AbstractAimsTranscatheter edge‐to‐edge repair of the mitral valve (M‐TEER) is known for its low complication rates. However, the optimal level and duration of post‐procedural care remain unclear. This study aimed to identify the specific timeframe of post‐procedural complications following M‐TEER.Methods and resultsWe conducted a retrospective analysis of 865 patients who underwent M‐TEER at the University Hospital Düsseldorf between August 2010 and August 2023. Our analysis focused on a comprehensive examination of all acute post‐procedural complications (1–100 h), considering the time point of occurrence or diagnosis. The complication analysed included cardiogenic shock, pericardial tamponade, stroke, cardiac arrhythmias, bleeding, acute kidney injury, myocardial infarction, peripheral vascular ischaemia and in‐hospital mortality.ResultsThe median age was 80 (74, 84) years, and the EuroScore II was high (6.5 [4.0, 12.0] %). Functional mitral regurgitation (MR) was more common than degenerative or mixed MR (69% vs. 20%. respectively; 11%). Technical success rate was 97.2%. Overall, acute post‐procedural complications occurred in 87 patients (10.1%). Most complications (75.9%) occurred within the first 4 h post‐procedure. 12.6% of the complications occurred during the period between 4 and 24 h post‐procedure, and 11.5% of the complications happened between 24 and 100 h post‐procedure. Life‐threatening complications were observed only within the first 4 h post‐procedure.ConclusionsThe majority of post‐procedural complications after M‐TEER occur within the first 4 h, with pericardial tamponade and major bleeding occurring only during this period. These findings provide valuable insight for physicians in determining the optimal surveillance and monitoring duration after M‐TEER within clinical settings.

Background Recent trials suggested that extracorporeal cardio-pulmonary resuscitation (ECPR) with veno-arterial extracorporeal membrane oxygenation (VA-ECMO) or “ECMELLA” (VA-ECMO plus Impella®) may improve short-term survival and neurological outcomes in selected patients with refractory cardiac arrest. However, long-term effects on cardiac, cognitive, physical and psychological health need further study. A multidisciplinary post-ECPR outpatient care program was developed at two centers, involving cardiologists, neurologists, psychologists and medical sociologists to assess seven key health dimensions. Methods This bicentric, multidisciplinary study, conducted from May 2021 to April 2023, included adult ECPR survivors. Outcomes were assessed approximately 22 months post-cardiac arrest, focusing on cardiac, neurological, psychological and multi-organ functions, as well as social, professional and physical performance. Results This study included 33 ECPR survivors, who were predominantly male (70%) with a mean age of 55 years. Left-ventricular ejection fraction improved significantly, from 22% during ICU stay to 51% at follow-up in the ECMELLA group and from 31% to 51% in the VA-ECMO group (p=0.006). Many patients reported dizziness or dyspnea (>52%) during daily activities, with a median New York Heart Association class of 2, EQ-5D-5L score of 53 and elevated NT-proBNP levels. Despite normal neurological scores, 46% had memory issues, 39% struggled with daily organization, 52% had depression and 12% had suicidal thoughts. Physical performance was reduced, with a mean distance of 394 meters in the 6-minute walk test and a 6-minute bicycle ergometry time. Conclusion ECPR patients showed significant improvement in left ventricular function over time but their neuropsychological and physical abilities remained compromised. Timely, multidisciplinary rehabilitation is required, starting in the intensive care unit and extending to include psychological support and community reintegration strategies after discharge.

In Europe, more than 300,000 persons per year experience out-of-hospital cardiac arrest (OHCA). Despite medical progress, only few patients survive with good neurological outcome. For many issues, evidence from randomized trials is scarce. OHCA often occurs for cardiac causes. Therefore, we established the national, prospective, multicentre German Cardiac Arrest Registry (G-CAR). Herein, we describe the first results of the pilot phase. Over a period of 16 months, 15 centres included 559 consecutive OHCA patients aged ≥ 18 years. The median age of the patients was 66 years (interquartile range 57;75). Layperson resuscitation was performed in 60.5

AbstractAimsMyocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown. We aimed at establishing a relevant role of cardiac inflammation in the impairment of mitochondrial energy production in advanced ischaemic and non‐ischaemic HF.MethodsWe included 81 patients with stage D HF (ICM, n = 44; DCM, n = 37) undergoing left ventricular assist device implantation (n = 59) or heart transplantation (n = 22) and obtained left ventricular tissue samples during open heart surgery. We quantified mitochondrial oxidative capacity, citrate synthase activity (CSA) and fibrosis and lymphocytic infiltration. We considered infiltration of >14 CD3+ cells/mm2 relevant inflammation.ResultsPatients with ICM or DCM did not differ regarding age (61.5 ± 5.7 vs. 56.5 ± 12.7 years, P = 0.164), sex (86% vs. 84% male, P = 0.725), type 2 diabetes mellitus (34% vs. 18%, P = 0.126) or chronic kidney disease (8% vs. 11%, P = 0.994). ICM exhibited oxidative capacity reduced by 23% compared to DCM (108.6 ± 41.4 vs. 141.9 ± 59.9 pmol/(s*mg), P = 0.006). Maximum production of reactive oxygen species was not significantly different between ICM and DCM (0.59 ± 0.28 vs. 0.69 ± 0.36 pmol/(s*ml), P = 0.196). Mitochondrial content, detected by CSA, was lower in ICM (359.6 ± 164.1 vs. 503.0 ± 198.5 nmol/min/mg protein, P = 0.002). Notably, relevant inflammation was more common in ICM (27% vs. 6%, P = 0.024), and the absolute number of infiltrating leucocytes correlated with lower oxidative capacity (r = −0.296, P = 0.019). Fibrosis was more prevalent in ICM (20.9 ± 21.2 vs. 7.2 ± 5.6% of area, P = 0.002), but not associated with oxidative capacity (r = −0.13, P = 0.327).ConclusionsMore than every fourth ICM patient with advanced HF displays myocardial inflammation in the range of inflammatory cardiomyopathy associated with reduced mitochondrial oxidative capacity. Future studies may evaluate inflammation in ICM at earlier stages in standardised fashion to explore the therapeutic potential of immunosuppression to influence trajectories of HF in ICM.

Background: The search for the best therapeutic approach in cardiopulmonary resuscitations (CPR) remains open to question. In this study, we evaluated if Amiodarone administration during CPR was associated with short-term mortality or neurological development. Methods: A total of 232 patients with sudden cardiac arrest (CA) with shockable rhythms were included in our analysis. Propensity score matching based on age, gender, type of CA, and CPR duration was used to stratify between patients with and without Amiodarone during CPR. Primary endpoints were short-term mortality (30-day) and neurological outcomes assessed by the cerebral performance category. Secondary endpoints were plasma lactate, phosphate levels at hospital admission, and the peak Neuron-specific enolase. Results: Propensity score matching was successful with a caliper size used for matching of 0.089 and a sample size of n = 82 per group. The 30-day mortality rates were similar between both groups (p = 0.24). There were no significant differences in lactate levels at hospital admission and during the following five days between the groups. Patients receiving Amiodarone showed slightly higher phosphate levels at hospital admission, while the levels decreased to a similar value during the following days. Among CA survivors to hospital discharge, no differences between the proportion of good neurological outcomes were detected between the two groups (p = 0.58), despite slightly higher peak neuron-specific enolase levels in CA patients receiving Amiodarone (p = 0.03). Conclusions: Amiodarone administration is not associated with short-term mortality or neurological outcomes in CA patients with shockable rhythms receiving CPR.

Abstract Aims Cancer therapy-related cardiac dysfunction (CTRCD) is a dreaded complication of anthracycline therapy. CTRCD most frequently appears in patients with cardiovascular risk factors (CVR) or known cardiovascular disease. However, limited data exist on incidence and course of anthracycline-induced CTRCD in patients without preexisting risk factors. We therefore aimed to longitudinally investigate a cohort of young women on anthracycline treatment due to breast cancer without cardiovascular risk factors or known cardiovascular disease (NCT03940625). Methods and results We enrolled 59 women with primary breast cancer and scheduled anthracycline-based therapy, but without CVR or preexisting cardiovascular disease. We conducted a longitudinal assessment before, immediately and 12 months after cancer therapy with general laboratory, electrocardiograms, echocardiography and cardiovascular magnetic resonance (CMR), including myocardial relaxometry with T1, T2 and extracellular volume mapping. Every single patient experienced a drop in CMR-measured left ventricular ejection fraction (LVEF) of 6 ± 3% immediately after cancer therapy. According to the novel definition 32 patients (54.2%) developed CTRCD after 12 months defined by reduction in LVEF, global longitudinal strain (GLS) and/or biomarkers elevation, two of them were symptomatic. Global myocardial T2 relaxation times as well as myocardial mass increased coincidently with a decline in wall-thickening. While T2 values and myocardial mass normalized after 12 months, LVEF and GLS remained impaired. Conclusion In every single patient anthracyclines induce a decline of myocardial contractility, even among patients without pre-existing risk factors for CTRCD. Our data suggest to thoroughly evaluate whether this may lead to an increased risk of future cardiovascular events. Graphical Abstract Reduced myocardial contractility in low-risk patients receiving anthracycline-based cancer therapy. This study included 59 otherwise healthy women with primary breast cancer undergoing anthracycline-based chemotherapy. CMR was performed at baseline, directly and 12 months after cancer therapy. A decline in left ventricular function was observed in every single patient accompanied by transient edema. More than 50% were diagnosed with cancer therapy related cardiovascular dysfunction. LVEF: left ventricular function, CTRCD: cancer therapy related cardiovascular dysfunction, GLS = Global longitudinal strain, hs-TnT = high sensitive Troponin T, NT-pro BNP = NT-pro brain natriuretic peptide

AbstractAimsData on the clinical profiles of patients with transthyretin amyloidosis cardiomyopathy (ATTR‐CM) in the post‐approval era of tafamidis 61 mg are lacking. Study aims were characterization of contemporary ATTR‐CM patients, analysis of potential eligibility for the ‘Transthyretin Amyloidosis Cardiomyopathy Clinical Trial’ (ATTR‐ACT) and identification of factors associated with the decision on tafamidis 61 mg treatment.Methods and resultsThis retrospective study analysed ATTR‐CM patients seen at eight University Hospitals in the first year after approval of tafamidis 61 mg for ATTR‐CM in Germany (April 2020 to March 2021). The cohort comprised 366 patients (median age 79 [74; 82] years, 84% male), with 47% and 45% of the cohort being in National Amyloidosis Centre ATTR stage ≥ II and NYHA class ≥ III, respectively. Sixty‐four per cent of patients met key eligibility criteria of the pivotal ATTR‐ACT. In recently diagnosed patients (58% with diagnosis ≤6 months), the rate of variant ATTR was significantly lower than in patients diagnosed more than 6 months ago (9.3% vs. 19.7%). Of the 293 patients without prior ATTR specific treatment, tafamidis 61 mg was newly initiated in 77%. Patients with tafamidis 61 mg treatment were significantly younger, were more often eligible for ATTR‐ACT, had lower NYHA class and higher serum albumin levels. These variables explained 16% of the variance of treatment decision. Unadjusted survival was higher in patients with than those without treatment (1‐year survival 98.6% vs. 87.3%, P < 0.001).ConclusionsWild‐type ATTR was the primary aetiology amongst contemporary ATTR‐CM patients and almost two‐thirds of patients were in an advanced disease stage. Clinical profiles of 64% of patients in routine care matched those of the ATTR‐ACT. Further effort is needed to detect patients at an earlier disease stage and to validate criteria justifying treatment initiation.

Percutaneous left ventricular assist devices (pVADs) may be used in patients with cardiogenic shock (CS) to stabilize hemodynamics and maintain sufficient end-organ perfusion. Vascular complications are commonly observed in patients with pVAD support. We aimed to assess the relationship between pVAD implantation time and access-site complication rates. This retrospective observational study included all patients who underwent pVAD insertion for the treatment of CS at our university hospital between 2014 and 2021 (n = 224). Depending on the pVAD insertion time, the patients were assigned to the on-hours (n = 120) or off-hours group (n = 104). Both groups had comparable baseline characteristics and comorbidities. The rate of access-site–related complications was higher in the off-hours group than in the on-hours group (26% vs. 10%, p = 0.002). Premature discontinuation of pVAD support to prevent limb ischemia or manage access-site bleeding was required more often in the off-hours group than in the on-hours group (14% vs. 5%, p = 0.016). Pre-existing peripheral artery disease and implantation time off-hours were independent predictors for access-siterelated vascular complications. In conclusion, patients with CS in whom pVAD was inserted during off-hours had higher rates of access-site–related complications and premature discontinuation of pVAD support than those in whom pVAD was inserted during on-hours.

Aims: Identifying patients who may benefit from mechanical circulatory support (MCS) after out-of-hospital cardiac arrest (OHCA) and return of spontaneous circulation (ROSC) remains challenging; thus, a search for helpful biomarkers is warranted. We aimed to evaluate phosphate and lactate levels on admission regarding their associations with survival with and without MCS. Methods: In 224 OHCA patients who achieved ROSC, the initial phosphate and lactate levels were investigated to discriminate in-hospital mortality by receiver operating characteristic (ROC) curves. According to the Youden Index (YI) from the respective ROC, the groups were risk stratified by both biomarkers, and 30-day mortality was analyzed in patients with and without MCS. Results: Within the entire collective, MCS was not associated with a better chance of survival. Both phosphate and lactate level elevations showed good yet comparable discriminations to predict mortality (areas under the curve: 0.80 vs. 0.79, p = 0.74). In patients with initial phosphate values > 2.2 mmol/L (>YI), 30-day mortality within the MCS cohort was lower (HR 2.3, 95% CI: 1.4–3.7; p = 0.0037). In patients with lower phosphate levels and groups stratified by lactate, 30-day mortality was similar in patients with and without MCS. Conclusions: We found a significant association between survival and MCS therapy in patients with phosphate levels above 2.2 mmol/L (Youden Index), and a similar discrimination of patient overall survival by lactate and phosphate. Prospective studies should assess the possible independent prognostic value of phosphate and its clearance for MCS efficiency.

Abstract Background Cytomegalovirus (CMV) infections after heart transplantation (HTx) can cause cardiac allograft vasculopathy. Consequently, monitoring and prophylaxis for cytomegalovirus deoxyribonucleic acid (CMV‐DNAemia) within the first weeks after HTx is recommended. Methods All patients who underwent HTx between September 2010 and 2021 surviving the first 90 days (n = 196) were retrospectively reviewed. The patients were divided on the prevalence of CMV‐DNAemia during the first postoperative year after the end of the prophylaxis. A total of n = 35 (20.1%) developed CMV‐DNAemia (CMV group) and were compared to patients without CMV‐DNAemia (controls, n = 139). The remaining patients (n = 22) were excluded due to incomplete data. Results Positive donors and negative recipients (D+/R−) and negative donors and positive recipients (D−/R+) serology was significantly increased and D−/R− decreased in the CMV group (p < .01). Furthermore, the mean age was 57.7 ± 8.7 years but only 53.6 ± 10.0 years for controls (p = .03). Additionally, the intensive care unit (p = .02) and total hospital stay (p = .03) after HTx were approximately 50% longer. Interestingly, the incidence of CMV‐DNAemia during prophylaxis was only numerically increased in the CMV group (5.7%, respectively, 0.7%, p = .10), the same effect was also observed for postoperative infections. Multivariate analyses confirmed that D+/R− and D−/R+ CMV immunoglobulin G match were independent risk factors for postprophylaxis CMV‐DNAemia. Conclusion Our data should raise awareness of CMV‐DNAemia after the termination of regular prophylaxis, as this affects one in five HTx patients. Especially old recipients as well as D+/R− and D−/R+ serology share an elevated risk of late CMV‐DNAemia. For these patients, prolongation, or repetition of CMV prophylaxis, including antiviral drugs and CMV immunoglobulins, may be considered.

BACKGROUND:Out-of-hospital cardiac arrest (OHCA) remains a frequent medical emergency with low survival rates even after a return of spontaneous circulation (ROSC). Growing evidence supports formation of dedicated teams in scenarios like cardiogenic shock to improve prognosis. Thus, the European Resuscitation Council (ERC) recommended introduction of Cardiac Arrest Centers (CAC) in their 2015 guidelines. Here, we aimed to elucidate the effects of newly introduced CACs in Germany regarding survival rate and neurological outcome. METHODS:A multicenter retrospective observational cohort study was performed at three university hospitals and outcomes after OHCA were compared before and after CAC accreditation. Primary outcomes were survival until discharge and favorable neurological status (CPC 1 or 2) at discharge. RESULTS:In total 784 patients (368 before and 416 after CAC accreditation) were analyzed. Rates of immediate percutaneous coronary intervention (40 vs. 52%, p = 0.01) and implementation of extracorporeal CPR (8 vs. 13%, p < 0.05) increased after CAC accreditation. Likelihood of favorable neurological status at discharge was higher after CAC accreditation (71 vs. 87%, p < 0.01), whereas overall survival remained similar (35 vs. 35%, p > 0.99). CONCLUSION:CAC accreditation is linked to higher rates of favorable neurological outcome and unchanged overall survival.

Background: Loss of functional capacity is one of the hallmarks in cardiovascular aging. Cocoa flavanols (CF) exert favorable effects on endothelial function, blood pressure, and inflammation. These cardiovascular health markers worsen with increasing age and limit functional exercise capacity. Aim: To investigate the effect of CF on cardiorespiratory-fitness in healthy elderly people. Methods: In a randomized, double-masked, placebo-controlled, parallel-group dietary intervention trial, 68 healthy elderly people (55-79 years, 28 female) received either 500 mg of CF or a nutrient-matched control capsule twice a day for 30 days. Primary endpoint was defined as peak oxygen consumption (VO2) in a cardiopulmonary exercise test (CPET). Secondary endpoints were oxygen pulse (VO2 per heart rate (HR)), resting blood pressure (BP), and resting vascular function. Results: After 30 days of CF intake peakVO2 increased by 190 ml min-1 (95% CI 1-371 ml min-1) and peakVO2 per kg by 2.5 ml (min kg)-1 (95% CI 0.30-4.2 ml (min kg)-1). O2-pulse increased by 1.7 ml (95% CI 0.29-3.2 ml) and max exercise capacity by 9.6 W (95% CI 2.1-17.7 W). CF decreased resting systolic and diastolic BP by 5.4 mmHg (95% CI -10.7 to -0.1 mmHg) and 2.9 mmHg (95% CI -5.5 to -0.4 mmHg), respectively. Flow-mediated vasodilation (FMD) increased by an absolute 1.3% (95% CI 0.76-1.79%) in the CF group. Indexes of pulmonary function were not affected. No changes for primary and secondary endpoints were detected in control. Conclusion: CF substantially improve markers of cardiorespiratory fitness in healthy elderly humans highlighting their potential to preserve cardiovascular health with increasing age.

Purpose: Although a moderate proportion of cardiac arrest (CA) patients achieve a return of spontaneous circulation (ROSC), few survive to discharge, mostly with poor neurological development. As serum phosphate levels were described as elevated after cardiopulmonary resuscitation (CPR), we asked whether these elevations would predict a higher risk of mortality and impaired neurological outcome in CA patients following ROSC. Methods: Initial serum phosphate levels, survival, and neurologic status at discharge of 488 non-traumatic CA patients treated at a single German hospital after achieving ROSC were analyzed. The cut-off value of phosphate for mortality prediction was determined using the receiver operator characteristic (ROC) curve, and patients were divided accordingly for comparison. Results were validated by analyzing phosphate levels in a multi-centric cohort containing 3299 CA patients from the eICU database of the United States. Results: In the German cohort, ROC analysis showed a 90% specificity for phosphate levels >2.7 mmol/L to predict mortality (AUC: 0.76, p < 0.0001), and phosphate level elevations were associated with higher in-hospital mortality (crude odds ratio 3.04, 95% CI 2.32 to 4.08). Patients with initial phosphate levels >2.7 mmol/L had significantly higher mortality in both analyzed collectives (p < 0.0001). Similarly, patients from the German cohort who initially had higher phosphate levels also showed a higher proportion of impaired neurological status at discharge and morphological signs of brain injury. Conclusions: In CA patients following ROSC, initial serum phosphate levels >2.7 mmol/L predict higher mortality and impaired neurological outcome. Our data suggests that phosphate determination might improve the preciseness of the overall and neurologic prognostication in patients after CPR following ROSC.

Purpose It was reported that mRNA-based Covid-19 vaccines rarely cause myocarditis. Although endomyocardial biopsy (EMB) is considered the gold standard for diagnosing myocarditis, no standardized study has been performed after Covid-19 vaccination in humans. Because routine EMB is frequently performed in heart transplant recipients (HTX), we aimed here to investigate effects of Covid-19 vaccination by analyzing myocardial inflammation with state-of-the-art quantitative immunohistochemistry. Methods Consecutive patients after HTX who underwent routine EMB at a median of 167 days before and 136 days after the first Covid 19 vaccination with an mRNA vaccine were included and divided into groups with and without postvaccination inflammatory response, defined as increased CD3+ lymphocyte count >14/ mm2. Patients with evidence of rejection (ISHLT grade >1) or >14 CD3+ lymphocytes/mm2 at baseline were excluded. Results The final analysis included 46 patients with a mean age of 63 years and a time after HTX of 2.4 years. Thirty-six (78%) patients remained below the threshold of 14 CD3+ lymphocytes/mm2. However, in 10 (22%) recipients, we detected significant leukocyte infiltration by quantitative analysis of EMB after vaccination (4 vs. 33.7 leukocytes/ mm2, p=0.001). The groups did not differ with respect to age (63 vs. 57 years, p=0.21), body mass index (25 vs. 24 kg/m2, p=0.24), NYHA class (≥2 at 19 vs. 10%, p=0.4), NT-ProBNP levels (592 vs. 514 ng/l, p=0.55) or myocardial CD3+ cell count (4.9 vs. 2.6 cells/mm2, p=0.07) before vaccination. Patients with leukocyte infiltration remained clinically inapparent with stable NYHA class (≥2 in 10 vs. 20%, p=0.99) and did not have increased NT-ProBNP levels (514 vs. 478 ng/l, p=0.03). No hospitalizations for suspected myocarditis were reported. Conclusion For the first time, we report subclinical myocardial leukocyte infiltration after Covid-19 mRNA vaccination in one in five patients without clinical sequelae during the short observation period.

Objective: Although the application of higher doses of norepinephrine (NE) in potential organ donors is a frequent reason for heart decline, its associations with outcomes after heart transplantation (HTx) are discussed controversially. Therefore, we aimed to explore donor NE support’s potential impact on outcomes in our single-center heart transplant cohort. Methods: All patients who had undergone HTx in our center between September 2010 and April 2022 (n = 241) were screened for eligibility. From those, all patients with complete data on donor NE support (n = 238) were included. Recipients were divided into three groups according to their donor NE support: without support (n = 26), with low support of 0.01–0.2 µg/kg/min (n = 132), and with high support of > 0.2 µg/kg/min (n = 80). Receiver operating characteristics (ROC) and Kaplan Meier analysis was used to investigate the association of donor NE support and mortality after heart transplantation. Recipient and donor variables, including peri- and postoperative characteristics, were reviewed and compared. Results: NE support in donors ranged between 0 and 2.94 µg/kg/min (median 0.13 µg/kg/min, IQR 0.05–0.26 µg/kg/min). No association between donor NE support and mortality after HTx was observed (AUC for overall survival 0.494). Neither Kaplan-Meier analysis in survival up to 5 years after transplantation (Log Rank p = 0.284) nor group comparisons showed significant differences between the groups. With few exceptions, baseline characteristics in recipients and donors were comparable between the groups. Regarding peri- and postoperative parameters, increasing donor NE support was associated with a longer duration of mechanical ventilation (68 h and 95 h vs. 47 h), longer postoperative IMC/ICU stay (14 vs. 15 vs. 19 days), and a higher need for mechanical life support post-HTx (26% and 39% vs. 12%). Conclusion: In this retrospective analysis, NE support in donors prior to heart transplantation was unrelated to differing survival after heart transplantation. However, higher doses of donor NE were associated with prolonged ventilation, longer duration on IMC/ICU, and a higher need for extracorporeal life support in recipients post-HTx.

BACKGROUND:Despite successful resuscitation with return of spontaneous circulation (ROSC), the prediction of survival in patients suffering out-of-hospital cardiac arrest (OHCA) remains difficult. Several studies have shown alterations in sublingual microcirculation in the critical ill. We hypothesized that early alterations in sublingual microcirculation may predict short-term survival after OHCA.METHODS:We prospectively included all adults admitted to our university hospital between April and September 2019 with ROSC following OHCA. Sidestream dark-field microscopy to obtain sublingual microcirculation was performed at admission and after 6, 12 and 24 hours. Primary outcome was survival until discharge.RESULTS:Twenty-five patients were included. Six hours after ROSC, the proportion of perfused small vessels (PPVsmall ) was lower in non-survivors than in survivors (85 ± 7.9 vs. 75 ± 6.6%; p = .01). PPVsmall did not correlate with serum lactate. Stratification for survival with cutoff values >78.4% for PPVsmall 6 h post-admission and <5.15 mmol/l for initial serum lactate as suggested by ROC-Analyses results in a positive predictive value of 100% and a negative one of 67% for our study population.CONCLUSION:Estimating short-term prognosis of OHCA patients with ROSC may be supported by measuring the PPVsmall at the sublingual microcirculation 6 hours after admission.

Acute kidney injury (AKI) is a common complication post-PCI. Here, in a single-center observational registry, we compared the frequency of AKI in patients at elevated risk for AKI (based on Mehran risk stratification scoring) who underwent VA-ECMO- or Impella-supported high-risk PCI. A total of 28 patients scheduled for elective high-risk PCI with mechanical circulatory support were studied prospectively. All patients were turned down for surgery due to exceedingly high risk. Allocation to VA-ECMO (n=11) or Impella (n=17) was performed according to site-specific restrictions on the daily availability of the VA-ECMO platform as a prospective enrollment and performed prior to initiation of PCI. We analyzed AKI incidence as our primary endpoint, as well as PCI success, duration, and peripheral complications. All patients were successfully revascularized and had MCS weaned at the end of the procedure. Baseline GFR and procedural contrast media were similar. Despite similar risks for AKI as calculated by the Mehran score (35 ± 18.9 vs. 31 ± 16.6 %; p=0.55), patients supported by Impella during PCI demonstrated a reduced incidence of AKI (55 vs. 12 %; p=0.03). MCS-assisted high-risk PCI with VA-ECMO or Impella is feasible. However, Impella is associated with a shorter procedure time and a lower incidence of AKI.

During circulatory shock, gastrointestinal microcirculation is impaired, especially via activation of the renin-angiotensin-aldosterone system. Therefore, inhibition of the renin-angiotensin-aldosterone system might be beneficial in maintaining splanchnic microcirculation. The aim of this study was to analyze whether locally applied losartan influences gastric mucosal perfusion (µflow, µvelo) and oxygenation (µHbO2) without systemic hemodynamic changes. In repetitive experiments six anesthetized dogs received 30 mg losartan topically on the oral and gastric mucosa during normovolemia and hemorrhage (-20% blood volume). Microcirculatory variables were measured with reflectance spectrometry, laser Doppler flowmetry and incident dark field imaging. Transpulmonary thermodilution and pulse contour analysis were used to measure systemic hemodynamic variables. Gastric barrier function was assessed via differential absorption of inert sugars. During normovolemia, losartan increased gastric µflow from 99 ± 6 aU to 147 ± 17 aU and µvelo from 17 ± 1 aU to 19 ± 1 aU. During hemorrhage, losartan did not improve µflow. µvelo decreased from 17 ± 1 aU to 14 ± 1 aU in the control group. Application of losartan did not significantly alter µvelo (16 ± 1 aU) compared to the control group and to baseline levels (17 ± 1 aU). No effects of topical losartan on macrohemodynamic variables or microcirculatory oxygenation were detected. Gastric microcirculatory perfusion is at least partly regulated by local angiotensin receptors. Topical application of losartan improves local perfusion via vasodilation without significant effects on systemic hemodynamics. During mild hemorrhage losartan had minor effects on regional perfusion, probably because of a pronounced upstream vasoconstriction.

Einleitung: Der hamorrhagische Schock stellt auch in Folge seiner Kompli-kationen, wie der Sepsis oder des Multiorganversagens, eine haufige und schwerwiegende Erkrankung dar. Bei der Entstehung dieser Komplikationen kommt es uber eine kompromittierte Mikrozirkulation zu einer gestorten Barrierefunktion der intestinalen Mukosa. Durch seine vasokonstriktive Wirkung scheint das im Schock vermehrt sezernierte Angiotensin (AT) II entscheidend daran beteiligt zu sein. Durch Applikation eines Antagonisten am AT1-Rezeptor (Losartan) im hamorrhagischen Schock konnte demnach die intestinale Mikrozirkulation aufrechterhalten werden und auf diese Weise das Auftreten der o.g. Komplikationen verhindert werden. Zur Vermeidung systemischer Nebenwirkungen sollte die Applikation des Losartans topisch erfolgen. Methoden: Nach Genehmigung durch die zustandige Behorde wurden die Experimente an sechs anasthesierten Foxhounds in wiederholter, randomisierter Reihenfolge verblindet durchgefuhrt. Dabei wurden jeweils 30mg Losartan bzw. NaCl-Losung unter physiologischen oder hamorrhagischen (20% des Blutvolumens) Kreislaufbedingungen und anschliesender Retransfusion appliziert. Die orale und gastrale Mikrozirkulation wurde mittels Reflektionsspektrofotometrie und Laser-Doppler-Technik kontinuierlich beurteilt. Parallel wurde intermittierend die orale Mukosa mittels incident dark field illumination untersucht. Systemische Kreislaufparameter wurden kontinuierlich aufgezeichnet. Die statistische Auswertung erfolgte mittels einer 2-way ANOVA und eines Bonferroni post-hoc Test. Dargestellt sind MW  SEM, p Ergebnisse: Lokal appliziertes Losartan verbesserte unter physiologischen Kreislaufbedingungen den gastralen µflow im Vergleich zur Kontrollgruppe (147  17 vs. 106  9 aU), wahrend dieser Effekt unter hypovolamischen Kreislaufbedingungen nur tendenziell (p=0.09) nachweisbar war (125  9 vs. 95  16 aU). Die µHbO2 der gastralen Mukosa wurde durch die lokale Losartan-Applikation nicht beeinflusst. Die Messungen an der oralen Mukosa, sowie die systemischen Kreislaufparameter zeigten keine Beeinflussung durch Losartan. Diskussion: Unterschiede in der Expression von AT-II-Rezeptoren in der oralen und gastralen Mukosa sowie histologische Unterschiede zwischen den beiden Messorten konnten den unterschiedlichen Messergebnissen zugrunde liegen. Verstarkte Ausschuttung von AT II im hamorrhagischen Schock konnte bei kompetitiver Antagonisierung durch Losartan zu einem verminderten Effekt im Schock gefuhrt haben. Unter Hamorrhagie vermehrt ausgeschuttetes Vasopressin konnte uber eine vorgeschaltete Vasokonstriktion ebenfalls einen verminderten Effekt durch Losartan im Schock erklaren. Diese Studie legt also folgende Schlusse nahe: 1. Die lokale Applikation von Losartan erhoht den Blutfluss der gastralen Mikrozirkulation unter physiologischen Kreislaufbedingungen. 2. Die lokale Applikation von Losartan erhoht tendenziell den Blutfluss der gastralen Mukosa unter hypovolamischen Kreislaufbedingungen. 3. Die lokale Applikation von Losartan an oraler und gastraler Mukosa hat keinen Einfluss auf systemische Kreislaufparameter.