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BackgroundEnhanced bleeding remains a serious problem after cardiac surgery, and fibrinolysis is often involved. We speculate that lower plasma concentrations of plasminogen activator inhibitor – 1 (PAI-1) preoperatively and tissue plasminogen activator/PAI-1 (t-PA/PAI-1) complex postoperatively might predispose for enhanced fibrinolysis and increased postoperative bleeding.MethodsTotally 88 adult patients (mean age 66 ± 10 years) scheduled for cardiac surgery, were enrolled into a prospective study. Blood samples were collected pre-operatively, on admission to the recovery and at 6 and 24 hours postoperatively. Patients with a surgical bleeding that was diagnosed during reoperation were discarded from the study. The patients were allocated to two groups depending on the 24-hour postoperative chest tube drainage (CTD): Group I > 500ml, Group II ≤ 500ml. Associations between CTD, PAI-1, t-PA/PAI-1 complex and D-dimer were analyzed with SPSS.ResultsNine patients were excluded because of surgical bleeding. Of the 79 remaining patients, 38 were allocated to Group I and 41 to Group II. The CTD volumes correlated with the preoperative plasma levels of PAI-1 (r = − 0.3, P = 0.009). Plasma concentrations of preoperative PAI-1 and postoperative t-PA/PAI-1 complex differed significantly between the groups (P < 0.001 and P = 0.012, respectively). Group I displayed significantly lower plasma concentrations of fibrinogen and higher levels of D-dimer from immediately after the operation and throughout the first 24 hours postoperatively.ConclusionsLower plasma concentrations of PAI-1 preoperatively and t-PA/PAI-1 complex postoperatively leads to higher plasma levels of D-dimer in association with more postoperative bleeding after cardiac surgery.

Background Conduit arteries, especially the aorta, play a major role in ensuring efficient cardiac function and optimal microvascular flow due to their viscoelastic properties. Studies in animals and on isolated arteries show that acute systemic inflammation can cause aortic stiffening which affects hemodynamic efficiency. Carotid-femoral pulse wave velocity, a measure of aortic stiffness, may be useful as a bedside investigational method in patients with early sepsis admitted to intensive care, as circulatory changes can lead to multiple organ failure and increased mortality. This study aims to investigate arterial stiffness in early sepsis and its association with clinical outcomes. Methods This prospective observational study included adult patients with severe sepsis or septic shock admitted to our intensive care unit ( n = 45). Their carotid-femoral pulse wave velocity was measured within 24 h of admission. We assessed the progression of multiple organ as well as cardiovascular failure by sequential SOFA scores. Prediction models for the progression of multiple organ and cardiovascular failure were constructed using multivariate logistic regression with pulse wave velocity and vasopressor use as predictors. A Cox proportional hazards model was used to examine the relationship between pulse wave velocity and survival time. Results The median pulse wave velocity for the cohort was 14.6 (8.1–24.7) m/s. There was no association between pulse wave velocity and the progression of multiple organ failure, before or after adjustment for vasopressor use. No association was found between pulse wave velocity and subsequent improvement in cardiovascular failure in the subgroup of patients who had cardiovascular instability at baseline. Cox regression and survival analyses with age, APACHE II, and baseline SOFA as confounders showed a shorter hospital survival time for patients with pulse wave velocity > 24.7 m/s (HR = 9.45, 95% CI 1.24–72.2; P = 0.03). Conclusions Patients with severe sepsis and septic shock admitted to intensive care have higher arterial stiffness than in the general population. No convincing association was found between pulse wave velocity at admission and the progression of multiple organ or cardiovascular failure, although the group with pulse wave velocity > 24.7 m/s had shorter survival time. Electronic supplementary material The online version of this article (10.1186/s40635-019-0252-3) contains supplementary material, which is available to authorized users.

Introduction Vascular dysfunction due to reduced nitric oxide bioavailability plays an important role in the pathogenesis of sepsis. This meta-analysis examines evidence from published literature to evaluate whether in the adult population the presence/severity of sepsis is associated with impaired vasoreactivity. Material and methods We performed a search of the Medline, Scopus, and EMBASE databases to identify observational studies using measurement of reactive hyperaemia in adult patients with sepsis. After data extraction using predefined protocol, qualitative synthesis of findings was performed regarding consistency of findings between methods, evidence of association between vascular reactivity and severity of sepsis, multiple organ failure, and death. A meta-analyses of standardised mean differences in vasoreactivity between groups was performed, in which data were available for relevant outcomes. Results Eighteen studies using four methods to measure vascular reactivity from a total of 466 were included in the analysis. The pooled standardised mean difference estimate showed that septic patients had less reactive hyperaemia than controls (–2.59, 95% CI: –3.46 to –1.72; p < 0.00001), and peak hyperaemic blood flow was lower in patients with sepsis than in the control group (SMD = –1.42, 95% CI: –2.14 to –0.70; p = 0.0001). The combined SMD between non survivors and survivors was –0.36 (95% CI: –0.67 to –0.06; p = 0.02) for reactive hyperaemia and –0.70 (95% CI: –1.13 to –0.27; p = 0.001) for peak hyperaemic blood flow. Conclusions Septic patients have attenuated vascular reactivity when compared to healthy volunteers. There are insufficient data indicating that these changes can identify patients at risk of worsening organ failure or death.