Search Results (33)

Background: Among patients with congenital heart disease, particularly those with a history of undergoing the Fontan operation, pregnancy presents a significant maternal–fetal risk, especially when complicated by severe valvular dysfunction. Lung reperfusion syndrome (LRS) is a rare but life-threatening complication occurring following valve intervention. Multidisciplinary management, including by Cardio-Obstetrics teams, is essential for optimizing outcomes in such high-risk cases. Methods: We present the case of a 37-year-old pregnant patient with previously repaired tetralogy of Fallot (via the Fontan procedure) who presented at 24 weeks gestation with worsening severe pulmonary stenosis and right-ventricular dysfunction. The patient had been lost to cardiac follow-up for over a decade. She experienced recurrent arrhythmias, including supraventricular and non-sustained ventricular tachycardia, prompting hospital admission. A multidisciplinary team recommended transcatheter pulmonic valve replacement (TPVR), performed at 28 weeks’ gestation. Results: Post-TPVR, the patient developed acute hypoxia and hypotension, consistent with Lung Reperfusion Syndrome, necessitating intensive cardiopulmonary support. Despite initial stabilization, progressive maternal respiratory failure and fetal compromise led to an emergent cesarean delivery. The neonate’s neonatal intensive care unit (NICU) course was complicated by spontaneous intestinal perforation, while the mother required intensive care unit (ICU)-level care and a bronchoscopy due to new pulmonary findings. She was extubated and discharged in stable condition on postoperative day five. Conclusions: This case underscores the complexity of managing severe congenital heart disease and valve pathology during pregnancy. Lung reperfusion syndrome should be recognized as a potential complication following TPVR, particularly in pregnant patients with Fontan physiology. Early involvement of a multidisciplinary Cardio-Obstetrics team and structured peripartum planning are critical to improving both maternal and neonatal outcomes. Full article

Introduction: Postreperfusion syndrome (PRS) is associated with complications following liver transplantation (LT). Mannitol may play a role in attenuating PRS as a free radical scavenger. This study aimed to evaluate the association between intraoperative mannitol administration and the incidence of PRS and postoperative acute kidney injury (AKI) in LT. Methods: A retrospective analysis of adult liver-only transplantation between August 2019 and January 2023 at the Mount Sinai Hospital was performed. Patients in the mannitol group received 25G of the drug intravenously prior to reperfusion. Any recipients with pre-existing renal diagnoses were excluded. Demographic, laboratory, intraoperative, and hospital course data were extracted from an institutional data warehouse. Multivariable logistic regressions were used to evaluate the association between mannitol administration and PRS, AKI, early allograft dysfunction, and postoperative cardiac complications. Negative binomial regression was used to evaluate the association with postoperative length of stay (LOS) and ICU LOS. Results: 495 LT cases were included. A total of 81 patients received mannitol before graft reperfusion, while 414 patients did not. The incidence of PRS in patients who received mannitol was 13% and 17% for those who did not receive mannitol (p = 0.53). Additionally, 79% of patients who received mannitol experienced AKI at 7 days, compared to 73% in those who did not receive mannitol (p = 0.48). In the multivariable regression models, mannitol administration was not associated with decreased incidence of PRS or postoperative AKI. It was, however, associated with increased postoperative cardiac complications (risk-adjusted odds ratio 2.70, 95% confidence interval 1.15–6.14, p = 0.02). Conclusions: Mannitol administration during LT was not an effective therapy for reducing PRS or postoperative AKI. Full article

Background: Cardiac arrest (CA) is a leading cause of mortality and morbidity, with survivors often developing post-cardiac arrest syndrome (PCAS), characterized by systemic inflammation, ischemia–reperfusion injury (IRI), and multiorgan dysfunction. Acute kidney injury (AKI), a frequent complication, is associated with increased mortality and prolonged intensive care unit (ICU) stays. This study evaluates AKI incidence and progression in cardiac arrest patients managed with different temperature protocols and explores urinary biomarkers’ predictive value for AKI risk. Methods: A prospective, single-center observational study was conducted, including patients with Return of Spontaneous Circulation (ROSC) post-cardiac arrest. Patients were stratified into three groups: therapeutic hypothermia (TH) at 33 °C, Targeted Temperature Management (TTM) at 35 °C, and no temperature management (No TTM). AKI was defined using KDIGO criteria, with serum creatinine and urinary biomarkers (TIMP-2 and IGFBP7) measured at regular intervals during ICU stay. Results: AKI incidence at 72 h was 31%, varying across protocols. It was higher in the No TTM group at 24 h and in the TH and TTM groups during rewarming. Persistent serum creatinine elevation and fluid imbalance were notable in the TH group. Biomarkers indicated moderate tubular stress in the TTM and No TTM groups. Conclusions: AKI is a frequent complication post-cardiac arrest, with the rewarming phase identified as critical for renal vulnerability. Tailored renal monitoring, biomarker-guided risk assessment, and precise temperature protocols are essential to improve outcomes. Full article

Pulmonary embolism (PE) is a life-threatening medical condition caused by the thrombotic occlusion of one or more branches of the lung vasculature, which represents the third most common cause of cardiovascular mortality after myocardial infarction and stroke. PE treatment requires a tailored approach based on accurate risk stratification and personalized treatment decision-making. Anticoagulation is the cornerstone of PE management, yet patients at higher clinical risk may require more rapid reperfusion therapies. In recent years, transcatheter treatment has emerged as a valuable option for patients with intermediate–high or high-risk PE who have contraindications to systemic thrombolysis. Recent advancements in catheter-directed therapies, such as catheter-directed thrombolysis (CDT) and catheter-directed mechanical thrombectomy (CDMT), provide minimally invasive options for swift symptom relief and hemodynamic stabilization. This review aims to provide a practical approach for optimal patient selection and management for PE percutaneous therapies, supported by a thorough evaluation of the current evidence base supporting these procedures. A focus on post-procedural management, the prevention of recurrence, and monitoring for long-term complications such as chronic pulmonary hypertension and post-PE syndrome is also specifically tackled. Full article

Cerebral hyperperfusion syndrome (CHS) is a serious post-procedural complication of carotid artery stenting (CAS). The pathophysiological mechanisms of CHS in the absence of arterial hypertension (AH) remain only partially understood. We performed a systematic literature search of the PubMed database using the terms »cerebral hyperperfusion syndrome«, »hypotension«, »hyperperfusion«, »stroke«, »intracranial hemorrhages«, »risk factors«, »carotid revascularization«, »carotid stenting«, »carotid endarterectomy«, »blood-brain barrier«, »endothelium«, »contrast encephalopathy«, and combinations. We present a case of a normotensive female patient who developed CHS post-CAS for symptomatic carotid stenosis while being hypotensive with complete recovery. We identified 393 papers, among which 65 were deemed relevant to the topic. The weighted average prevalence of CHS after CAS is 1.2% [0.0–37.7%] with that of intracranial hemorrhage (ICH) being 0.51% [0–9.3%]. Recently symptomatic carotid stenosis or contralateral carotid revascularization, urgent intervention, acute carotid occlusion, contralateral ≥70% stenosis, and the presence of leptomeningeal collaterals were associated with CHS. A prolonged hemodynamic instability after CAS conveys a higher risk for CHS. However, none of the articles mentioned isolated hypotension as a risk factor for CHS. Whereas mortality after ICH post-CAS ranges from 40 to 75%, in the absence of ICH, CHS generally carries a good prognosis. AH is not obligatory in CHS development. Even though impaired cerebral autoregulation and post-revascularization changes in cerebral hemodynamics seem to play a pivotal role in CHS pathophysiology, our case highlights the complexity of CHS, involving factors like endothelial dysfunction and sudden reperfusion. Further research is needed to refine diagnostic and management approaches for this condition. Full article

Background and Objectives: Postreperfusion syndrome (PRS) is a significant challenge in liver transplantation (LT), leading to severe circulatory and metabolic complications. Ischemic preconditioning (IPC), including remote IPC (RIPC), can mitigate ischemia-reperfusion injury, although its efficacy in LT remains unclear. This study evaluated the impact of paired RIPC, involving the application of RIPC to both the recipient and the living donor, on the incidence of PRS and the need for rescue epinephrine during living-donor LT (LDLT). Materials and Methods: This retrospective observational cohort analysis included 676 adult patients who had undergone elective LDLT between September 2012 and September 2022. After applying exclusion criteria and propensity score matching (PSM), 664 patients were categorized into the paired RIPC and non-RIPC groups. The primary outcomes were the occurrence of PRS and the need for rescue epinephrine during reperfusion. Results: The incidence of PRS and the need for rescue epinephrine were significantly lower in the paired RIPC group than in the non-RIPC group. Furthermore, the incidence of postoperative acute kidney injury was lower in the paired RIPC group. Multivariable logistic regression adjusted for propensity scores indicated that paired RIPC was significantly associated with a reduced occurrence of PRS (odds ratio: 0.672, 95% confidence interval: 0.479–0.953, p = 0.021). Conclusions: Paired RIPC, involving both the recipient and the living donor, effectively reduces the occurrence of PRS and the need for rescue epinephrine during LDLT. These findings suggest that paired RIPC protects against ischemia-reperfusion injury in LDLT. Future randomized controlled trials are needed to verify our results and to explore the underlying mechanisms of the protective effects of RIPC. Full article

The close interaction between neurons and astrocytes has been extensively studied. However, the specific behavior of these cells after ischemia-reperfusion injury and hypothermia remains poorly characterized. A growing body of evidence suggests that mitochondria function and putative transference between neurons and astrocytes may play a fundamental role in adaptive and homeostatic responses after systemic insults such as cardiac arrest, which highlights the importance of a better understanding of how neurons and astrocytes behave individually in these settings. Brain injury is one of the most important challenges in post-cardiac arrest syndrome, and therapeutic hypothermia remains the single, gold standard treatment for neuroprotection after cardiac arrest. In our study, we modeled ischemia-reperfusion injury by using in vitro enhanced oxygen-glucose deprivation and reperfusion (eOGD-R) and subsequent hypothermia (HPT) (31.5 °C) to cell lines of neurons (HT-22) and astrocytes (C8-D1A) with/without hypothermia. Using cell lysis (LDH; lactate dehydrogenase) as a measure of membrane integrity and cell viability, we found that neurons were more susceptible to eOGD-R when compared with astrocytes. However, they benefited significantly from HPT, while the HPT effect after eOGD-R on astrocytes was negligible. Similarly, eOGD-R caused a more significant reduction in adenosine triphosphate (ATP) in neurons than astrocytes, and the ATP-enhancing effects from HPT were more prominent in neurons than astrocytes. In both neurons and astrocytes, measurement of reactive oxygen species (ROS) revealed higher ROS output following eOGD-R, with a non-significant trend of differential reduction observed in neurons. HPT after eOGD-R effectively downregulated ROS in both cells; however, the effect was significantly more effective in neurons. Lipid peroxidation was higher after eOGD-R in neurons, while in astrocytes, the increase was not statistically significant. Interestingly, HPT had similar effects on the reduction in lipoperoxidation after eOGD-R with both types of cells. While glutathione (GSH) levels were downregulated after eOGD-R in both cells, HPT enhanced GSH in astrocytes, but worsened GSH in neurons. In conclusion, neuron and astrocyte cultures respond differently to eOGD-R and eOGD-R + HTP treatments. Neurons showed higher sensitivity to ischemia-reperfusion insults than astrocytes; however, they benefited more from HPT therapy. These data suggest that given the differential effects from HPT in neurons and astrocytes, future therapeutic developments could potentially enhance HPT outcomes by means of neuronal and astrocytic targeted therapies. Full article

The KOSovan Acute Coronary Syndrome (KOS-ACS) Registry is established as a prospective, continuous, nationwide, web-based registry that is operated online. The KOS-ACS registry is designed with the following objectives: (1) to obtain data on the demographic, clinical, and laboratory characteristics of ACS patients treated in Kosovo; (2) to create a national database with information on health care in ACS patients treated in Kosovo; (3) to identify the national features of associations between ACS characteristics and clinical outcomes, including mortality, complications, the length of hospital stay, and the quality of clinical care; and (4) to propose a practical guide for improving the quality and efficiency of ACS treatment in Kosovo. The Kosovo Society of Cardiology and University of Prishtina will be responsible for the development of the KOS-ACS registry and centralized data analysis at the national level. The KOS-ACS Registry will enroll all patients admitted, at any of the registered clinical centers, with the diagnosis of ACS and who will be clinically managed at any of the Kosovo hospitals. Data on patient demographics, clinical characteristics, previous and hospital drug treatment, and reperfusion therapy will be collected. The type of ACS (unstable angina, NSTEMI, or STEMI) will also be clearly defined. The time from first medical contact to balloon inflation (FMC-to-balloon) and door-to-ballon time will be registered. In-hospital death and complications will be registered. Data on the post-hospital primary outcome (MACE: cardiac death, all-cause mortality, hospitalization, stroke, need for coronary revascularization) of patients, at 30 days and 1 year, will be included in the registry. Full article

Background: Mitochondrial dysfunction, which is triggered by systemic ischemia–reperfusion (IR) injury and affects various organs, is a key factor in the development of post-cardiac arrest syndrome (PCAS). Current research on PCAS primarily addresses generalized mitochondrial responses, resulting in a knowledge gap regarding organ-specific mitochondrial dynamics. This review focuses on the organ-specific mitochondrial responses to IR injury, particularly examining the brain, heart, and kidneys, to highlight potential therapeutic strategies targeting mitochondrial dysfunction to enhance outcomes post-IR injury. Methods and Results: We conducted a narrative review examining recent advancements in mitochondrial research related to IR injury. Mitochondrial responses to IR injury exhibit considerable variation across different organ systems, influenced by unique mitochondrial structures, bioenergetics, and antioxidative capacities. Each organ demonstrates distinct mitochondrial behaviors that have evolved to fulfill specific metabolic and functional needs. For example, cerebral mitochondria display dynamic responses that can be both protective and detrimental to neuronal activity and function during ischemic events. Cardiac mitochondria show vulnerability to IR-induced oxidative stress, while renal mitochondria exhibit a unique pattern of fission and fusion, closely linked to their susceptibility to acute kidney injury. This organ-specific heterogeneity in mitochondrial responses requires the development of tailored interventions. Progress in mitochondrial medicine, especially in the realms of genomics and metabolomics, is paving the way for innovative strategies to combat mitochondrial dysfunction. Emerging techniques such as mitochondrial transplantation hold the potential to revolutionize the management of IR injury in resuscitation science. Conclusions: The investigation into organ-specific mitochondrial responses to IR injury is pivotal in the realm of resuscitation research, particularly within the context of PCAS. This nuanced understanding holds the promise of revolutionizing PCAS management, addressing the unique mitochondrial dysfunctions observed in critical organs affected by IR injury. Full article

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a frequent, debilitating and still enigmatic disease. There is a broad overlap in the symptomatology of ME/CFS and the Post-COVID-19 Syndrome (PCS). A fraction of the PCS patients develop the full clinical picture of ME/CFS. New observations in microvessels and blood from patients suffering from PCS have appeared and include microclots and malformed pathological blood cells. Capillary blood flow is impaired not only by pathological blood components but also by prothrombotic changes in the vascular wall, endothelial dysfunction, and the expression of adhesion molecules in the capillaries. These disturbances can finally cause a low capillary flow and even capillary stasis. A low cardiac stroke volume due to hypovolemia and the inability of the capacitance vessels to adequately constrict to deliver the necessary cardiac preload generate an unfavorable low precapillary perfusion pressure. Furthermore, a predominance of vasoconstrictor over vasodilator influences exists, in which sympathetic hyperactivity and endothelial dysfunction play a strong role, causing the constriction of resistance vessels and of precapillary sphincters, which leads to a fall in capillary pressure behind the sphincters. The interaction of these two precapillary cardiovascular mechanisms causing a low capillary perfusion pressure is hemodynamically highly unfavorable in the presence of a primary capillary stasis, which is already caused by the pathological blood components and their interaction with the capillary wall, to severely impair organ perfusion. The detrimental coincidence of microcirculatory and precapillary cardiovascular disturbances may constitute the key disturbance of the Post-COVID-19 syndrome and finally lead to ME/CFS in predisposed patients because the interaction causes a particular kind of perfusion disturbance—capillary ischemia/reperfusion—which has a high potential of causing mitochondrial dysfunction by inducing sodium- and calcium-overload in skeletal muscles. The latter, in turn, worsens the vascular situation through the generation of reactive oxygen species to close a vicious cycle from which the patient can hardly escape. Full article

Background and Objectives: Survival with favorable neurologic outcomes after out-of-hospital cardiac arrest (OHCA) remains elusive. Post-cardiac arrest syndrome (PCAS) involves myocardial and neurological injury, ischemia-reperfusion response, and underlying pathology. Neurologic injury is a crucial determinant of survival and functional outcomes, with damage caused by free radicals among the responsible mechanisms. This study explores the feasibility of adding intravenous vitamin C to the treatment of OHCA survivors, aiming to mitigate PCAS. Vitamin C, a nutrient with antioxidative and free radical-scavenging properties, is often depleted in critically ill patients. Materials and Methods: This randomized, double-blinded trial was conducted at a tertiary-level university hospital with adult OHCA survivors. Participants received either standard care or the addition of 1.5 g of intravenous vitamin C every 12 h for eight consecutive doses. Neurologic injury was assessed using neuron-specific enolase (NSE) levels, with additional clinical and laboratory outcomes, such as enhanced neuroprognostication factors, inflammatory markers, and cardiac parameters. Results: NSE levels were non-significantly higher in patients who received vitamin C compared to the placebo group (55.05 µg/L [95% confidence interval (CI) 26.7–124.0] vs. 39.4 µg/L [95% CI 22.6–61.9], p > 0.05). Similarly, a non-significantly greater proportion of patients in the vitamin C group developed myoclonus in the first 72 h. We also observed a non-significantly shorter duration of mechanical ventilation, fewer arrhythmias, and reduced length of stay in the intensive care unit in the group of patients who received vitamin C (p = 0.031). However, caution is warranted in interpretation of our results due to the small number of participants. Conclusions: Our findings suggest that intravenous vitamin C should not be used outside of clinical trials for OHCA survivors. Due to the small sample size and conflicting results, further research is needed to determine the potential role of vitamin C in post-cardiac arrest care. Full article

Building collapse leads to mechanical injury, which is the main cause of injury and death, with crush syndrome as its most common complication. During the post-disaster search and rescue phase, if rescue personnel hastily remove heavy objects covering the bodies of injured individuals and fail to provide targeted medical care, ischemia-reperfusion injury may be triggered, leading to rhabdomyolysis. This may result in disseminated intravascular coagulation or acute respiratory distress syndrome, further leading to multiple organ failure, which ultimately leads to shock and death. Using bio-radar to detect vital signs and identify compression states can effectively reduce casualties during the search for missing persons behind obstacles. A time-domain ultra-wideband (UWB) bio-radar was applied for the non-contact detection of human vital sign signals behind obstacles. An echo denoising algorithm based on PSO-VMD and permutation entropy was proposed to suppress environmental noise, along with a wounded compression state recognition network based on radar-life signals. Based on training and testing using over 3000 data sets from 10 subjects in different compression states, the proposed multiscale convolutional network achieved a 92.63% identification accuracy. This outperformed SVM and 1D-CNN models by 5.30% and 6.12%, respectively, improving the casualty rescue success and post-disaster precision. Full article

(1) Background: Post-cardiac arrest syndrome (PCAS) is a type of global ischemic reperfusion injury that occurs after the return of spontaneous circulation (ROSC). The procalcitonin to albumin ratio (PAR) has been studied as an independent prognostic factor of various diseases. There are no previous studies of PAR in patients with PCAS. We assessed if PAR is more effective than procalcitonin (PCT) in predicting prognosis for patients with PCAS. (2) Methods: This retrospective cohort study included a total of 187 patients with PCAS after non-traumatic out-of-hospital cardiac arrest (OHCA) between January 2016 and December 2020. Multivariate logistic regression analysis was conducted to assess the association between PAR and PCAS prognosis. The predictive performance of PAR was compared with PCT via the receiver-operating characteristic (ROC) analysis and DeLong test.; (3) Results: PAR at 24 and 48 h after hospital admission were independently associated with one-month neurological outcome (OR: 1.167, 95% CI: 1.023–1.330; OR: 1.077, 95% CI: 1.012–1.146, p < 0.05). By ROC analysis, PAR showed better performance over PCT at 48 h after admission in predicting one-month CPC (0.763 vs. 0.772, p = 0.010). (4) Conclusions: Our findings suggest that PAR at 48 h after admission is more effective in predicting a one-month neurological outcome than PCT at 48 h after admission in patients with PCAS after OHCA. Full article

Acute kidney injury (AKI) leads to acute cardiac injury and dysfunction in cardiorenal syndrome Type 3 (CRS3) through oxidative stress (OS). The stress-inducible Sestrin2 (Sesn2) protein reduces reactive oxygen species (ROS) accumulation and activates AMP-dependent protein kinase (AMPK) to regulate cellular metabolism and energetics during OS. Sesn2 levels and its protective effects decline in the aged heart. Antidiabetic drug metformin upregulates Sesn2 levels in response to ischemia–reperfusion (IR) stress. However, the role of metformin in CRS3 remains unknown. This study seeks to explore how the age-related decrease in cardiac Sesn2 levels contributes to cardiac intolerance to AKI-induced insults, and how metformin ameliorates CRS3 through Sesn2. Young (3–5 months) and aged (21–23 months) C57BL/6J wild-type mice along with cardiomyocyte-specific knockout (cSesn2^−/−) and their wild type of littermate (Sesn2^f/f) C57BL/6J mice were subjected to AKI for 15 min followed by 24 h of reperfusion. Cardiac and mitochondrial functions were evaluated through echocardiograms and seahorse mitochondria respirational analysis. Renal and cardiac tissue was collected for histological analysis and immunoblotting. The results indicate that metformin could significantly rescue AKI-induced cardiac dysfunction and injury via Sesn2 through an improvement in systolic and diastolic function, fibrotic and cellular damage, and mitochondrial function in young, Sesn2^f/f, and especially aged mice. Metformin significantly increased Sesn2 expression under AKI stress in the aged left-ventricular tissue. Thus, this study suggests that Sesn2 mediates the cardioprotective effects of metformin during post-AKI. Full article

Cardiac arrest is an important public health issue, with a survival rate of approximately 15 to 22%. A great proportion of these deaths occur after resuscitation due to post-cardiac arrest syndrome, which is characterized by the ischemia-reperfusion injury that affects the role body. Understanding physiopathology is mandatory to discover new treatment strategies and obtain better results. Besides improvements in cardiopulmonary resuscitation maneuvers, the great increase in survival rates observed in recent decades is due to new approaches to post-cardiac arrest care. In this review, we will discuss physiopathology, etiologies, and post-resuscitation care, emphasizing targeted temperature management, early coronary angiography, and rehabilitation. Full article