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Right heart failure (RHF) is a clinical syndrome in which symptoms and signs are caused by dysfunction and/or overload of the right heart structures, predominantly the right ventricle (RV), resulting in systemic venous hypertension, peripheral oedema and finally, the impaired ability of the right heart to provide tissue perfusion. Pathogenesis of RHF includes the incompetence of the right heart to maintain systemic venous pressure sufficiently low to guarantee an optimal venous return and to preserve renal function. Virtually, all myocardial diseases involving the left heart may be responsible for RHF. This may result from coronary artery disease, hypertension, valvular heart disease, cardiomyopathies and myocarditis. The most prominent clinical signs of RHF comprise swelling of the neck veins with an elevation of jugular venous pressure and ankle oedema. As the situation worsens, fluid accumulation becomes generalised with extensive oedema of the legs, congestive hepatomegaly and eventually ascites. Diagnosis of RHF requires the presence of signs of elevated right atrial and venous pressures, including dilation of neck veins, with at least one of the following criteria: (1) compromised RV function; (2) pulmonary hypertension; (3) peripheral oedema and congestive hepatomegaly. Early recognition of RHF and identifying the underlying aetiology as well as triggering factors are crucial to treating patients and possibly reversing the clinical manifestations effectively and improving prognosis. [ABSTRACT FROM AUTHOR]

Objective: This study quantifies the change in intraocular pressure (IOP) secondary to wearing neck seals in scuba diving drysuits. Previous work demonstrates significant pressures exerted by these seals; we hypothesize that they would reduce craniofacial venous drainage and increase IOP through elevation of episcleral venous pressure. Methods: IOP was measured in 33 divers before and while wearing a drysuit using rebound tonometry. The drysuit neck seal pressures were measured using a manometer. A paired two-sample t-test was used to compare IOP before and after drysuit donning. Pearson correlation coefficients were calculated between neck sealing pressures and IOP by side. Results: The mean IOP in the right eye was similar pre- and post-drysuit donning, with baseline mean 15.9 mmHg (3.7 mmhg) versus 15.4 mmHG (4.3 mmHg) post-donning, p=0.41. Similarly, the mean IOP in the left eye was also similar, with mean pre-donning IOP 15.6 (3.8 mmHg) versus 15.4 mmHg (4.7 mmHg) post-donning, p=0.75. The mean right and left neck seal pressures were 23.66 (10.60) mmHg and 23.67 (7.87) mmHg, respectively. Only the correlation between right neck sealing pressure for silicone neck seals and right IOP, pre- and post-donning was significant (pre: 0.97, p-value 0.03, post: 0.98, p-value 0.02). Conclusion: No significant difference overall was detected in IOP with drysuit donning. [ABSTRACT FROM AUTHOR]

It is unclear to what extent systemic arterial blood pressure influences portal pressure. This relationship is clinically important as drugs, which are conventionally used for therapy of portal hypertension, may also influence systemic arterial blood pressure. This study investigated the potential correlation between mean arterial (MAP) and portal venous pressure (PVP) in rats with healthy livers. In a rat model with healthy livers, we investigated the effect of manipulation of MAP on PVP. Interventions consisted of 0.9% NaCl (group 1), 0.1 mg/kg body weight (bw) Sildenafil (low dose), an inhibitor of phosphodiesterase-5 (group 2), and 1.0 mg/kg bw Sildenafil (high dose, group 3) in 600 µL saline injected intravenously. Norepinephrine was used to increase MAP in animals with circulatory failure while PVP was monitored. Injection of the fluids induced a transient drop in MAP and PVP, probably due to a reversible cardiac decompensation. The drop in MAP and drop in PVP are significantly correlated. The time lag between change in MAP and change in PVP by 24 s in all groups suggests a cause-and-effect relationship. Ten minutes after the injection of the fluid, cardiac function was normalized. Thereafter, MAP gradually decreased. In the NaCl group, PVP decreases by 0.485% for a 1% drop of MAP, by 0.550% in the low-dose sildenafil group, and by 0.651% in the high-dose sildenafil group (p < 0.05 for difference group two vs. group one, group three vs. group one, and group three vs. group two). These data suggest that Sildenafil has an inherent effect on portal pressure that exceeds the effect of MAP. Injection of norepinephrine led to a sudden increase in MAP followed by an increase in PVP after a time lag. These data show a close relationship between portal venous pressure and systemic arterial pressure in this animal model with healthy livers. A change in MAP is consequently followed by a change in PVP after a distinct time lag. This study, furthermore, suggests that Sildenafil influences portal pressure. Further studies should be performed in a model with cirrhotic livers, as these may be important in the evaluation of vasoactive drugs (e.g., PDE-5-inhibitors) for therapy of portal hypertension. [ABSTRACT FROM AUTHOR]

Cryptococcal meningoencephalitis can occur in both previously healthy and immunocompromised hosts. Here, we describe a 55 year-old HIV-negative male with no known prior medical problems, who presented with three months of worsening headaches, confusion, and memory changes without fever. Magnetic resonance imaging of the brain demonstrated bilateral enlargement/enhancement of the choroid plexi, with hydrocephalus, temporal and occipital horn entrapments, as well as marked periventricular transependymal cerebrospinal fluid (CSF) seepage. CSF analysis yielded a lymphocytic pleocytosis and cryptococcal antigen titer of 1:160 but sterile fungal cultures. Despite standard antifungal therapy and CSF drainage, the patient had worsening confusion and persistently elevated intracranial pressures. External ventricular drainage led to improved mental status but only with valve settings at negative values. Ventriculoperitoneal shunt placement could thus not be considered due to a requirement for drainage into the positive pressure venous system. Due to this persistent CSF inflammation and cerebral circulation obstruction, the patient required transfer to the National Institute of Health. He was treated for cryptococcal post-infectious inflammatory response syndrome with pulse-taper corticosteroid therapy, with resultant reductions in CSF pressures along with decreased protein and obstructive material, allowing successful shunt placement. After tapering of corticosteroids, the patient recovered without sequelae. This case highlights (1) the necessity to consider cryptococcal meningitis as a rare cause of neurological deterioration in the absence of fever even in apparently immunocompetent individuals and (2) the potential for obstructive phenomena from inflammatory sequelae and the prompt response to corticosteroid therapy. [ABSTRACT FROM AUTHOR]

Primary biliary cholangitis (PBC) is an immune-mediated liver disease characterized by cholestasis, biliary injuries, liver fibrosis, and chronic nonsuppurative cholangitis. The pathogenesis of PBC is multifactorial and involves immune dysregulation, abnormal bile metabolism, and progressive fibrosis, ultimately leading to cirrhosis and liver failure. Ursodeoxycholic acid (UDCA) and obeticholic acid (OCA) are currently used as first- and second-line treatments, respectively. However, many patients do not respond adequately to UDCA, and the long-term effects of these drugs are limited. Recent research has advanced our understanding the mechanisms of pathogenesis in PBC and greatly facilitated development of novel drugs to target mechanistic checkpoints. Animal studies and clinical trials of pipeline drugs have yielded promising results in slowing disease progression. Targeting immune mediated pathogenesis and anti-inflammatory therapies are focused on the early stage, while anticholestatic and anti-fibrotic therapies are emphasized in the late stage of disease, which is characterized by fibrosis and cirrhosis development. Nonetheless, it is worth noting that currently, there exists a dearth of therapeutic options that can effectively impede the progression of the disease to its terminal stages. Hence, there is an urgent need for further research aimed at investigating the underlying pathophysiology mechanisms with potential therapeutic effects. This review highlights our current knowledge of the underlying immunological and cellular mechanisms of pathogenesis in PBC. Further, we also address current mechanism-based target therapies for PBC and potential therapeutic strategies to improve the efficacy of existing treatments. [ABSTRACT FROM AUTHOR]

Therapeutic Physical Exercise Programs reduce certain comorbidities and complications in patients with chronic diseases. Therapeutic Physical Exercise Programs APA have been shown to decrease hypertension and reduce mortality in patients with type 2 diabetes. Diabetes and obesity are frequently associated with the development of non-alcoholic fatty liver disease (NAFLD). These can progress to liver fibrosis and ultimately to metabolic cirrhosis (NASH cirrhosis). Our systematic review of the literature found an improvement in the aerobic capacity and quality of life of cirrhotic patients who received Therapeutic Physical Exercise Programs. Physical exercise could reduce the intrahepatic venous pressure gradient without causing any side effects. It could reduce the length of stay of liver transplant patients and could combat the recurrence or de novo appearance of NAFLD after transplantation. [ABSTRACT FROM AUTHOR]

Sigmoid sinus wall dehiscence (SSWD) is an important etiology of venous pulsatile tinnitus (VPT) and is treated by sigmoid sinus wall reconstruction (SSWR). This study aimed to investigate the therapeutic effects of the different degrees of SSWR and the prognostic effect in patients with VPT. Personalized models of three patients with SSWD (control), 3/4SSWD, 1/2SSWD, 1/4SSWD, and 0SSWD were reconstructed. A multiphysics interaction approach was applied to elucidate the biomechanical and acoustic changes. Results revealed that after SSWR, the average pressure of venous vessel on the SSWD region reduced by 33.70 ± 12.53%, 35.86 ± 12.39%, and 39.70 ± 12.45% (mean ± SD) in three patients with 3/4SSWD, 1/2SSWD, and 1/4SSWD. The maximum displacement of the SSWR region reduced by 25.91 ± 30.20%, 37.20 ± 31.47%, 52.60 ± 34.66%, and 79.35 ± 18.13% (mean ± SD) in three patients with 3/4SSWD, 1/2SSWD, 1/4SSWD, and 0SSWD, with a magnitude approximately 10−3 times that of the venous vessel in the SSWD region. The sound pressure level at the tympanum reduced by 23.72 ± 1.91%, 31.03 ± 14.40%, 45.62 ± 19.11%, and 128.46 ± 15.46% (mean ± SD). The SSWR region was still loaded with high stress in comparison to the surrounding region. The SSWR region of the temporal bone effectively shielded the high wall pressure and blocked the transmission of venous vessel vibration to the inner ear. Patients with inadequate SSWR still had residual VPT symptoms despite the remission of VPT symptoms. Complete SSWR could completely solve VPT issues. High-stress distribution of the SSWR region may be the cause of the recurrence of VPT symptoms. [ABSTRACT FROM AUTHOR]

Background & Objective: Many factors can contribute to the development of acute kidney injury (AKI) following major abdominal surgery, including the effect of fluid extravasation into interstitial space due to capillary leakage. Microalbuminuria is also brought on by capillary leakage. Increased central venous pressure (CVP) or intraabdominal pressure (IAP) will decrease renal filtration according to the degree of pressure transmission to the glomeruli. The objective of this study was to know the correlation of capillary leakage index (CLI), microalbuminuria [urine albumin to creatinine ratio (ACR)] and renal perfusion pressure (RPP) with the incidence of AKI. Methodology: A prospective longitudinal cohort design with consecutive sampling was used in this study. The parameters capillary leakage index (CLI), microalbuminuria (ACR) and renal perfusion pressure (RPP) were examined preoperatively, and at 12 h and 36 h postoperatively, and the incidence of AKI was observed till the fourth postoperative day. CLI was defined as C-reactive protein (CRP mg/dL) over albumin (g/L) multiplied by 100. RPP as glomerular pressure was obtained from mean arterial pressure (MAP), IAP, and renal venous pressure estimated by CVP, by the formula RPP = MAP-(IAP+CVP). Results: Following major abdominal surgery, 19 (25.68%) of the 74 subjects developed AKI. There was no significant difference in CLI and ACR between patients with and without AKI. Renal perfusion measurements examined at 0, 12, and 36 h showed significantly lower values in AKI patients. The relative risk (RR) of RPP was 9.125 with a 95 % CI of 1.141293-72.95725 (P = 0.037) after data analysis with Cox Regression to establish the correlation between CLI, ACR, and RPP, as well as covariate variables on the occurrence of AKI at 0 h. Compared to participants without AKI, those with AKI had a mortality risk of 2.384 times higher (P = 0.0351, 95 % CI = 1.133-5.018). Conclusion: Renal perfusion pressure showed a significant correlation with acute kidney injury. Additionally, there is a strong connection between acute kidney injury and mortality. Abbreviations: ACR- albumin to creatinine ratio; AKI- acute kidney injury; CLI- capillary leakage index; CVP- central venous pressure; IAP- intra-abdominal pressure; MAP- mean arterial pressure; RPP- renal perfusion pressure [ABSTRACT FROM AUTHOR]

Hepatic venous pressure gradient (HVPG) is the criterion for assessing sinusoidal portal hypertension. Using HVPG to assess the degree of liver fibrosis by transjugular liver biopsy (TJLB) is still being explored, as no data has been shown that portal hypertension may already be present in patients with advanced hepatic fibrosis (Scheuer stage ≥ S3). The objective of this study was to observe whether portal hypertension exists before progressing to cirrhosis (Scheuer stage = S4). Fifty patients who underwent TJLB and HVPG were enrolled. The correlation between Scheuer stage and HVPG was analyzed using the Pearson correlation coefficient, and the ROC curve predicted the diagnostic value of HVPG in patients with hepatic fibrosis. The Scheuer stage and HVPG significantly correlated (r = 0.654, p < 0.001). The AUC of HVPG in predicting advanced liver fibrosis was 0.896, and of cirrhosis was 0.810. There were 45 patients with portal hypertension (HVPG> 5 mmHg), 12 with S3, 29 with S4; There were 42 patients with CSPH (HVPG≥ 10 mmHg), 11 with S3, and 29 with S4. HVPG is valuable in evaluating the Scheuer stage of liver fibrosis in patients with TJLB. Portal hypertension might already exist before the progression to cirrhosis in some patients. [ABSTRACT FROM AUTHOR]

Online healthcare portals have become prevalent worldwide in recent years. One common form of healthcare portal is the online consultation website, which provides a bridge between patients and doctors and reduces patients' time and cost when seeking healthcare services. Another form is the healthcare service appointment website, which facilitates offline visits for patients. Though nominally separate, the behaviors of the users (including patients and doctors) on these two types of websites could be related to each other. In particular, how does opening online consultation services impact the offline appointments of doctors? Although this is an important question for healthcare portals, doctors, and policy makers, it has not been rigorously examined in the literature. We examine the overall impact of opening online consultation services on offline appointments and show that the number of offline appointments for doctors increases after opening online consultation services. Given that online consultation is a new but important way to connect patients and doctors, our findings provide useful implications for all the stakeholders—doctors, patients, hospitals, and policy makers—regarding how to integrate online and offline channels in the healthcare context. Online healthcare portals have become prevalent worldwide in recent years. One common form of a healthcare portal is the online consultation website, which provides a bridge between patients and doctors and reduces patients' time and cost when seeking healthcare services. Another form is the healthcare service appointment website, which facilitates offline visits for patients. Although nominally separate, the behaviors of the users (including patients and doctors) on these two types of websites could be related to each other. In particular, how does opening online consultation services impact the offline appointments of doctors? Although this is an important question for healthcare portals, doctors, and policy makers, it has not been rigorously examined in the literature. In this paper, we attempt to bridge this important gap by examining the overall impact of offering online consultations on offline appointments. Our results show that the number of offline appointments for doctors increases after opening an online consultation service. Additionally, we examine how several factors, such as recommendation heat, hospital ranking, and doctor title, moderate the impact of opening online consultation services on doctors' offline appointments. Given that online consultation is a new but important way to connect patients and doctors, our findings provide useful implications for all the stakeholders—doctors, patients, hospitals, and policy makers—regarding how to integrate online and offline channels in the healthcare context. History: Param Singh, Senior Editor; Yuliang (Oliver) Yao, Associate Editor. Funding: This work was supported by the National Natural Science Foundation of China [Grants 72071057, 71922009, 71871080, and 72188101]. Supplemental Material: The online appendix is available at https://doi.org/10.1287/isre.2022.1145. [ABSTRACT FROM AUTHOR]

Background: Idiopathic intracranial hypertension (IIH) is a common neurosurgical condition, and the exact pathophysiology remains elusive. Cerebral sinovenous stenosis (CSS) and the resultant decreased venous outflow have been labelled as a potential contributors to the pathophysiology of IIH. We describe the effect of cerebrospinal fluid (CSF) drainage on sinovenous pressure in a patient with IIH and a radiographic evidence of CSS. Case description: A patient in their 40s with a diagnoses of IIH and imaging finding of focal stenosis of the distal left transverse sinus. To assess the nature of the stenosis, we performed venous sinus pressure monitoring with concurrent CSF drainage (5 ml at one minute intervals) through a lumbar drain with continuous mean sinovenous pressures recording. We observed a progressive decline in the pressure recording while draining CSF, after draining 40ml of CSF, the final pressure gradient recording of the TS-SS trans-stenotic was (7 mm Hg from 27 mm Hg), mean SSS pressure (37 mm Hg from 60 mm Hg), and mean TS pressure (35 mm Hg from 56 mm Hg). The mean SS pressure remained relatively unperturbed. Conclusion: Our findings indicate that the cerebral sinovenous pressure response to CSF removal generally conforms to a monophasic exponential decay model. [ABSTRACT FROM AUTHOR]

There is a limit beyond which increasing either the concentration of a prostaglandin analog (PGA) or its dosing frequency fails to produce increases in ocular hypotensive efficacy with topical dosing. Intracameral PGA dosing with a bimatoprost implant, however, does not exhibit the same intraocular pressure (IOP)-lowering plateau at studied concentrations, and the maximum-achievable ocular hypotensive effects are not yet known. This suggests that the bimatoprost intracameral implant may activate another mechanism of action in addition to the mechanism(s) activated by topical application. Episcleral venous pressure (EVP) is a key determinant of IOP, and experimental manipulation of the episcleral vasculature can change both EVP and IOP. The recent observation that topical and intracameral PGA drug delivery routes produce different patterns of conjunctival hyperemia suggested that the differences in the IOP-lowering profiles may be caused by differing effects on the episcleral vasculature. Recent experiments in animals have shown that topical PGAs increase EVP, while the bimatoprost intracameral implant causes a smaller, transient increase in EVP, followed by a sustained decrease. The increase in EVP could be limiting the IOP-lowering efficacy of topical PGAs. In contrast, the decrease in EVP associated with the bimatoprost implant could explain its enhanced IOP-lowering effects. Further research on EVP as a target for IOP lowering is indicated to improve our understanding of this potentially important pathway for treating patients with glaucoma.

The article in the Journal of Physiology discusses the markers of cerebral autoregulation dynamics, focusing on critical closing pressure (CrCP) and resistance-area product (RAP). The study by Panerai et al. (2020) and Payne (2024) highlights the different time constants associated with dynamic cerebral autoregulation, with CrCP and RAP exhibiting distinct responses. The analysis suggests that CrCP tracks outlet pressure, potentially corresponding to venous pressure, while RAP is primarily governed by changes in radius. Further research is needed to explore the implications of these dynamics for clinical applications. [Extracted from the article]

The document discusses an analysis of the NEUROPROTECT study, comparing hemodynamic therapy in comatose survivors of cardiac arrest. The authors used hemodynamic data to calculate measures related to venous return physiology, highlighting the ambiguity of certain derived measures due to assumptions about resistance to venous return. The study emphasizes the importance of interpreting measures related to venous return alongside cardiac output and resistance, revealing novel insights into interventions like IV fluids. The authors stress the need to consider multiple factors when analyzing measures dependent on the pressure gradient for venous return. [Extracted from the article]

Background: Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide, and has a poor prognosis unless treated. Transarterial chemoembolization of HCC lesions is a promising treatment option for patients who are not eligible for surgery. Objective: To study the short termeffect of TACE on portal venous pressure by assessing it indirectly through measuring hepatic venous pressure gradient before and after TACE procedure. Patients and Methods: Our study was a Prospective cohort analysis of patients who were been referred to our IR unit (in our university hospital) diagnosed with HCC for performance of TACE at the period between January 2022 and December 2022. (21 patients). Results: Our study showed that there is no short term effect of TACE on HVPG (which reflects the portal pressure). We also recommend doing a follow up measurement of HVPG after 6 months and compare it with the baseline measurements to assess the long term effect of TACE on the portal pressure. Conclusion: Our study is in agreement with previous studies that there is no short term effect of TACE on HVPG (which reflects the portal pressure). [ABSTRACT FROM AUTHOR]

Background: Germinal matrix hemorrhage and subsequent posthemorrhagic hydrocephalus are common among pre-term infants due to multiple factors including fragility of germinal matrix vasculature, swinging increases of arterial and venous pressure, periodic hypoxia, and high metabolic demand. Aim of the Work: To compare between Ventricular access device (VAD) and Neuroendoscopic lavage (NEL) as temporary measures for management of posthemorrhagic hydrocephalus in premature infants in terms of incidence of permanent shunt placement, and post operative complications like infection. This will be done through a systematic review of literatures addressing this research question. Patients and Methods: Our study included 13 observational studies (12 retrospective and 1 prospective) comparing ventricular access device insertion vs neuroendoscopic lavage in management of posthemorrhagic hydrocephalus in pre-term infants regarding the need for VP shunt insertion and post operative complications mainly post operative infection and malfunction of the temporary CSF diversion, most of the cases had germinal matrix hemorrhage G III-IV according to papille classification, the results showed that while the neuroendoscopic lavage group had lower rate of VP shunt insertion, they had higher rate of post operative complications mainly malfunction of CSF diversion (The incidence of post operative infection was similar in both groups). Results: In this review while comparing the need for VP shunt insertion in both groups was somewhat simple, comparing complications on the other hand was problematic due to the heterogenicity between types of complications and the underlying comorbidities, with different follow up periods and most of the complications is not shared by both groups. Conclusion: Based on our systematic review and other available data in the literature, the neuroendoscopic lavage may be the preferred intervention for management of posthemorrhagic hydrocephalus in preterm infants regarding the incidence of permanent VP shunt insertion, although it has higher rate of malfunction and no statistical difference in post operative infection compared with the ventricular access device group. [ABSTRACT FROM AUTHOR]

Background: Clinically significant portal hypertension (CSPH), which causes a number of problems such variceal haemorrhage, ascites, and hepatorenal syndrome and is linked to a drastically decreased chance of survival, is a turning point in the development of liver cirrhosis. Therefore, the diagnosis of CSPH has significant prognostic significance. The measurement of the invasive hepatic venous pressure gradient (HVPG) is the gold standard for the diagnosis of portal hypertension. Objective: To evaluate plasma level of cyclic guanosine monophosphate as a possible biomarker in patients with liver cirrhosis and portal hypertension Patients and Methods: The type of study is a case control study; which were performed at Ain Shams university hospitals inpatients and outpatients settings for one year. The study population includes 80 patients with liver cirrhosis (40 cirrhotic patients without portal hypertension and 40 cirrhotic patients with portal hypertension 20 healthy controls). Inclusion Criteria involves adult over 18years old patients form both sexes. Results: In this study we found that there was high statistically significant difference between the studied groups as regard Plasma cGMP, as level of cGMP in patients with portal hypertension is higher than in patients without portal hypertension (p<0.001). In the present study we found that there was no statistically significant relation between Plasma cGMP and varices in patients with portal hypertension or without portal hypertension (mean 85614.96 range:46.4-111.3, mean 82.05620.96 range 62.5-111.3 respectively, p=0.608). Conclusion: The current investigation shows that cirrhotic patients with CSPH have dramatically disturbed plasma cGMP homeostasis. Our findings suggest that cGMP may be used as a blood-derived CSPH biomarker, particularly in the context of esophageal varices screening. [ABSTRACT FROM AUTHOR]

The commentary discusses a study comparing the accuracy of end-hole catheter and balloon catheter methods in measuring portal pressure in cirrhotic patients, with a focus on patients with intrahepatic venous shunts. The study found that the end-hole method was more accurate in patients with IHVS, but questions remain about the methodology and patient demographics. While some studies suggest the balloon method is more reliable, further research is needed to determine the most reliable technique for measuring portal pressure and predicting complications in patients with portal hypertension. The study was not funded and the author declared no conflicts of interest. [Extracted from the article]

Background: The hemodynamics of patients with cirrhosis and portal hypertension are complex and variable. We aimed to investigate differences in venous pressures determined by innovative angiography and conventional angiography using balloon occlusion of the hepatic veins in patients with alcoholic cirrhosis and portal hypertension. Methods: A total of 134 patients with alcoholic cirrhosis who fulfilled the inclusion criteria from June 2017 to June 2020 were included. During transjugular intrahepatic portosystemic shunt, conventional and innovative angiography were performed, and venous pressures were measured. A paired t-test and Pearson's correlation coefficient were used for analysis. Results: Conventional and innovative hepatic angiography detected lateral branches of the hepatic vein in 26 (19.4%) and 65 (48.5%) cases, respectively (P < 0.001). Innovative angiography detected a total of 65 patients with lateral shunts, of whom 37 (56.9%) had initial shunts. The average wedged hepatic venous pressure and portal venous pressure of the initial lateral branches were 21.27 ± 6.66 and 35.84 ± 7.86 mmHg, respectively, with correlation and determination coefficients of 0.342 (P < 0.05) and 0.117, respectively. The mean hepatic venous pressure gradient and portal pressure gradient were 9.59 ± 7.64 and 26.86 ± 6.78 mmHg, respectively, with correlation and determination coefficients of 0.292 (P = 0.079) and 0.085, respectively. Conclusions: Innovative angiography reveals collateral branches of the hepatic veins more effectively than conventional angiography. Hepatic vein collateral branches are the primary factors leading to underestimation of wedged hepatic venous pressures and hepatic venous pressure gradients, with the initial hepatic vein collateral branches resulting in the most severe underestimations. [ABSTRACT FROM AUTHOR]

Background and Aims: Assessment of clinically significant portal hypertension (CSPH) non-invasively using a combination of liver stiffness measurement (LSM) and platelet counts is proposed as an alternative to hepatic venous pressure gradient (HVPG) estimation. Utility of these criteria in compensated advanced chronic liver disease (cACLD) patients of different etiologies including nonalcoholic steatohepatitis (NASH) with BMI > 30 kg/m2 was studied in a large cohort. Methods: Consecutive patients of cACLD with available anthropometric and laboratory details, LSM, and HVPG were included in a retrospective analysis. A LSM of ≥ 25 kPa alone and LSM ≤ 15 kPa plus platelets ≥ 150 × 109/L were evaluated as non-invasive rule-in and rule-out criteria for CSPH, respectively. The NASH-ANTICPATE model (composite of BMI, platelets, and LSM) was evaluated in patients with obese NASH. Results: Patients with cACLD (n = 626) (mean age: 50.8 ± 12.4 years, 74.2% males) with alcohol (ALD, 30.3%), NASH (26.4%), hepatitis C (HCV, 16.6%), hepatitis B (HBV,10.2%) etiology were included. The prevalence of CSPH was > 80% across all etiologies except in HBV (62.5%) and in obese non-NASH (71–72%). The rule-in criteria had a PPV > 90% for all etiologies except in HBV (80.8%). The rule-out criteria had a negative predictive value (NPV) of 65%, 53%, and 40% in ALD, HCV, and NASH, respectively. The NASH-ANTCIPATE model had specificity of 100% and NPV of 33% to detect CSPH in obese NASH (n = 62). Conclusions: LSM ≥ 25 kPa predicted CSPH in most etiologies except HBV. A significant proportion of patients have CSPH despite satisfying the rule-out criteria. The NASH-ANTICIPATE model is specific but fails to exclude CSPH in nearly two-third patients with obesity and NASH. There is a need for precise disease-specific non-invasive models for detecting CSPH. [ABSTRACT FROM AUTHOR]

Introduction: Carbon dioxide production (VCO2i), oxygen consumption and oxygen delivery can be monitored during cardiopulmonary bypass (CPB) as markers for tissue perfusion. This study examines if inline venous pCO2 (PvCO2) monitoring can be used as an alternative to exhaust gas pCO2 (ExCO2) to calculate VCO2i. Methods: PvCO2 and ExCO2 were monitored continuously during 40 elective coronary artery bypass grafting (CABG) procedures. VCO2i was calculated with ExCO2 as well as PvCO2. Results: Mean PvCO2 was 0.27 mmHg higher than mean ExCO2 (p <.001). The 95% limits of agreement of PvCO2 and ExCO2 were [‐2.99, 3.53] mmHg which is within the limits proposed by the Clinical Laboratory Improvement Amendments of 2019. VCO2i was calculated using both PvCO2 and ExCO2 (PvVCO2i; ExVCO2i). A strong linear correlation was found for ExVCO2i and PvVCO2i (R2=.94, p <.001). Conclusion: In conclusion, the differences in VCO2i calculation between the two methods are unlikely to be clinically relevant during normothermic CABG procedures. VCO2i can be calculated with either a capnograph or inline venous pCO2 monitoring. [ABSTRACT FROM AUTHOR]

Vascular complications after liver transplantation (LT) can be lethal and require immediate treatment to prevent graft failure. Nowadays, with interventional radiology (IR), approaches such as the percutaneous transhepatic (PTH) and transileocolic venous (TIC), have become major treatment options. We reviewed the safety and efficacy of a hybrid operating room (OR) for portal vein complications after LT. Patients who underwent IR for post-LT vascular complications in the hybrid OR from May 2014 to May 2022 were enrolled. Patients who underwent post-LT IR in conventional angiography rooms were excluded. Nine patients developed portal vein complications; eight after living donor LT and one after deceased donor LT. Six patients had portal vein stenosis, two had portal vein thrombosis, and one had both. In the hybrid OR, PTH and TIC were used in five and three cases, respectively. The Rendezvous technique was used in one case. Angioplasty was performed in all patients. A stent was placed in four patients. The portal venous pressure gradient across the stenotic site significantly decreased after IR (P &= 0.031). The IR success rate in the hybrid OR was 100%. The hybrid OR enables us to accomplish IR for post-LT vascular complications safely and effectively. [ABSTRACT FROM AUTHOR]

We analyzed RNA-sequencing (RNA-seq) and clinical data from head and neck squamous cell carcinoma (HNSCC) patients in The Cancer Genome Atlas (TCGA) Genomic Data Commons (GDC) portal to investigate the prognostic value of anoikis-related genes (ARGs) in HNSCC and develop new targeted drugs. Differentially expressed ARGs were screened using bioinformatics methods; subsequently, a prognostic model including three ARGs (CDKN2A, BIRC5, and PLAU) was constructed. Our results showed that the model-based risk score was a good prognostic indicator, and the potential of the three ARGs in HNSCC prognosis was validated by the TISCH database, the model’s accuracy was validated in two independent cohorts of the Gene Expression Omnibus database. Immune correlation analysis and half-maximal inhibitory concentration were also performed to reveal the different landscapes of TIME between risk groups and to predict immuno- and chemo-therapeutic responses. Potential small-molecule drugs for HNSCC were subsequently predicted using the L1000FWD database. Finally, in vitro experiments were used to verify the database findings. The relative ARG mRNA expression levels in HNSCC and surrounding normal tissues remained consistent with the model results. BIRC5 knockdown inhibited anoikis resistance in WSU-HN6 and CAL27 cells. Molecular docking, real-time PCR, cell counting kit-8 (CCK-8), plate clone, and flow cytometry analyses showed that small-molecule drugs predicted by the database may target the ARGs in the prognostic model, inhibit HNSCC cells survival rate, and promote anoikis in vitro. Therefore, we constructed a new ARG model for HNSCC patients that can predict prognosis and immune activity and identify a potential small-molecule drug for HNSCC, paving the way for clinically targeting anoikis in HNSCC. [ABSTRACT FROM AUTHOR]

Background: Clinically significant portal hypertension (CSPH) drives cirrhosis-related complications (i.e. hepatic decompensation). Impaired nitric oxide (NO) bioavailability promotes sinusoidal vasoconstriction, which is the initial pathomechanism of CSPH development. Activation of soluble guanylyl cyclase (sGC), a key downstream effector of NO, facilitates sinusoidal vasodilation, which in turn may improve CSPH. Two phase II studies are being conducted to assess the efficacy of the NO-independent sGC activator BI 685,509 in patients with CSPH due to various cirrhosis aetiologies. Methods: The 1366.0021 trial (NCT05161481) is a randomised, placebo-controlled, exploratory study that will assess BI 685,509 (moderate or high dose) for 24 weeks in patients with CSPH due to alcohol-related liver disease. The 1366.0029 trial (NCT05282121) is a randomised, open-label, parallel-group, exploratory study that will assess BI 685,509 (high dose) alone in patients with hepatitis B or C virus infection or non-alcoholic steatohepatitis (NASH) and in combination with 10 mg empagliflozin in patients with NASH and type 2 diabetes mellitus for 8 weeks. The 1366.0021 trial will enrol 105 patients, and the 1366.0029 trial will enrol 80 patients. In both studies, the primary endpoint is the change from baseline in hepatic venous pressure gradient (HVPG) until the end of treatment (24 or 8 weeks, respectively). Secondary endpoints include the proportion of patients with an HVPG reduction of > 10% from baseline, the development of decompensation events and the change from baseline in HVPG after 8 weeks in the 1366.0021 trial. In addition, the trials will assess changes in liver and spleen stiffness by transient elastography, changes in hepatic and renal function and the tolerability of BI 685,509. Discussion: These trials will enable the assessment of the short-term (8 weeks) and longer-term (24 weeks) effects and safety of sGC activation by BI 685,509 on CSPH due to various cirrhosis aetiologies. The trials will use central readings of the diagnostic gold standard HVPG for the primary endpoint, as well as changes in established non-invasive biomarkers, such as liver and spleen stiffness. Ultimately, these trials will provide key information for developing future phase III trials. Trial registration: 1366.0021: EudraCT no. 2021–001,285-38; ClinicalTrials.gov NCT05161481. Registered on 17 December 2021, https://www.clinicaltrials.gov/ct2/show/NCT05161481. 1366.0029: EudraCT no. 2021–005,171-40; ClinicalTrials.gov NCT05282121. Registered on 16 March 2022, https://www.clinicaltrials.gov/ct2/show/NCT05282121. [ABSTRACT FROM AUTHOR]

Objective: Using the novel imaging method of high-speed modified photoplethysmography we measured the retinal venous pulse wave velocity in a single case. Results: A healthy 30-year-old subject underwent high-speed modified photoplethysmography (120 frames per second) with simultaneous ophthalmodynamometry at 26 Meditron units. A video of the optic nerve was analyzed using custom software. A harmonic regression model was fitted to each pixel in the time series and used to quantify the retinal vascular pulse wave parameters. Retinal venous pulsation at the optic disc was observed as a complex dynamic wall motion, whereas contraction commenced at a point in the vein at the center of the optic disc, and progressed centrifugally. The empirically estimated retinal venous pulse wave velocity at this segment was approximately 22.24694 mm/s. This measurement provides an estimate for future studies in the field. [ABSTRACT FROM AUTHOR]

Objectives: Portal venous thrombosis (PVT) in cirrhotic patients is usually asymptomatic and diagnosed incidentally. In this study we aimed to investigate the prevalence and characteristics of advanced PVT in cirrhotic patients with a recent episode of gastroesophageal variceal hemorrhage (GVH). Methods: Cirrhotic patients with recent GVH at one month before their admission for further treatment to prevent rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurements, contrast‐enhanced computed tomography (CT) scan of the portal vein system, and endoscopy were performed. PVT was diagnosed by CT examination and classified as none, mild and advanced. Results: Of the 356 patients enrolled, 80 (22.5%) had advanced PVT. Elevated levels of white blood cells (WBC) and serum D‐dimer were observed in advanced PVT patients compared with those with no or mild PVT. Moreover, HVPG was lower in patients with advanced PVT, with fewer patients having HVPG exceeding 12 mmHg, while grade III esophageal varices and varices with red signs were more prevalent. Multivariate analysis showed that WBC count (odds ratio [OR] 1.401, 95% confidence interval [CI] 1.171–1.676, P < 0.001), D‐dimer level (OR 1.228, 95% CI 1.117–1.361, P < 0.001), HVPG (OR 0.942, 95% CI 0.900–0.987, P = 0.011), and grade III esophageal varices (OR 4.243, 95% CI 1.420–12.684, P = 0.010) were associated with advanced PVT. Conclusions: Advanced PVT, which is associated with a more severe hypercoagulable and inflammatory status, causes severe prehepatic portal hypertension in cirrhotic patients with GVH. [ABSTRACT FROM AUTHOR]

Infrahepatic inferior vena cava (IVC) clamping has already been proven as a safe and effective technique to reduce intraoperative blood loss (BL) in open liver resection (OLR).[1] However, its effectiveness and safety in laparoscopic liver resection (LLR) remains unclear. Laparoscopic Infrahepatic Inferior Vena Cava Clamping During Liver Resection - a Feasibility Study Keywords: Hepatectomy; Central venous pressure; Minimal invasive; Blood loss; Outcome EN Hepatectomy Central venous pressure Minimal invasive Blood loss Outcome 794 797 4 04/06/23 20230401 NES 230401 Patrick Téoule and Niccolo Schmidt contributed equally to this work. [Extracted from the article]

Introduction: The risk for the occurrence of esophageal varices in a cirrhotic patient is assessed by two gold standard invasive tests: hepatic venous pressure gradient measurement and esophagogastroduodenoscopy. We aim to find the association between spleen and liver stiffness with the occurrence of esophageal varices in our settings. Methods: This was a prospective cross-sectional study. In the study duration of one year, 94 cirrhotic patients who met the inclusion and exclusion criteria were included. All patients were subjected to transient elastography for measuring liver and spleen stiffness and endoscopy. Results: Of 94 patients, only 77 (81.9%) had esophageal varices. The mean liver stiffness in patients with and without varices was 19.46±4.9SD kPa and 12.92±1.52 SD kPa respectively. The difference was statistically significant, p<0.001. The mean spleen stiffness in patients with and without varices was 22.26±4.6 SD kPa and 14.08±1.20 SD kPa respectively. The difference was statistically significant, p<0.001. The optimal cut-off value of liver and spleen to detect patients with any grade of esophageal varices was 14 and 16.15 kPa respectively. Conclusion: The stiffness of liver and spleen using transient elastography can be considered an equivalent method for screening cirrhotic patients for esophageal varices in clinical settings. [ABSTRACT FROM AUTHOR]

To demonstrate that patients with pre-cirrhotic bridging fibrosis (Meta-analysis of Histological Data in Viral Hepatitis, METAVIR stage F3) and clinically significant portal hypertension (CSPH, Hepatic Venous Pressure Gradient ≥10 mmHg) experience a higher rate of clinical decompensation than patients without CSPH. 128 consecutive patients with pathology proven bridging fibrosis without cirrhosis between 2012 and 2019 were reviewed. Inclusion criteria were patients with HVPG measurement obtained during the same outpatient transjugular liver biopsy and clinical follow up of at least two years. Primary endpoint included rate of overall complication related to portal hypertension including evidence of either ascites, presence of varices on imaging or endoscopy, or evidence of hepatic encephalopathy. Among 128 patients with bridging fibrosis (67 females and 61 males; average age 56 years), 42 (33%) and 86 (67%) were with and without CSPH (HVPG ≥10 mmHg). Median follow-up time was 4 years. Rate of overall complication (either ascites, varices or hepatic encephalopathy) in patients with and without CSPH was 36/42 (86%) and 39/86 (45%) (p <.001) respectively. Rate of developing ascites, varices and hepatic encephalopathy in patients with and without CSPH was 21/42 (50%) vs 26/86 (30%) (p =.034), 32/42 (76%) vs 26/86 (30%) (p ≤.001) and 18/42 (43%) vs 12/86 (14%) (p =.001) respectively. Patients with pre-cirrhotic bridging fibrosis and CSPH were associated with higher rates of developing ascites, varices and hepatic encephalopathy. Measuring HVPG during transjugular liver biopsy provides additional prognostic value in anticipating clinical decompensation in patients with pre-cirrhotic bridging fibrosis. • Higher rates of clinical complications occurred in bridging fibrosis with hepatic venous pressure gradient ≥10 mmHg. • Developments of ascites, non-bleeding varices and hepatic encephalopathy are the predominant clinical complications. • Hepatic venous pressure gradient has prognostic values in patients with non-cirrhotic bridging fibrosis liver disease. [ABSTRACT FROM AUTHOR]

Background: For a long time, trans-femoral venous pressure (FVP) measurement was considered a simple alternative for estimating intra-abdominal pressure (IAP). Since intravesical [IVP] and intragastric [IGP] pressure measurements are sometimes contraindicated for anatomical and pathophysiological reasons, FVP raised hopes, especially among pediatricians. Pediatric FVP validation studies have never been published; recent results from adult studies cast doubt on their interchangeability. Therefore, we compared for the first time the measurement agreement between FVP and IVP and IGP in children. Material and methods: We prospectively compared FVP with IVP and IGP, according to the Abdominal Compartment Society validation criteria. Additionally, we analyzed the agreement as a function of IAP or right heart valve regurgitation and pulmonary hypertension. Results: In a real-life PICU study design, n = 39 children were included (median age 4.8 y, LOS-PICU 23 days, PRISM III score 11). In n = 660 FVP–IGP measurement pairs, the median IAP was 7 (range 1 to 23) mmHg; in n = 459 FVP–IVP measurement pairs, the median IAP was 6 (range 1to 16) mmHg. The measurement agreement was extremely low with both established methods (FVP–IGP: r2 0.13, mean bias −0.8 ± 4.4 mmHg, limits of agreement (LOA) −9.6/+8.0, percentage error (PE) 55%; FVP–IVP: r2 0.14, bias +0.5 ± 4.2 mmHg, limit of agreement (LOA) −7.9/+8.9, percentage error (PE) 51%). No effect of the a priori defined influencing factors on the measurement agreement could be demonstrated. Conclusions: In a study cohort with a high proportion of critically ill children suffering from IAH, FVP did not agree reliably with either IVP or IGP. Its clinical use in critically ill children must therefore be strongly discouraged. [ABSTRACT FROM AUTHOR]

Background: It is unclear whether hepatocyte function and/or portal hypertension improves if a sustained virologic response (SVR) is achieved with direct-acting antivirals in patients with decompensated hepatitis C-related cirrhosis. Methods: We examined the safety and efficacy of a 12-week course of sofosbuvir/velpatasvir (SOF/VEL) in 20 patients with decompensated hepatitis C-related cirrhosis. We also investigated changes in the hepatocyte receptor index (LHL15) and blood clearance index (HH15) by Tc-99 m-galactosyl human serum albumin scintigraphy, liver stiffness measurement (LSM) by transient elastography, and hepatic venous pressure gradient (HVPG) in patients who achieved an SVR at 24 weeks after treatment (SVR24). Results: One patient discontinued treatment because of rectal variceal hemorrhage, and 19 patients completed treatment. SVR24 was achieved in 17 patients (89%). Median LHL15 increased from 0.72 pre-treatment to 0.82 after SVR24 (p = 0.012), and median HH15 decreased from 0.82 pre-treatment to 0.76 after SVR24 (p = 0.010). The percentage of patients with LSM ≥ 20 kPa was 90% before treatment and remained at 90% after SVR24. However, the percentage with severe portal hypertension (defined as HVPG ≥ 12 mmHg) decreased from 92% pre-treatment to 58% after SVR24 (p = 0.046). Patients with a decreased HVPG from pre-treatment to after SVR24 had a smaller pre-treatment spleen volume than those with an increased HVPG (median, 252 vs. 537 mL, p = 0.028). Conclusion: Achieving SVR24 with SOF/VEL treatment in patients with decompensated hepatitis C-related cirrhosis can be expected to improve hepatocyte function and portal hypertension on short-term follow-up. [ABSTRACT FROM AUTHOR]

Introduction: Stasis dermatitis (SD), also known as venous dermatitis, is a form of inflammatory dermatitis of the lower extremities that typically occurs in older individuals and represents a cutaneous manifestation of venous hypertension. Venous hypertension (also known as sustained ambulatory venous pressure) is most often due to retrograde blood flow, which occurs due to calf muscle pump failure. This failure is most commonly secondary to incompetent venous valves, valve destruction, or obstruction of the venous system. Many of the common symptoms associated with SD are caused by inflammatory processes. Methods: This review summarizes the pathogenesis and key role of inflammation in SD by reviewing inflammatory biomarkers associated with SD. The literature was selected though a high-level PubMed search focusing on keywords relating to inflammation associated with SD. Results: Venous reflux at the lower extremities causes venous hypertension, which leads to chronic venous insufficiency. High venous pressure due to venous hypertension promotes the local accumulation and extravasation of inflammatory cells across the vascular endothelium. Leukocyte trapping in the microcirculation and perivascular space is associated with trophic skin changes. Cell adhesion molecules are linked with the perpetuated influx of activated leukocytes into inflammatory sites. Here, inflammatory cells may influence the remodeling of the extracellular matrix by inducing the secretion of proteinases such as matrix metalloproteinases (MMPs). The increased expression of MMPs is associated with the formation of venous leg ulcers and lesions. Phosphodiesterase 4 activity has also been shown to be elevated in individuals with inflammatory dermatoses compared to healthy individuals. Discussion: Because inflammation is a key driver of the signs and symptoms of SD, several of the highlighted biomarkers of inflammation represent potential opportunities to target and interrupt molecular pathways of cutaneous inflammation and, therefore, remediate the signs and symptoms of SD. Conclusion: Understanding the pathogenesis of SD may help clinicians identify drivers of inflammation to use as potential targets for the development of new treatment options. Plain Language Summary: Stasis dermatitis is a skin disease that affects the legs, most often of older people, with chronic venous insufficiency. Chronic venous insufficiency is when veins cannot return blood from the legs back to the heart. This leads to high blood pressure in veins and causes blood in those veins to flow backwards. If stasis dermatitis is left untreated, complications, including skin ulcers, can result. Other skin symptoms of stasis dermatitis include itchiness, scaling, and discoloration. Such skin symptoms can have a negative effect on a person's quality of life. Inflammation that lasts a long time is likely the main link between the skin changes seen in people with stasis dermatitis and the increased pressure in leg veins. Several molecules are associated with the inflammation observed in stasis dermatitis, including white blood cells, matrix metalloproteinases, phosphodiesterase 4, and interleukin-31. Treatment for stasis dermatitis should focus both on the underlying chronic venous insufficiency and the associated skin issues. Identifying inflammatory markers and pathways could help treat the signs and symptoms associated with stasis dermatitis, including the skin symptoms. [ABSTRACT FROM AUTHOR]

More than a half of patients undergoing liver transplantation (LT) receive intraoperative transfusion. Portal hypertension (PHT) may contribute to perioperative blood loss. We study the relationship between preoperative hepatic venous pressure gradient (HVPG) values and intraoperative transfusion requirements in adult patients undergoing LT. 160 cirrhotic patients undergoing first elective LT (2009–2019) with an HVPG measurement within the previous 6 months were included. Surgical technique was piggyback with portocaval shunt (PCS). The association of HVPG and other variables with transfusion requirements and blood loss were studied. Blood loss (ml/kg) was positively correlated with HVPG, among other variables, but at multivariable analysis it only remained associated with MELD-Na and HCC indication. Regarding RBC transfusion, MELD-Na and hemoglobin were independently associated with the need and magnitude of RBC transfusion. Subanalysis by surgical stage (hepatectomy, anhepatic, neohepatic) and by serial HVPG cut-offs found no clear associations with either bleeding or transfusion. The severity of PHT plays a minor role on bleeding and transfusion during LT in a contemporary cohort with systematic PCS. Main determinants of transfusion are liver function and baseline hemoglobin, which would seem the suitable goal to optimize transfusion in LT. [ABSTRACT FROM AUTHOR]

Background & Aims: Severity of portal hypertension is usually quantified by measuring the hepatic venous pressure gradient (HVPG). However, due to its invasiveness, alternative markers are being sought. Bile acids (BA), being synthesized, metabolized, and transported by the liver, seem to have the potential to serve as endogenous markers. The aim of the present study was to determine whether serum BA reflect the severity of portal hypertension. Methods: We correlated serum concentrations of individual BA with portal pressure (as HVPG) in an exploratory cohort of 21 cirrhotic patients with portal hypertension. The predictive potential of selected candidates was then confirmed in an independent validation cohort (n = 214). Additionally, nine previously published noninvasive markers were added to the stepwise logistic regression model to identify the most relevant ones, which were eventually used to create a prognostic index of portal hypertension. Results: Serum levels of taurochenodeoxycholic acid (TCDCA) significantly correlated with HVPG and showed a high potential to predict clinically significant portal hypertension (HVPG ≥ 10 mm Hg: AUROC = 0.97 ± 0.06). This was confirmed in the validation cohort (AUROC = 0.96 ± 0.01). The predictive index (constructed based on AST/ALT, spleen diameter, and TCDCA concentration) was able to distinguish clinically significant portal hypertension with 95% sensitivity and 76% specificity. Conclusions: TCDCA seems to be a promising noninvasive marker of clinically significant portal hypertension. Its predictive potential may be further enhanced when it is combined with both the AST/ALT ratio and spleen diameter. [ABSTRACT FROM AUTHOR]

Aims: The impact of mitral regurgitation (MR) in patients hospitalized for acute heart failure (AHF) is not well established. We assessed the role of MR in patients enrolled in the Relaxin in Acute Heart Failure 2 (RELAX‐AHF‐2) trial. Methods and results: Patients enrolled in RELAX‐AHF‐2 with available data regarding MR status were included in this analysis. Baseline characteristics, in‐hospital data, and clinical outcomes through 180‐day follow‐up were evaluated. The impact of moderate/severe MR was assessed. Among 6420 AHF patients with known MR status, 1810 patients (28.2%) had moderate/severe MR. Compared to patients with no/mild MR, those with moderate/severe MR were more likely to have history of heart failure (HF), prior HF hospitalization, more comorbidities, symptoms/signs of HF, lower left ventricular ejection fraction and higher N‐terminal pro‐B‐type natriuretic peptide levels. Moderate/severe MR was associated with longer length of hospital stay, higher rates of residual dyspnoea, increased jugular venous pressure through the index hospitalization and a higher unadjusted risk of the composite of cardiovascular (CV) death or rehospitalization for HF/renal failure (RF) through 180 days (crude hazard ratio [HR] 1.15, 95% confidence interval [CI] 1.03–1.27, p = 0.01). The association between moderate/severe MR and poorer outcomes was not maintained in a multivariable model including several covariates of interest (adjusted HR 1.03, 95% CI 0.91–1.17, p = 0.65). Similar findings were observed for HF/RF rehospitalization alone. Conclusions: In patients with AHF, moderate/severe MR was associated with a worse clinical profile but did not have an independent prognostic impact on clinical outcomes. [ABSTRACT FROM AUTHOR]

Background: Congestion is central to the pathophysiology of heart failure (HF); thus, tracking congestion is crucial for the management of patients with HF. In this study we aimed to compare changes in inferior vena cava diameter (IVCD) with venous pressure following manipulation of volume status during ultrafiltration in patients with cardiac dysfunction.Methods and Results: Patients with stable hemodialysis and with systolic or diastolic dysfunction were studied. Central venous pressure (CVP) and peripheral venous pressure (PVP) were measured before and after hemodialysis. IVCD and PVP were measured simultaneously just before dialysis, 3 times during dialysis and immediately after dialysis. Changes in IVCD and PVP were compared at each timepoint with ultrafiltration volumes. We analyzed 30 hemodialysis sessions from 20 patients. PVP was validated as a surrogate for CVP. Mean ultrafiltration volume was 2102 ± 667 mL. IVCD discriminated better ultrafiltration volumes ≤ 500 mL or ≤ 750 mL than PVP (AUC 0.80 vs 0.62, and 0.80 vs 0.56, respectively; both P< 0.01). IVCD appeared to track better ultrafiltration volume (P< 0.01) and hemoconcentration (P< 0.05) than PVP. Changes in IVCD were of greater magnitude than those of PVP (average change from predialysis: -58 ± 30% vs -28 ± 21%; P< 0.001).Conclusions: In patients undergoing ultrafiltration, changes in IVCD tracked changes in volume status better than venous pressure. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of LncRNA-NEAT1 on JAK2/STAT3 signaling pathway, inflammatory response and pregnancy outcome in hypertensive rats during pregnancy. Methods: The hypertensive rat model of pregnancy was established by injecting L-arginine methyl ester. The protein expression of JAK2/STAT3 signaling pathway was detected by Western blot. Inflammatory factors and vascular endothelial injury factors were detected by ELISA. Proteinuria, caudal venous pressure and stillbirth rate were observed and recorded. Results: Compared with blank group, the protein expression levels of JAK2 and STAT3 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P＜0.05). Compared with model group, the protein expression levels of JAK2 and STAT3 in LncRNA-NEAT1 inhibition group were significantly lower (P＜0.05), while the protein expression levels of JAK2 and STAT3 in LncRNA-NEAT1 overexpression group were significantly higher (P＜0.05). Compared with blank group, the levels of ET-1 and s ICAM-1 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher, while the level of NO was significantly lower (P＜0.05). Compared with model group, the levels of ET-1 and s ICAM-1 in LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P＜0.05), while the level of NO was significantly lower (P＜0.05). The expression levels of ET-1 and s ICAM-1 in LncRNA-NEAT1 overexpression group were significantly higher, but NO was significantly lower (P＜0.05). Compared with blank group,the expression levels of TNF-α, IL-1β and IL-18 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1inhibition group were significantly higher (P＜0.05). Compared with model group, the expression levels of TNF-α, IL-1β and IL-18 in LncRNA-NEAT1 inhibition group were significantly lower (P＜0.05), while the expression levels of TNF-α, IL-1β and IL-18 in LncRNA-NEAT1 overexpression group were significantly higher (P＜0.05). Compared with blank group, caudal venous pressure and 24 h proteinuria levels in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P＜0.05). Compared with model group, the caudal venous pressure and 24 h proteinuria expression levels in LncRNA-NEAT1inhibited group were significantly lower (P＜0.05), while the caudal venous pressure and 24 h proteinuria expression levels in LncRNA-NEAT1 overexpression group were significantly higher (P＜0.05). The stillbirth rate of LncRNA-NEAT1 overexpression group (21.56%) was higher than that of model group (16.72%) and LncRNA-NEAT1 inhibition group (5.65%). Conclusions: Down-regulation of LncRNA-NEAT1 in gestational diabetes rats can inhibit the expression of JAK2/STAT3 signaling pathway and down-regulate the expression of downstream pro-inflammatory factors, so as to alleviate vascular endothelial injury and reduce the stillbirth rate. [ABSTRACT FROM AUTHOR]

Background: Blood gas analysis is integral to assessing emergency department (ED) patients with acute respiratory or metabolic disease. Arterial blood gas (ABG) is the gold standard for oxygenation, ventilation, and acid–base status but is painful to obtain. Peripheral venous blood gas (VBG) is a valuable alternative as it is less painful and easy to collect. The comparability of ABG and VBG was studied in various conditions. But in hypotension, previous findings were inconsistent. So, we studied the correlation and agreement between ABG and VBG in hypotensive patients. Methodology: The study was conducted at the emergency department of a tertiary healthcare center in Northern India. Patients with hypotension above 18 years who satisfied the inclusion criteria were clinically evaluated. Patients who require ABG as a part of routine care were sampled. ABG was collected from the radial artery. VBG was obtained from the cubital or dorsal hand veins. Both samples were collected within 10 min and were analyzed. All ABG and VBG variables were entered in premade proforma. The patient was then treated and disposed of according to institutional protocol. Results: A total of 250 patients were enrolled. The mean age was 53.25 ± 15.71 years. 56.8% were male. The study included 45.6% septic, 34.4% hypovolemic, 18% cardiogenic, and 2% obstructive shock patients. The study found a strong correlation and agreement for ABG and VBG pH, pCO2, HCO3, lactate, sodium, potassium, chloride, ionized calcium, blood urea nitrogen, base excess, and arterial/alveolar oxygen ratio. Hence, regression equations were made for the aforementioned. There was no correlation observed between ABG and VBG pO2 and SpO2. Our study concluded that VBG could be a reasonable alternative for ABG in hypotensive patients. We can also mathematically predict values of ABG from VBG using regression equations derived. Conclusions: ABG sampling causes most unpleasant experiences to patients and is associated with complications like arterial injury, thrombosis, air or clotted-blood embolism, arterial occlusion, hematoma, aneurysm formation, and reflex sympathetic dystrophy. The study has shown strong correlations and agreements for most ABG and VBG parameters and can predict ABG mathematically using regression formulas formulated from VBG. This will decrease needle stick injury, consume less time, and make blood gas evaluation easy in hypotensive settings. [ABSTRACT FROM AUTHOR]

Congestion is a major cause of hospitalization for heart failure (HF). Peripheral venous pressure (PVP) strongly correlates with right atrial pressure. We recently reported that high PVP at discharge portends a poor prognosis in patients hospitalized for HF. In the same population, we aimed to analyze changes in PVP after discharge and to evaluate prognostic implications of post-discharge PVP. PVP was measured at the forearm vein of 163 patients in the 1-month post-discharge follow-up visit. The primary outcome was a composite of cardiovascular death or re-hospitalization for HF after the 1-month follow-up visit up to 1 year after discharge. Post-discharge PVP correlated with jugular venous pressure, the inferior vena cava diameter, and brain-type natriuretic peptide levels. The cumulative incidence of the primary outcome event was significantly higher in patients with PVP above the median (6 mmHg) than in those with median PVP or lower (39.8% versus 16.9%, Log-rank P = 0.04). Age- and sex-adjusted risk of PVP per 1 mmHg for the primary outcome measure was significant (hazard ratio: 1.12 [95% confidence interval 1.03–1.21]). 35% of patients who had PVP ≤6 mmHg at discharge had PVP >6 mmHg at the 1-month follow-up. PVP significantly decreased from discharge to 1-month follow-up in patients without the primary outcome event (from 6 [4–10] to 6 [4–8] mmHg, P =0.01), but remained high in those with the primary outcome event (from 8 [5–11] to 7 [5–10.5] mmHg, P = 0.9). PVP measurements during the early post-discharge period may be useful to identify high risk patients. Trial registration number: UMIN000034279. [Display omitted] • Post-discharge congestion can be assessed by peripheral venous pressure (PVP). • PVP at 1-month post-discharge correlated with subsequent clinical outcomes. • Sustained increase in PVP after discharge portends worse clinical outcomes. • PVP may be useful to monitor congestion status and identify high risk patients. [ABSTRACT FROM AUTHOR]

In the EARLIER (Efficacy and Safety of Early Initiation of Eplerenone Treatment in Patients with Acute Heart Failure) trial, eplerenone did not reduce heart failure (HF) hospitalizations or all-cause mortality in 300 patients admitted for acute HF (AHF). However, the trial might have been underpowered for these endpoints, and a comprehensive overview of the effect of eplerenone on diuretic doses and patients' clinical stability is warranted. The EARLIER trial included Japanese patients hospitalized for AHF randomly assigned to eplerenone or placebo over 6 months. Cox proportional hazards and mixed-effects models were used for analyses. Three hundred patients were included (mean age, 67 ± 13 years; 73% males). The median furosemide equivalent dose was 40 (20–62) mg at randomization. Patients with higher furosemide-equivalent doses had more severe signs and symptoms of congestion and a higher risk of all-cause mortality or HF hospitalization during 6-month follow-up (adjusted-hazard ratio per 10 mg/day increase = 1.25, 95% confidence interval: 1.05–1.49). Eplerenone significantly decreased furosemide-equivalent diuretic doses and b-type natriuretic levels throughout the follow-up (overall-joint- p < 0.05 for both) and reduced E/e' and inferior vena cava diameter at 4 weeks (both p < 0.05). Additionally, eplerenone significantly reduced left ventricular (LV) end-diastolic diameter at 24 weeks (p < 0.05). Eplerenone treatment improved the clinical stability particularly during short period following hospitalization for AHF, translated by lower diuretic doses, natriuretic peptide levels, indirect markers of filling pressure and venous congestion, and a smaller LV volume. • Higher diuretic doses were associated with more severe congestion and risk of HF-related events. • Eplerenone decreased diuretic doses both in-hospital and out-of-hospital settings. • Eplerenone decreased natriuretic peptide levels throughout the follow-up period. • Eplerenone improved echocardiographic markers of congestion and LV volume. [ABSTRACT FROM AUTHOR]

Introduction: A wide variety of diseases lead to pericardial effusion including systemic inflammatory diseases, pericarditis, reduced pericardial fluid reabsorption due to increased systemic venous pressure, pneumonia, pulmonary embolism, endocrine diseases, postcardiotomy syndrome, trauma, hypothyroidism, renal-hepatic failure, collagen-vascular diseases, infectious, and malignancy. In this study, we aimed to evaluate the underlying etiology of pericardial effusions in patients underwent surgical pericardial drainage or pericardial window and contemporary management. Materials and methods: Between January 2006 and January 2018, a total of 81 patients (49 males, 32 females; mean 52.9±10.6 years; range 5 to 84 years) who underwent subxiphoid pericardiostomy, pericardial window procedure with left anterior thoracotomy or subxiphoid approach, due to moderate or severe pericardial effusion and cardiac tamponade, were retrospectively analyzed. Results: Malignancy was diagnosed either with histopathological examination of the pericardial biopsy and/or fluid in 17 (80.9%) of 21 patients had a previous history of malignancy. Of the 21 patients diagnosed with malignancy, six patients (7.5%) had leukemia/lymphoma, and six patients (7.5%) had thyroid papillary cancer. Mycobacterium tuberculosis was identified in only one (1.2%) patient's culture of the pericardial fluid. No etiology was found in the remaining 38 patients (46.9%); thus, they were considered as idiopathic pericarditis. Conclusion: Tuberculosis is no longer the leading cause of pericarditis. Idiopathic pericarditis is the leading cause of pericardial effusion and malignancy is the next most common cause of pericardial effusion in our region. [ABSTRACT FROM AUTHOR]

Identifying individuals at higher risk of developing hepatocellular carcinoma (HCC) is pivotal to improve the performance of surveillance strategies. Herein, we aimed to evaluate the ability of single nucleotide polymorphisms (SNPs) to refine HCC risk stratification. Six SNPs in PNPLA3, TM6SF2, HSD17B13, APOE, and MBOAT7 affecting lipid turnover and one variant involved in the Wnt–β-catenin pathway (WNT3A-WNT9A rs708113) were assessed in patients with alcohol-related and/or HCV-cured cirrhosis included in HCC surveillance programmes (prospective CirVir and CIRRAL cohorts). Their prognostic value for HCC occurrence was assessed using Fine-Gray models combined into a 7-SNP genetic risk score (GRS). The predictive ability of two clinical scores (a routine non-genetic model determined by multivariate analysis and the external aMAP score) with/without the GRS was evaluated by C-indices. The standardised net benefit was derived from decision curves. Among 1,145 patients, 86 (7.5%) developed HCC after 43.7 months. PNPLA3 and WNT3A-WNT9A variants were independently associated with HCC occurrence. The GRS stratified the population into three groups with progressively increased 5-year HCC incidence (Group 1 [n = 627, 5.4%], Group 2 [n = 276, 10.7%], and Group 3 [n = 242, 15.3%]; p < 0.001). The multivariate model identified age, male sex, diabetes, platelet count, gamma-glutamyltransferase levels, albuminemia and the GRS as independent risk factors. The clinical model performance for 5-year HCC prediction was similar to that of the aMAP score (C-Index 0.769). The addition of the GRS to both scores modestly improved their performance (C-Indices of 0.786 and 0.783, respectively). This finding was confirmed by decision curve analyses showing only fair clinical net benefit. Patients with cirrhosis can be stratified into HCC risk classes by variants affecting lipid turnover and the Wnt–β-catenin pathway. The incorporation of this genetic information modestly improves the performance of clinical scores. The identification of patients at higher risk of developing liver cancer is pivotal to improve the performance of surveillance. Risk assessment can be achieved by combining several clinical and biological parameters used in routine practice. The addition of patients' genetic characteristics can modestly improve this prediction and will ultimately pave the way for precision medicine in patients eligible for HCC surveillance, allowing physicians to trigger personalised screening strategies. [Display omitted] • HCC risk stratification will ultimately enable refinement of surveillance strategies in patients with cirrhosis. • Universal scoring systems based on routine parameters may currently be applied regardless of the cause of liver disease. • Seven genetic variants can be combined into a genetic risk score for HCC in patients in surveillance programs. • The addition of this genetic information to clinical scoring systems modestly improves their performance for risk stratification. [ABSTRACT FROM AUTHOR]

Background and Study Aims: Weight reduction is the mainstay treatment for Nonalcoholic steatohepatitis (NASH). intragastric balloon (IGB) placement has proven benefit in terms of weight reduction. The aim of the present study is to assess the safety and efficacy of IGB placement in compensated NASH cirrhosis. Patients and Methods: Nonalcoholic steatohepatitis cirrhosis patients with CTP ≤ 7, BMI of > 30, and who were unable to achieve weight reduction with lifestyle modification in past 3 months were prospectively enrolled. Spatz3™ adjustable gastric balloon was placed endoscopically. Primary objective was to determine efficacy in weight loss at 6 months, with secondary objectives of reduction in hepatic venous pressure gradient (HVPG), liver fat (controlled attenuation parameter, CAP), liver stiffness measurement (LSM) and clinical events as well as the tolerability and adverse events due to IGB placement. Results: Altogether 56 cirrhosis patients, with a baseline BMI of 35.24 ± 3.92 and a CTP score of 6.27 ± 1.28 underwent IGB placement. The absolute weight reduction achieved was 15.88 kg (− 16.46%) and reduction in BMI was − 10.1% at 6 months. The percentage total body weight loss of ≥ 10% was achieved in 31 (55.35%) patients. The reduction in HVPG at 6-months was 11.12% (n = 16, 14.18 ± 2.12 to 12.60 ± 1.67 mmHg). The mean reduction in LSM was 28.6% and in CAP was 10.09%. Three (5.36%) patients required removal of IGB before 6-months due to persisting vomiting. No patient developed new-onset decompensation or any serious adverse event. Conclusion: IGB placement is a safe, well tolerated and effective option for reduction in weight and portal pressure in compensated obese cirrhosis patients. Trial Registry: Clinicaltrails.gov identifier no: NCT03753438. [ABSTRACT FROM AUTHOR]

Aims Evidence for the effect of elevated blood pressure (BP) on the risk of venous thromboembolism (VTE) has been conflicting. We sought to assess the association between systolic BP and the risk of VTE. Methods and results Three complementary studies comprising an observational cohort analysis, a one-sample and two-sample Mendelian randomization were conducted using data from 5 588 280 patients registered in the Clinical Practice Research Datalink (CPRD) dataset and 432 173 UK Biobank participants with valid genetic data. Summary statistics of International Network on Venous Thrombosis genome-wide association meta-analysis was used for two-sample Mendelian randomization. The primary outcome was the first occurrence of VTE event, identified from hospital discharge reports, death registers, and/or primary care records. In the CPRD cohort, 104 017(1.9%) patients had a first diagnosis of VTE during the 9.6-year follow-up. Each 20 mmHg increase in systolic BP was associated with a 7% lower risk of VTE [hazard ratio: 0.93, 95% confidence interval (CI): (0.92–0.94)]. Statistically significant interactions were found for sex and body mass index, but not for age and subtype of VTE (pulmonary embolism and deep venous thrombosis). Mendelian randomization studies provided strong evidence for the association between systolic BP and VTE, both in the one-sample [odds ratio (OR): 0.69, (95% CI: 0.57–0.83)] and two-sample analyses [OR: 0.80, 95% CI: (0.70–0.92)]. Conclusion We found an increased risk of VTE with lower BP, and this association was independently confirmed in two Mendelian randomization analyses. The benefits of BP reduction are likely to outweigh the harms in most patient groups, but in people with predisposing factors for VTE, further BP reduction should be made cautiously. [ABSTRACT FROM AUTHOR]

The liver is often involved in both primary and secondary forms of amyloidosis. Significant clinical evidence of portal hypertension is relatively uncommon and seems to be related to the reduced sinusoidal lumen and increased resistance to blood flow due to massive perisinusoidal amyloid deposits. The relationships between the pattern and extent of amyloid deposition in patients presenting with portal hypertension have not yet been clearly demonstrated. This study is focusing on the topographic distribution of amyloidosis in patients presenting with portal hypertension. The study included biopsy-proven cases of hepatic amyloidosis. The clinical, biochemical, and serological data, involvement of the extrahepatic organs, and HVPG values were recorded. Tissue sections were re-evaluated for the distribution patterns of amyloid deposits. We had 41 patients with hepatic amyloidosis, of which, 32 were male. A mixed pattern (sinusoidal and vascular) was the most common (32/41; 78%). Hepatic venous pressure gradient was available in 21 cases. Portal hypertension was found in 14 patients (14/21; 67%). Cases of portal hypertension were found to have a sinusoidal pattern (3/14; 21.4%), vascular pattern (1/14; 7.1%), or a mixed sinusoidal and vascular pattern (10/14; 71.4%). Those not having portal hypertension showed hepatic artery (HA) involvement in 6/7 (85.7%) cases. A comparative analysis between portal hypertension (PTH) and non-PTH groups showed that HA amyloid deposition was dominant in the non-PTH group (6/7; 85.7%) and sinusoidal deposition in the PTH group (13/14; 92.8%). The difference was found to be significant (P < 0.05) We found that portal hypertension was noted in cases with diffuse sinusoidal deposition or mixed sinusoidal with portal vein deposition. In the non-PHT group, the deposition was mainly in HA alone. [ABSTRACT FROM AUTHOR]

Non-selective beta-blockers (NSBBs) have a role in the management of portal hypertension. They are currently advocated in patients with clinically significant portal hypertension (CSPH) based on Baveno-VII consensus. Current survey aimed to evaluate the practice and perceptions of prescribing NSBBs in portal hypertension by gastroenterologists and hepatologists in Asia–Pacific region in patients with compensated cirrhosis. Out of 1500 gastroenterologists approached in the region, 328 gastroenterologists responded and completed the survey. 75% of the respondents were found not to be following practice of evaluating CSPH as they prescribed NSBBs in patients of compensated cirrhosis with high-risk varices only. Major concerns raised were non-availability of hepatic venous pressure gradient and reliable non-invasive tests as surrogate of CSPH to adapt PREDESCI methodology. While 56.7% used carvedilol as the preferred NSBB to treat patients with compensated cirrhosis, 43.3% used propranolol. This survey assessed the real-world scenario of prescribing NSBBs among practicing gastroenterologists/hepatologists in patients with compensated cirrhosis. [Display omitted] [ABSTRACT FROM AUTHOR]

The aim of this study is to investigate risk factors associated with gastroesophageal variceal rebleeding after endoscopic combined treatment. Patients who had liver cirrhosis and underwent endoscopic treatment to prevent variceal rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurement and CT examination of portal vein system were performed before endoscopic treatment. Endoscopic obturation for gastric varices and ligation for esophageal varices were performed simultaneously at the first treatment. One hundred and sixty-five patients were enrolled, and after the first endoscopic treatment, recurrent hemorrhage occurred in 39 patients (23.6%) during 1-year follow-up. Compared to the non-rebleeding group, HVPG was significantly higher (18 mmHg vs.14 mmHg, P = 0.024) and more patients had HVPG exceeding 18 mmHg (51.3% vs.31.0%, P = 0.021) in the rebleeding group. No significant difference was found in other clinical and laboratory data between two groups (P > 0.05 for all). By a logistic regression analysis, high HVPG was the only risk factor associated with failure of endoscopic combined therapy (OR = 1.071, 95%CI, 1.005–1.141, P = 0.035). The poor efficacy of endoscopic treatment to prevent variceal rebleeding was associated with high HVPG. Therefore, other therapeutic options should be considered for the rebleeding patients with high HVPG. [ABSTRACT FROM AUTHOR]

Mesenchymal stem cell (MSC) therapy is a promising approach to curing bone diseases and disorders. In treating genetic bone disorders, MSC therapy is local or systemic transplantation of isolated and in vitro proliferated MSC rather than bone marrow transplantation. Recent evidence showed that bone marrow MSC engraftment to bone regeneration has been controversial in animal and human studies. Here, our modified bone marrow transplantation (BMT) method solved this problem. Like routine BMT, our modified method involves three steps: (i) isolation of bone marrow cells from the donor, (ii) whole‐body lethal irradiation to the recipient, and (iii) injection of isolated bone marrow cells into irradiated recipient mice via the tail vein. The significant modification is imported at the bone marrow isolation step. While the bone marrow cells are flushed out from the bone marrow with the medium in routine BMT, we applied the enzymes' (collagenase type 4 and dispase) integrated medium to wash out the bone marrow cells. Then, cells were incubated in enzyme integrated solution at 37°C for 10 minutes. This modification designated BMT as collagenase‐integrated BMT (c‐BMT). Notably, successful engraftment of bone marrow MSC to the new bone formation, such as osteoblasts and chondrocytes, occurs in c‐BMT mice, whereas routine BMT mice do not recruit bone marrow MSC. Indeed, flow cytometry data showed that c‐BMT includes a higher proportion of LepR+, CD51+, or RUNX2+ non‐hematopoietic cells than BMT. These findings suggested that c‐BMT is a time‐efficient and more reliable technique that ensures the disaggregation and collection of bone marrow stem cells and engraftment of bone marrow MSC to the recipient. Hence, we proposed that c‐BMT might be a promising approach to curing genetic bone disorders. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research. [ABSTRACT FROM AUTHOR]