Search

Background: Inflammatory responses play an important role in the pathophysiology of cardiogenic shock (CS). The aim of this study was to investigate the kinetics of procalcitonin (PCT), C-reactive protein (CRP), and interleukin-6 (IL-6) in CS and to assess their relation to clinical presentation, other biochemical variables, and prognosis. Methods: Levels of PCT, CRP and IL-6 were analyzed in serial plasma samples (0-120h) from 183 patients in the CardShock study. The study population was dichotomized by PCTmax >= and < 0.5 mu g/L, and IL-6 and CRPmax above/below median. Results: PCT peaked already at 24 h [median PCTmax 0.71 mu g/L (IQR 0.24-3.4)], whereas CRP peaked later between 48 and 72 h [median CRPmax 137mg/L (59-247)]. PCT levels were significantly higher among non-survivors compared with survivors from 12 h on, as were CRP levels from 24 h on (p < 0.001). PCTmax >= 0.5 mu g/L (60% of patients) was associated with clinical signs of systemic hypoperfusion, cardiac and renal dysfunction, acidosis, and higher levels of blood lactate, IL-6, growth-differentiation factor 15 (GDF-15), and CRPmax. Similarly, IL-6 > median was associated with clinical signs and biochemical findings of systemic hypoperfusion. PCTmax >= 0.5 mu g/L and IL-6 > median were associated with increased 90-day mortality (50% vs. 30% and 57% vs. 22%, respectively; p < 0.01 for both), while CRPmax showed no prognostic significance. The association of inflammatory markers with clinical infections was modest. Conclusions: Inflammatory markers are highly related to signs of systemic hypoperfusion in CS. Moreover, high PCT and IL-6 levels are associated with poor prognosis. (C) 2020 Elsevier B.V. All rights reserved.

Background: Cardiogenic shock (CS) is the most life-threatening manifestation of acute heart failure. Its complexity and high in-hospital mortality may justify the need for invasive monitoring with a pulmonary artery catheter (PAC). Methods: Patients with CS included in the CardShock Study, an observational, prospective, multicenter, European registry, were analyzed, aiming to describe the real-world use of PAC, evaluate its impact on 30-day mortality, and the ability of different hemodynamic parameters to predict outcomes. Results: Pulmonary artery catheter was used in 82 (37.4%) of the 219 patients. Cardiogenic shock patients who managed with a PAC received more frequently treatment with inotropes and vasopressors, mechanical ventilation, renal replacement therapy, and mechanical assist devices ( P < .01). Overall 30-day mortality was 36.5%. Pulmonary artery catheter use did not affect mortality even after propensity score matching analysis (hazard ratio = 1.17 [0.59-2.32], P = .66). Cardiac index, cardiac power index (CPI), and stroke volume index (SVI) showed the highest areas under the curve for 30-day mortality (ranging from 0.752-0.803) and allowed for a significant net reclassification improvement of 0.467 (0.083-1.180), 0.700 (0.185-1.282), 0.683 (0.168-1.141), respectively, when added to the CardShock risk score. Conclusions: In our contemporary cohort of CS, over one-third of patients were managed with a PAC. Pulmonary artery catheter use was associated with a more aggressive treatment strategy. Nevertheless, PAC use was not associated with 30-day mortality. Cardiac index, CPI, and SVI were the strongest 30-day mortality predictors on top of the previously validated CardShock risk score.

Background: The aim of this study was to assess the levels, kinetics, and prognostic value of growth differentiation factor 15 (GDF-15) in cardiogenic shock (CS). Methods and Results: Levels of GDF-15 were determined in serial plasma samples (0-120 h) from 177 CS patients in the CardShock study. Kinetics of GDF-15, its association with 90-day mortality, and incremental value for risk stratification were assessed. The median GDF-15(0h) level was 9647 ng/L (IQR 4500-19,270 ng/L) and levels above median were significantly associated with acidosis, hyperlactatemia, renal dysfunction, and higher 90-day mortality (56% vs 28%, P7000 ng/L was identified as a strong predictor of death (OR 5.0; 95% CI 1.9-3.8, P=.002). Adding GDF-15(12h) >7000 ng/L to the CardShock risk score improved discrimination and risk stratification for 90-day mortality. Conclusions: GDF-15 levels are highly elevated in CS and associated with markers of systemic hypoperfusion and end-organ dysfunction. GDF-15 helps to discriminate survivors from non-survivors very early in CS.

Changes in QRS duration and pattern are regarded to reflect severe ischemia in acute coronary syndromes (ACS), and ventricular conduction blocks (VCBs) are recognized high-risk markers in both ACS and acute heart failure. Our aim was to evaluate the prevalence, temporal evolution, association with clinical and angiographic parameters, and impact on mortality of VCBs in ACS-related cardiogenic shock (CS). Data of 199 patients with ACS-related CS from a prospective multinational cohort were evaluated with electrocardiogram data from baseline and day 3. VCBs including left or right bundle branch block, right bundle branch block and hemiblock, isolated hemiblocks, and unspecified intraventricular conduction delay were assessed. Fifty percent of patients had a VCB at baseline; these patients were older, had poorer left ventricular function and had more often left main disease compared with those without VCB. One-year mortality was over 2-fold in patients with VCB compared with those without VCB (68% vs 32%, p

BackgroundThe most common aetiology of cardiogenic shock (CS) is acute coronary syndrome (ACS), but even up to 20%-50% of CS is caused by other disorders. ST-segment deviations in the electrocardiogram (ECG) have been investigated in patients with ACS-related CS, but not in those with other CS aetiologies. We set out to explore the prevalence of different ST-segment patterns and their associations with the CS aetiology, clinical findings and 90-day mortality. MethodsWe analysed the baseline ECG of 196 patients who were included in a multinational prospective study of CS. The patients were divided into 3 groups: (a) ST-segment elevation (STE). (b) ST-segment depression (STDEP). (c) No ST-segment deviation or ST-segment impossible to analyse (NSTD). A subgroup analysis of the ACS patients was conducted. ResultsST-segment deviations were present in 80% of the patients: 52% had STE and 29% had STDEP. STE was associated with the ACS aetiology, but one-fourth of the STDEP patients had aetiology other than ACS. The overall 90-day mortality was 41%: in STE 47%, STDEP 36% and NSTD 33%. In the multivariate mortality analysis, only STE predicted mortality (HR 1.74, CI95 1.07-2.84). In the ACS subgroup, the patients were equally effectively revascularized, and no differences in the survival were noted between the study groups. ConclusionST-segment elevation is associated with the ACS aetiology and high mortality in the unselected CS population. If STE is not present, other aetiologies must be considered. When effectively revascularized, the prognosis is similar regardless of the ST-segment pattern in ACS-related CS.

Objectives The aim was to assess the extent of coronary artery disease and revascularization using baseline SYNTAX Score (bSS) and residual SYNTAX Score (rSS) in patients with cardiogenic shock (CS) secondary to ST-segment elevation myocardial infarction (STEMI). The prognostic impact of SYNTAX Score (SS) was evaluated and assessed for additive value over clinical risk scores. Background bSS and rSS have been proven to be useful in risk stratification in stable coronary artery disease as well as in acute coronary syndromes, but they have not been studied in STEMI related CS. Methods Patients from a multinational prospective study of CS were analyzed. The study population was divided into tertiles according to bSS. The Cox regression and receiver operating characteristic (ROC) curves were used to assess the predictive power of SS. Results Of the 61 studied patients, 85% were male and the mean age was 67 years. Median bSS was 22 (15-32) and rSS 7 (0-13). Ninety-day mortality was 43%. bSS had negative prognostic value in multivariable analysis (HR 1.06, 95% CI 1.01-1.10). However, additive value over clinical risk scores was limited. rSS was not associated with mortality, whereas post-percutaneous coronary intervention (PCI) TIMI flow 3 of infarct-related artery (IRA) predicted better survival. Conclusions In STEMI related CS, the added value of bSS and rSS over clinical assessment and risk scores is limited. Our results suggest that while immediate PCI in order to restore blood flow to the IRA is essential, deferring the treatment of residual lesions does not seem to be associated with worse prognosis.

final draft, peerReviewed

Familial Atrial Fibrillation Introduction One-third of lone atrial fibrillation (AF) presents as familial disorder. Heterogeneity of both genetic background and clinical manifestations remains largely uncharacterized. We aimed to evaluate the clinical characteristics and especially the triggering factors of familial AF. Methods and Results Probands were screened from 84 consecutive lone AF patients seen in our tertiary hospital arrhythmia clinic. Those confirmed to have at least 1 first-degree relative with lone AF were included. 12-lead ECG, Holter recording, and cardiac ultrasound were performed. Data concerning arrhythmias and other medical history were collected. Altogether 17 kindreds with 59 AF patients, 52 of whom had lone AF, were identified. Initiation of AF was atrial extrasystolia (PACs) related in 35%, and vagal or sympathetic in 30% of cases. Within any given family, the characteristics related to AF initiation were the same in two-thirds of kindreds. AV conduction abnormalities were found in 2 families, sinus node dysfunction in 2 families, and both in 3 families. Frequent premature ventricular complexes (>1,000/24 hours) were observed in 9 families. Additional comorbidities included dilative cardiomyopathy and sudden death in 3 families. Conclusions In familial AF the proportion of PACs-related AF is lower than expected. The arrhythmia triggers for lone AF in general are heterogeneous but often family specific. Concomitant rhythm disorders, as well as cardiomyopathies, are common in patients with familial AF. A positive family history for AF in an apparently lone AF patient may be a marker for wider spectrum of cardiac pathology.

Objective Mutations in the LMNA gene encoding lamins A and C of the nuclear lamina are a frequent cause of cardiomyopathy accounting for 5–8% of familial dilated cardiomyopathy (DCM). Our aim was to study disease onset, presentation and progression among LMNA mutation carriers. Methods Clinical follow-up data from 27 LMNA mutation carriers and 78 patients with idiopathic DCM without an LMNA mutation were collected. In addition, ECG data were collected and analysed systematically from 20 healthy controls. Results Kaplan-Meier analysis revealed no difference in event-free survival (death, heart transplant, resuscitation and appropriate implantable cardioverter-defibrillator therapy included as events) between LMNA mutation carriers and DCM controls (p=0.5). LMNA mutation carriers presented with atrial fibrillation at a younger age than the DCM controls (47 vs 57 years, p=0.003). Male LMNA mutation carriers presented with clinical manifestations roughly a decade earlier than females. In close follow-up non-sustained ventricular tachycardia was detected in 78% of LMNA mutation carriers. ECG signs of septal remodelling were present in 81% of the LMNA mutation carriers, 21% of the DCM controls and none of the healthy controls giving a high sensitivity and specificity for the standard ECG in distinguishing LMNA mutation carriers from patients with DCM and healthy controls. Conclusions Male LMNA mutation carriers present clinical manifestations at a younger age than females. ECG septal remodelling appears to distinguish LMNA mutation carriers from healthy controls and patients with DCM without LMNA mutations.

We wanted to illustrate the right-to-left impulse propagation routes during sinus in patients with paroxysmal atrial fibrillation (PAF), as alterations in conduction patterns have been linked to the pathogenesis of PAF, and as no large patient materials have been published. Patients underwent 3-D electroanatomical contact mapping prior to catheter ablation. The site of the earliest left atrial (LA) activation was determined. Three different interatrial routes were identified, either as solitary pathways (36/50 patients, 72%) or in their combinations (14/50). Bachmann’s bundle (BB) was involved in the majority of the cases with solitary routes (25/36). More seldom, impulse propagation occurred near the oval fossa (FO) (7/36) or the coronary sinus ostium (4/36). In patients with combined routes, both the BB (10/14) and FO routes (11/14) were included in most cases. In PAF patients, LA can be activated during sinus rhythm through three distinct connections, either encompassing a single route or via any combination of these connections. In one third, the earliest LA activation occurs outside BB. The knowledge of the propagation patterns may give insight into the pathophysiology of PAF and into refining ablation therapy.

Aims Alteration in conduction from right to left atrium (LA) is linked to susceptibility to atrial fibrillation (AF). We examined whether different inter-atrial conduction pathways can be identified non-invasively by magnetocardiographic mapping (MCG). Methods and results In 27 patients undergoing catheter ablation of paroxysmal AF, LA activation sequence was determined during sinus rhythm using invasive electroanatomic mapping. Before this, 99-channel magnetocardiography was recorded over anterior chest. The orientation of the magnetic fields during the early (40–70 ms from P onset) and later part (last 50%) of LA depolarization was determined using pseudocurrent conversion. Breakthrough of electrical activation to LA occurred through Bachmann bundle (BB) in 14, margin of fossa ovalis (FO) in 3, coronary sinus ostial region (CS) in 2, and their combinations in 10 cases by invasive reference in total of 29 different P-waves. Based on the combination of pseudocurrent angles over early and late parts of LA activation, the MCG maps were divided to three types. These types correctly identified the LA breakthrough sites to BB, CS, FO, or their combinations in 27 of 29 (93%) cases. Conclusion Magnetocardiographic mapping seems capable of distinguishing inter-atrial conduction pathways. Recognizing the inter-atrial conduction pattern may assist in understanding the pathogenesis of AF and identifying the subgroups for patient-tailored therapy.

Background: Abnormalities in the electromagnetic signal of the atria during sinus rhythm could serve as markers of triggering foci or substrate for atrial fibrillation (AF). We examined atrial electrophysiologic properties noninvasively by using magnetocardiographic mapping (MCG) in patients with paroxysmal lone AF to find whether any difference exists between those who have frequent triggers of AF and who don't. Methods: MCG was recorded over anterior chest during sinus rhythm in 80 patients with paroxysmal lone AF (44 ± 12 years, 61 males) and 80 matched controls. Atrial wave duration (Pd) and root mean square amplitudes of the last 40 ms (RMS40) of the averaged filtered atrial complex were determined automatically. Patients expressing atrial arrhythmias triggering AF episodes were classified as focal AF. Results: The Pd was 109 ms in patients and 104 ms in controls (P = 0.007). In focal AF (72%) the Pd was slightly prolonged and its proportion of the PR interval was larger, but RMS40 was normal compared to controls. In other patients, the Pd was close to controls, but the RMS40 was reduced (59 ± 17 vs74 ± 36 fT, P = 0.006). Pd and atrial RMS amplitudes were unrelated to duration of AF history or frequency of recurrences. Conclusion: Clinical subclasses of lone AF seem to possess distinct signal profiles of atrial depolarization. Differences in electrophysiological properties between these subclasses may reflect pathogenetic variation and could have implications on diagnostics and therapy.

Objective Mutations in the LMNA gene encoding lamins A and C of the nuclear lamina are a frequent cause of cardiomyopathy accounting for 5–8% of familial dilated cardiomyopathy (DCM). Our aim was to study disease onset, presentation and progression among LMNA mutation carriers. Methods Clinical follow-up data from 27 LMNA mutation carriers and 78 patients with idiopathic DCM without an LMNA mutation were collected. In addition, ECG data were collected and analysed systematically from 20 healthy controls. Results Kaplan-Meier analysis revealed no difference in event-free survival (death, heart transplant, resuscitation and appropriate implantable cardioverter-defibrillator therapy included as events) between LMNA mutation carriers and DCM controls (p=0.5). LMNA mutation carriers presented with atrial fibrillation at a younger age than the DCM controls (47 vs 57 years, p=0.003). Male LMNA mutation carriers presented with clinical manifestations roughly a decade earlier than females. In close follow-up non-sustained ventricular tachycardia was detected in 78% of LMNA mutation carriers. ECG signs of septal remodelling were present in 81% of the LMNA mutation carriers, 21% of the DCM controls and none of the healthy controls giving a high sensitivity and specificity for the standard ECG in distinguishing LMNA mutation carriers from patients with DCM and healthy controls. Conclusions Male LMNA mutation carriers present clinical manifestations at a younger age than females. ECG septal remodelling appears to distinguish LMNA mutation carriers from healthy controls and patients with DCM without LMNA mutations., published version, peerReviewed

One-third of lone atrial fibrillation (AF) presents as familial disorder. Heterogeneity of both genetic background and clinical manifestations remains largely uncharacterized. We aimed to evaluate the clinical characteristics and especially the triggering factors of familial AF.Probands were screened from 84 consecutive lone AF patients seen in our tertiary hospital arrhythmia clinic. Those confirmed to have at least 1 first-degree relative with lone AF were included. 12-lead ECG, Holter recording, and cardiac ultrasound were performed. Data concerning arrhythmias and other medical history were collected. Altogether 17 kindreds with 59 AF patients, 52 of whom had lone AF, were identified. Initiation of AF was atrial extrasystolia (PACs) related in 35%, and vagal or sympathetic in 30% of cases. Within any given family, the characteristics related to AF initiation were the same in two-thirds of kindreds. AV conduction abnormalities were found in 2 families, sinus node dysfunction in 2 families, and both in 3 families. Frequent premature ventricular complexes (1,000/24 hours) were observed in 9 families. Additional comorbidities included dilative cardiomyopathy and sudden death in 3 families.In familial AF the proportion of PACs-related AF is lower than expected. The arrhythmia triggers for lone AF in general are heterogeneous but often family specific. Concomitant rhythm disorders, as well as cardiomyopathies, are common in patients with familial AF. A positive family history for AF in an apparently lone AF patient may be a marker for wider spectrum of cardiac pathology.

Background The purpose of this study was to identify early features of lamin A/C gene mutation related dilated cardiomyopathy (DCM) with cardiovascular magnetic resonance (CMR). We characterise myocardial and functional findings in carriers of lamin A/C mutation to facilitate the recognition of these patients using this method. We also investigated the connection between myocardial fibrosis and conduction abnormalities. Methods Seventeen lamin A/C mutation carriers underwent CMR. Late gadolinium enhancement (LGE) and cine images were performed to evaluate myocardial fibrosis, regional wall motion, longitudinal myocardial function, global function and volumetry of both ventricles. The location, pattern and extent of enhancement in the left ventricle (LV) myocardium were visually estimated. Results Patients had LV myocardial fibrosis in 88% of cases. Segmental wall motion abnormalities correlated strongly with the degree of enhancement. Myocardial enhancement was associated with conduction abnormalities. Sixty-nine percent of our asymptomatic or mildly symptomatic patients showed mild ventricular dilatation, systolic failure or both in global ventricular analysis. Decreased longitudinal systolic LV function was observed in 53% of patients. Conclusions Cardiac conduction abnormalities, mildly dilated LV and depressed systolic dysfunction are common in DCM caused by a lamin A/C gene mutation. However, other cardiac diseases may produce similar symptoms. CMR is an accurate tool to determine the typical cardiac involvement in lamin A/C cardiomyopathy and may help to initiate early treatment in this malignant familiar form of DCM.

Aims Patients with a history of atrial fibrillation (AF) have previously been shown to have altered atrial conduction, as seen non-invasively using signal-averaged P-wave analysis. However, little is known about the P-wave morphology in patients in the early phases of AF with structurally normal hearts. Methods and results Thirty-six patients with lone AF were included before the age of 40 years (34 ± 4 years, 34 men) and compared with age- and gender-matched control subjects. Standard 12-lead electrocardiogram (ECG) was recorded for at least 10 s. P-wave morphology and duration were estimated using signal-averaged P-wave analysis. Echocardiography was performed in association with the ECG recording. Heart rate (67 ± 13 vs. 65 ± 7 b.p.m., P = 0.800) and PQ-interval (163 ± 16 vs. 164 ± 23 ms, P = 0.629) were similar in AF cases and controls, as was P-wave duration (136 ± 13 vs. 129 ± 13 ms, P = 0.107). The distribution of P-wave morphology differed between the AF cases and controls [33/58/0/8 vs. 75/25/0/0% (Type 1/Type 2/Type 3/atypical), P = 0.001], with a larger proportion of patients with AF exhibiting signs of impaired interatrial conduction. Conclusion A significant difference in P-wave morphology distribution was seen between patients with early-onset, lone paroxysmal AF and age- and gender-matched healthy control subjects. This finding indicates that alterations in atrial electrophysiology are common in the early stage of the arrhythmia, and since it occurs in young patients without co-morbidity may well be the cause rather than the consequence of AF. (Less)

Background: Atrial fibrillation (AF) causes electrical, functional, and structural changes in the atria. We examined electrophysiologic remodeling caused by AF and its reversal noninvasively by applying a new atrial signal analysis based on magnetocardiography (MCG). Methods: In 26 patients with persistent AF, MCG, signal-averaged electrocardiography (SAECG), and echocardiography were performed immediately after electrical cardioversion (CV), and repeated after 1 month in 15 patients who remained in sinus rhythm (SR). Twenty-four matched subjects without history of AF served as controls. P-wave duration (Pd) and dispersion (standard deviation of Pd values in individual channels) and root mean square amplitudes of the P wave over the last 40 ms portions (RMS40) were determined. Results: In MCG Pd was longer (122.8 ± 18.2 ms vs 101.5 ± 14.6 ms, P < 0.01) and RMS40 was higher (60.4 ± 28.2 vs 46.9 ± 19.1 fT) in AF patients immediately after CV as compared to the controls. In SAECG Pd dispersion was increased in AF patients. Mitral A-wave velocity and left atrial (LA) contraction were decreased and LA diameter was increased (all P < 0.01). After 1 month, Pd in MCG still remained longer and LA diameter greater (both P < 0.05), while RMS40 in MCG, Pd dispersion in SAECG, mitral A-wave velocity, and LA contraction were recovered. Conclusions: Magnetocardiographically detected atrial electrophysiologic alterations in persistent AF diminish rapidly although incompletely during maintained SR after CV. This might be related to the known early high and late lower, but still existent tendency to AF relapses.

Background Different P-wave morphologies during sinus rhythm as displayed on standard ECGs have been postulated to correspond to differences in interatrial conduction. Objective The purpose of this study was to evaluate the hypothesis by comparing P-wave morphologies using left atrial activation maps. Methods Twenty-eight patients (mean age 49 ± 9 years) admitted for ablation of paroxysmal atrial fibrillation were studied. Electroanatomic mapping of left atrial activation was performed at baseline during sinus rhythm with simultaneous recording of standard 12-lead ECG. Unfiltered signal-averaged P waves were analyzed to determine orthogonal P-wave morphology. The morphology was subsequently classified into one of three predefined types. All analyses were blinded. Results The primary left atrial breakthrough site was the fossa ovalis in 8 patients, Bachmann bundle in 18, and coronary sinus in 2. Type 1 P-wave morphology was observed in 9 patients, type 2 in 17, and type 3 in 2. Seven of eight patients with fossa ovalis breakthrough had type 1 P-wave morphology, 16 of 18 patients with Bachmann bundle breakthrough had type 2 morphology, and both patients with coronary sinus breakthrough had type 3 P-wave morphology. Overall, P-wave morphology criteria correctly identified the site of left atrial breakthrough in 25 (89%) of 28 patients. Conclusion In the vast majority of patients, P-wave morphology derived from standard 12-lead ECG can be used to correctly identify the left atrial breakthrough site and the corresponding route of interatrial conduction.

O18 Atrial fibrillation shows recurrent spatial characteristics in magnetocardiography Ville Mantynen, Raija Jurkko, Lauri Toivonen, Juha Montonen BioMag Laboratory, HUSLAB, Helsinki University Central Hospital, Helsinki, Finland Department of Biomedical Engineering and Computational Science, Aalto University School of Science and Technology, Helsinki, Finland Department of Internal Medicine, Helsinki University Central Hospital, Helsinki, Finland

Encephalitis has been described as a rare complication of pandemic 2009 (H1N1) influenza A infection in children and adolescents. This report is on two adult patients who presented with encephalitis in relation to acute H1N1 influenza. Encephalitis is therefore also a potential complication of pandemic 2009 (H1N1) influenza infection in adults.

Dilated cardiomyopathy (DCM) is a major cause of heart failure and sudden cardiac death. About one third of DCM is familial. Several DCM disease genes have been identified, many of them limited to only single individuals or families. A/C gene (LMNA) is sofar the most significant disease gene of DCM. Cardiac magnetic resonance imaging (MRI) plays an important role in characterization and risk stratification of patients with DCM. About one third of DCM patients have demonstrated mid-myocardial linear enhancement on DE-MRI in a non-coronary distribution, due to fibrosis.

Aims Optimal outcome after cardiogenic shock (CS) depends on a coordinated healing response in which both debris removal and extracellular matrix tissue repair play a crucial role. Excessive inflammation can perpetuate a vicious circle, positioning leucocytes as central protagonists and potential therapeutic targets. High levels of circulating Triggering Receptor Expressed on Myeloid cells-1 (TREM-1), were associated with death in acute myocardial infarction confirming excessive inflammation as determinant of bad outcome. The present study aims to describe the association of soluble TREM-1 with 90-day mortality and with various organ injuries in patients with CS. Methods and results This is a post-hoc study of CardShock, a prospective, multicenter study assessing the clinical presentation and management in patients with CS. At the time of this study, 87 patients had available plasma samples at either baseline, and/or 48 h and/or 96-120 h for soluble TREM-1 (sTREM-1) measurements. Plasma concentration of sTREM-1 was higher in 90-day non-survivors than survivors at baseline [median: 1392 IQR: (724-2128) vs. 621 (525-1233) pg/mL, p = 0.008), 48 h (p = 0.019) and 96-120 h (p = 0.029). The highest tertile of sTREM-1 at baseline (threshold: 1347 pg/mL) was associated with 90-day mortality with an unadjusted HR 3.08 CI 95% (1.48-6.42). sTREM-1 at baseline was not associated to hemodynamic parameters (heart rate, blood pressure, use of vasopressors or inotropes) but rather with organ injury markers: renal (estimated glomerular filtration rate, p = 0.0002), endothelial (bio-adrenomedullin, p = 0.018), myocardial (Suppression of Tumourigenicity 2, p = 0.002) or hepatic (bilirubin, p = 0.008). Conclusion In CS patients TREM-1 pathway is highly activated and gives an early prediction of vital organ injuries and outcome. [GRAPHICS] .