Cardiac fibrosis is a major driver of heart failure, a leading cause of morbidity and mortality worldwide. Advances in single-cell transcriptomics have revealed the pivotal role of SPP1+ macrophages in the pathogenesis of cardiac fibrosis, positioning them as critical mediators and promising therapeutic targets. SPP1+ macrophages, characterized by elevated expression of secreted phosphoprotein 1 (SPP1) and often co-expressing Triggering Receptor Expressed on Myeloid Cells 2 (TREM2), localize to fibrotic niches in the heart and other organs. These cells interact with activated fibroblasts and myofibroblasts, driving extracellular matrix remodeling and fibrosis progression. Their differentiation is orchestrated by signals such as CXCL4, GM-CSF, and IL-17A, further emphasizing their regulatory complexity. Therapeutic strategies targeting SPP1+ macrophages have shown encouraging preclinical results. Approaches include silencing Spp1 using antibody–siRNA conjugates and modulating key pathways involved in macrophage differentiation. These interventions have effectively reduced fibrosis and improved cardiac function in animal models. The mechanisms underlying SPP1+ macrophage function in cardiac fibrosis provide a foundation for innovative therapies aimed at mitigating pathological remodeling and improving outcomes in patients with heart failure. This emerging field has significant potential to transform the treatment of fibrotic heart disease.

Background: Coronary physiology assessment in rodents by ultrasound is an excellent noninvasive and easy to perform technique, including pulsed-wave Doppler (PWD) and myocardial contrast echocardiography (MCE). Both techniques and the corresponding calculated parameters were investigated in this study at rest as well as their response to pharmacologically induced stress. Methods: Left ventricular myocardial function was assessed in eight anaesthetised rats using transthoracic echocardiography. Coronary physiology was assessed by both PWD of the left coronary artery and MCE using a bolus method. Measurements were performed at rest and under stimulation with adenosine and dobutamine. Effects of stimulation on the calculated parameters were evaluated and rated by effect size (η²). Results: Changes could be demonstrated by selected parameters of PWD and MCE. The clearest effect in PWD was found for diastolic peak velocity (η² = 0.58). It increased from 528 ± 110 mm/s (mean ± standard deviation) at rest to 839 ± 342 mm/s (p = 0.001) with adenosine and 1093 ± 302 mm/s with dobutamine (p = 0.001). The most distinct effect from MCE was found for the normalised wash-in rate (η² = 0.58). It increased from 1.95 ± 0.35% at rest to 3.87 ± 0.85% with adenosine (p = 0.001) and 3.72 ± 1.03% with dobutamine (p = 0.001). Conclusion: Induced changes in coronary physiology by adenosine and dobutamine could successfully be monitored using MCE and PWD in anaesthetised rats. Due to the low invasiveness of the measurements, this protocol could be used for longitudinal animal studies.

The survival rate of cardiac arrest (CA) can be improved by utilizing percutaneous left ventricular assist devices (pLVADs) instead of conventional chest compressions. However, existing pLVADs require complex fluoroscopy-guided placement along a guidewire and suffer from limited blood flow due to their cross-sectional area. The recently developed self-expandable Impella CP (ECP) pLVAD addresses these limitations by enabling guidewire-free placement and increasing the pump cross-sectional area. This study evaluates the feasibility of resuscitation using the Impella ECP in a swine CA model. Eleven anesthetized pigs (73.8 ± 1.7 kg) underwent electrically induced CA, were left untreated for 5 min and then received pLVAD insertion and activation. Vasopressors were administered and defibrillations were attempted. Five hours after the return of spontaneous circulation (ROSC), the pLVAD was removed, and animals were monitored for an additional hour. Hemodynamics were assessed and myocardial function was evaluated using echocardiography. Successful guidewire-free pLVAD placement was achieved in all animals. Resuscitation was successful in 75% of cases, with 3.5 ± 2.0 defibrillations and 1.8 ± 0.4 mg norepinephrine used per ROSC. Hemodynamics remained stable post-device removal, with no adverse effects or aortic valve damage observed. The Impella ECP facilitated rapid guidewire-free pLVAD placement in fibrillating hearts, enabling successful resuscitation. These findings support a broader clinical adoption of pLVADs, particularly the Impella ECP, for CA.

Sufficient ventilation during cardiopulmonary resuscitation (CPR) is increasingly recognised as a critical determinant of patient outcomes. The effectiveness of ventilation training, however, likely depends on the anatomical and mechanical fidelity of CPR manikins. While chest compression mechanics of manikins have been studied extensively, ventilation-related anatomy, airflow pathways, and respiratory mechanics have not been evaluated systematically. This study analysed 10 adult CPR manikins from three manufacturers. Airway and lung replicas were documented using photography, video laryngoscopy, and bronchoscopy. Expiratory tidal volume and air leakage were measured during volume-controlled mechanical ventilation via facemask, supraglottic airway devices and endotracheal tube. Mechanics of the respiratory system were described by the peak and plateau airway pressures and respiratory compliance. Manikins differed substantially in airway design and expiratory airflow design. Three distinct expiratory mechanisms were identified, of which only one permitted exhalation through the airway and thus quantification of expiratory tidal volumes. Air leakage varied across manikins and airway devices, including during ventilation via advanced airway devices. Respiratory mechanics showed marked variability, with peak inspiratory pressures ranging from 21 ± 1 to 56 ± 1 mbar and compliances from 7 ± 0 to 51 ± 4 mL/mbar. Several models exhibited substantial leakage via the gastric channel of the i-gel® supraglottic airway. CPR manikins exhibited substantial variability in ventilation-related anatomy, airflow pathways, leakage and respiratory mechanics. None of the assessed manikins consistently approximated human ventilation characteristics across airway devices, underscoring the need for local evaluation of manikin-airway device combinations to optimise ventilation fidelity in CPR training.

Background: Previous studies have shown cardiac abnormalities in acute liver injury, suggesting a potential role in the associated high mortality. Methods: We designed an experimental study exploring the short-term effects of acute cholestasis-induced liver injury on cardiac function and structure in a rodent bile duct ligation (BDL) model to elucidate the potential interplay. Thirty-seven male Sprague-Dawley rats were subjected to BDL surgery (n = 28) or served as sham-operated (n = 9) controls. Transthoracic echocardiography, Doppler evaluation of the left anterior descending coronary artery, and myocardial contrast echocardiography were performed at rest and during adenosine and dobutamine stress 5 days after BDL. Immunohistochemical staining of myocardial tissue samples for hypoxia and inflammation as well as serum analysis were performed. Results: BDL animals exhibited acute liver injury with elevated transaminases, bilirubin, and total circulating bile acids (TBA) 5 days after BDL (TBA control: 0.81 ± 2.54 µmol/L vs. BDL: 127.52 ± 57.03 µmol/L; p < 0.001). Concurrently, cardiac function was significantly impaired, characterized by reduced cardiac output (CO) and global longitudinal strain (GLS) in the echocardiography at rest and under pharmacological stress (CO rest control: 120.6 ± 24.3 mL/min vs. BDL 102.5 ± 16.6 mL/min, p = 0.041; GLS rest control: −24.05 ± 3.8% vs. BDL: −18.5 ± 5.1%, p = 0.01). Myocardial perfusion analysis revealed a reduced myocardial blood flow at rest and a decreased coronary flow velocity reserve (CFVR) under dobutamine stress in the BDL animals (CFVR control: 2.1 ± 0.6 vs. BDL: 1.7 ± 0.5 p = 0.047). Immunofluorescence staining indicated myocardial hypoxia and increased neutrophil infiltration. Conclusions: In summary, acute cholestasis-induced liver injury can lead to impaired cardiac function mediated by coronary microvascular dysfunction, suggesting that major adverse cardiac events may contribute to the mortality of acute liver failure. This may be due to endothelial dysfunction and direct bile acid signaling.

Zusammenfassung: Die Aortenklappenstenose ist eine häufige Erkrankung, die dem behandelnden Anästhesisten profundes Wissen über die Pathophysiologie, Diagnostik und die perioperativen Besonderheiten der Erkrankung abverlangt. Eine neu aufgetretene Aortenklappenstenose wird vielfach erst durch klinische Leitsymptome (Dyspnoe, Synkopen, Angina pectoris) bzw. einen auffälligen Auskultationsbefund im Rahmen der anästhesiologischen Prämedikationsvisite entdeckt und erfordert ein interdisziplinäres Management, um die optimale Behandlung der Patienten im perioperativen Setting zu gewährleisten. Für die individuelle Auswahl des Anästhesieverfahrens ist eine präzise Befunderhebung im Rahmen der Prämedikationsvisite erforderlich, und darüber hinaus eine genaue Kenntnis der hämodynamischen Besonderheiten der Aortenklappenstenose. Der folgende Übersichtsartikel führt nach einer kurzen Rekapitulation der allgemeinen Pathophysiologie der Erkrankung durch die anästhesiologischen Besonderheiten, die Risikofaktoren für Komplikationen und das perioperative Management bei nichtkardiochirurgischen Operationen von Patienten mit Aortenklappenstenose.