-proBNP during the first 2 days, which is in full agreement with the above-cited reports showing a direct link between the degree of acute inflammation and the severity of hemodynamic deterioration in CS.…”

“…Although the precise mechanisms responsible for triggering such inflammation in CS remain undefined, they may include innate immune activation in response to the release of damage associated molecular patterns (DAMPs or alarmins) by injured cells in ischemic tissues [13][14][15] , or the translocation of pathogen-associated molecular patterns (PAMPs), such as endotoxin, from the ischemic intestine 16 . Heart rate (bpm) 84 ( 23) 92 ( 24) 87 ( 26) 89 (16) Systolic BP (mm Hg) 89 ( 15) 98 ( 14) 100 ( 14)* 112 (39)* Diastolic BP (mm Hg) 54 ( 12) 58 ( 13) 57 ( 7) 58 (15) Mean BP (mm Hg) 63 ( 8) 70 ( 12 www.nature.com/scientificreports www.nature.com/scientificreports/ blood pressure, and positive correlation with norepinephrine treatment and NT-proBNP during the first 2 days, which is in full agreement with the above-cited reports showing a direct link between the degree of acute inflammation and the severity of hemodynamic deterioration in CS. In contrast, IL-1β and IFNy were not elevated, and even displayed lower values than in our control population, suggesting that these two cytokines do not play a major role in the acute phase of CS.…”

Prognostic role of procalcitonin in ST-elevation myocardial infarction complicated by cardiogenic shock

“…6,8,15,16 Although most studies included a small number of patients with CS-STEMI, 16 few have studied the role of PCT in the prediction of outcomes in this subgroup. 8,[17][18][19] A comparison of studies assessing the role of PCT in CS-STEMI is depicted in Table 3. The patients in our study were younger.…”

Endotoxemia in Acute Heart Failure and Cardiogenic Shock: Evidence, Mechanisms and Therapeutic Options

“…Indeed, endotoxemia is not measured directly by this method, but is suggested by the drop of endotoxin antibodies in patients’ plasma, and the underlying hypothesis of antibody consumption is due to endotoxin exposure. However, the actual endotoxins were not measured, and the antibody titer, which provides only indirect assessment of endotoxemia, was not associated with mortality [ 52 ]. In the third article, endotoxin activity was measured in 16 patients with cardiogenic shock, but only one of the patients was found to have high endotoxin activity [ 53 ].…”