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Severe early graft dysfunction (EGD) is defined by mechanical circulatory support (MCS) <24 hours of heart transplantation (HT). We classified severe EGD based on timing of post-HT MCS: "Immediate" intra-operative vs "Delayed" post-operative MCS (after admission into intensive care unit (ICU) from operating theater). We hypothesized that (1) risk factors and clinical course differ between "Immediate" and "Delayed" MCS; and (2) diastolic perfusion pressure (DPP = diastolic blood pressure-central venous pressure) and Norepinephrine equivalents (NE = sum of vasopressor doses), as measures of vasoplegia are related to "Delayed" MCS. Two-center study of 216 consecutive patients who underwent HT. Recipient, donor, vasopressor doses and hemodynamic data at T0 and T6 (on admission and 6 hours after admission into ICU) were collected. Of the 216 patients, 67 patients had severe EGD ("Immediate" MCS: n = 43, "Delayed" MCS: n = 24). The likelihood of "immediate" MCS but not "delayed" MCS increased with increasing warm ischemic and cardiopulmonary bypass times on multinomial regression analysis with "no MCS" as the referent group. One-year mortality was highest in "Immediate" MCS vs "no MCS" and "delayed" MCS (34.9% vs 3.4% and 8% respectively, p < 0.001). Of the patients who had no immediate post-transplant MCS, DPP and NE at T6 were independently associated with subsequent "delayed" MCS. Sensitivity and specificity of NE ≥ 0.2 mcg/kg/min for "Delayed" MCS were 71% and 81%. Sensitivity and specificity of DPP of ≥40 mm Hg for No MCS were 83% and 74%. The discriminatory value of systemic vascular resistance for "Delayed" MCS was poor. Risk factors and 1-year survival differed significantly between "Immediate" and "Delayed" post-HT MCS. The latter is related to lower DPP and higher NE, which is consistent with vasoplegia as the dominant pathophysiology. [ABSTRACT FROM AUTHOR]

Background: Ultrasonographic assessment of the diameters of various veins and their indices are among the most applied diagnostic tools for evaluating fluid responsiveness in clinical practice. Despite their widespread use, there is no definitive answer on which is preferable. Our study aimed to investigate the diagnostic accuracy of different venous diameters and their indices to assess fluid responsiveness. Methods: We conducted a systematic review and network meta-analysis, analyzing prospective studies evaluating the diagnostic accuracy of venous diameters (inferior vena cava [IVC], internal jugular vein [IJV], superior vena cava, and subclavian vena) and their indices for fluid responsiveness. Electronic databases were searched from inception until March 2024; this search was supplemented by snowballing methods. The risk of bias was evaluated with QUADAS-2, and evidence certainty was assessed using the GRADE approach. Nine prospective cohort studies (560 patients) were included. Results: The network meta-analysis revealed that the ΔCaval index exhibited a significant performance advantage over other "venous" test parameters. The caval index significantly outperformed IJV min/max and IVCmax. IJV index and IVCmin significantly outperformed IJVmin/max. The caval index was comparable to the IJV index. The caval index was comparable during mechanical ventilation and spontaneous breathing. Conclusions: In this meta-analysis, the ΔCaval index test showed higher diagnostic accuracy for fluid responsiveness compared with other venous tests. Caval and jugular indices displayed similar accuracy, and caval indices were consistent under mechanical ventilation and spontaneous breathing. Indices generally outperformed absolute values, except for IVCmin, which equaled the caval index in efficacy. This study was registered on the International Platform for Registered Protocols for Systematic Reviews and Meta-Analyses: INPLASY202430104. [ABSTRACT FROM AUTHOR]

Background: Cerebral autoregulation is a robust regulatory mechanism that stabilizes cerebral blood flow in response to reduced blood pressure, thereby preventing cerebral ischaemia. Scientists have long believed that cerebral autoregulation also stabilizes cerebral blood flow against increases in intracranial pressure, which is another component that determines cerebral perfusion pressure. However, this idea was inconsistent with the complex pathogenesis of normal pressure hydrocephalus, which includes components of chronic cerebral ischaemia due to mild increases in intracranial pressure. Methods: Twenty-one patients who underwent ventriculoperitoneal shunt surgery for normal pressure hydrocephalus were included in this study. To determine the pressure setting of the Codman-Hakim programmable valve, intracranial pressure was measured after shunt surgery by puncturing the Ommaya reservoir, which formed a closed circuit with the needle and the syringe. Then, intracranial pressure was continuously measured with intermittent infusion of cerebrospinal fluid from the same closed circuit. We also continuously measured oximetry data, such as regional cerebral oxygen saturation derived from near-infrared spectroscopy monitoring. These data were digitized, recorded, and used for calculating intracranial compliance and the relationship between cerebrospinal fluid volume loading and intracranial pressure. Results: This study demonstrates that in patients with normal pressure hydrocephalus, cerebral venous vascular bed compression induces mild cerebral ischaemia when intracranial pressure is slightly higher than physiological venous pressure. Cerebral venous compression impairs cerebral blood flow by quadratically increasing circulatory resistance according to Poiseuille's law. Furthermore, chronic cerebral ischaemia occurred even at low or normal intracranial pressures when deep and subcortical white matter hyperintensities (DSWMHs) were severe. Conclusion: The fact that cerebral blood flow impairment begins at very low intracranial pressures indicates that cerebral autoregulation to compensate for reduced venous blood flow is not functioning adequately in NPH. These processes provide a link between impaired cerebrospinal fluid circulation, cerebral autoregulation, and neurological dysfunction, which has been missing in patients with NPH involving small vessel arteriosclerosis. These findings may provide insight into similar conditions, such as normal-tension glaucoma and chronic kidney disease, in which a mild increase in local compartment pressure leads to chronic ischemia in organs protected by autoregulatory mechanisms. [ABSTRACT FROM AUTHOR]

Background and Aims: In response to direct‐acting antivirals (DAAs) therapy, patients who experience a decrease in hepatic venous pressure gradient (HVPG) considerably reduce liver complications and have increased survival. This study aimed to assess the metabolomic changes associated with the changes in HVPG from the start of DAA therapy until 48 weeks after effective DAA therapy in patients with advanced HCV‐related cirrhosis. Methods: We carried out a multicenter longitudinal study in 31 patients with advanced hepatitis C virus (HCV)‐related cirrhosis. We performed a non‐targeted metabolomic analysis using gas chromatography–mass spectrometry and liquid chromatography‐mass spectrometry, as well as analysis of inflammation‐related biomarkers using Luminex technology. The statistical analysis was performed by Generalised Linear Mixed‐effects Models (GLMM), correcting for multiple testing. Results: We found that increases of 2,3‐butanediol (AMR = 1.15; q‐value = 0.023) and taurocholic acid (AMR = 1.06; q‐value < 0.001) were significantly associated with increases in HVPG and inflammatory biomarker levels from before DAA therapy to one year after completion of successful HCV treatment. Conclusions: These metabolites have a potential role as indicators of portal hypertension evolution. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: We aimed to characterise insulin‐like growth factor‐1 (IGF‐1) signalling in patients with advanced chronic liver disease (ACLD). Methods: Consecutive patients undergoing hepatic venous pressure gradient [HVPG] measurement were prospectively included. Clinical stages were defined as follows: probable ACLD (pACLD): liver stiffness ≥10 kPa and HVPG ≤5 mmHg, S0: mild PH (HVPG 6–9 mmHg), S1: clinically significant PH (CSPH), S2: CSPH with varices, S3: past variceal bleeding, S4: past/current non‐bleeding hepatic decompensation and S5: further decompensation. Results: In total, 269 patients were included; 105 were compensated (pACLD: n = 18; S0: n = 30; S1: n = 20; S2: n = 37), and 164 were decompensated (S3: n = 11; S4: n = 89; S5: n = 64). Median levels of IGF‐1 decreased with progressive cirrhosis (from pACLD: 88.5 ng/mL to S5: 51.0 ng/mL; p < 0.001). Patients with CSPH had significantly lower IGF‐1 levels (63.5 ng/mL vs. 81.0 ng/mL; p = 0.001). IGF‐1 showed an independent negative association with body mass index (BMI; aB: −1.56; p < 0.001), enhanced liver fibrosis (ELF) test (aB: −8.43; p < 0.001), MELD (aB: −1.13; p = 0.042) and age (per 10 years; aB: −6.87; p < 0.001). IGF‐1 exhibited an excellent AUROC (0.856) for the prediction of liver‐related death at 6 months of follow‐up. Lower IGF‐1 (per 10 ng/mL) was linked to higher risk of (further) decompensation (0.90; 95% CI: 0.83–0.98; p = 0.016), acute‐on‐chronic liver failure (ACLF; asHR: 0.80; 95% CI: 0.68–0.93; p = 0.004) and liver‐related death (asHR: 0.76; 95% CI: 0.63–0.91; p = 0.004). Conclusion: Decreased levels of IGF‐1 reflect impaired hepatic function and fibrogenesis in patients with cirrhosis, which seems particularly relevant in obesity since low IGF‐1 was independently linked to high BMI. Lower IGF‐1 in cirrhosis predicts decompensation, ACLF and liver‐related death. [ABSTRACT FROM AUTHOR]

Background Hepatic venous portal gradient (HVPG) measurement remains the gold standard for estimating portal pressure gradient (PPG). This study aimed to evaluate the correlation between endoscopic ultrasound (EUS)-guided PPG and HVPG in patients with chronic portal hypertension. Methods Patients with chronic portal hypertension in whom HVPG assessment was clinically indicated were invited to undergo transjugular HVPG and EUS-PPG with a 22-G needle in separate sessions for comparison. Intraclass correlation coefficient (ICC) and the Bland–Altman method were used to evaluate the agreement between techniques. Results 33 patients were included. No significant differences in technical success were observed: EUS-PPG (31/33, 93.9%) vs. HVPG (31/33, 93.9%). Overall, 30 patients who underwent successful EUS-PPG and HVPG were analyzed. Correlation between the two techniques showed an ICC of 0.82 (0.65–0.91). Four patients had major discrepancies (≥5 mmHg) between HVPG and EUS-PPG. No significant differences in adverse events were observed. Conclusions The correlation between EUS-PPG and HVPG was almost perfect. EUS-PPG could be a safe and reliable method for direct PPG measurement in patients with cirrhosis and a valid alternative to HVPG. [ABSTRACT FROM AUTHOR]

Objectives Methods Results Conclusion This study aimed to evaluate the performance of virtual portal pressure gradient (vPPG) and its associated hemodynamic parameters of 3‐dimensional (3D) model in patients with cirrhosis.Seventy cirrhotic patients who underwent both hepatic venous pressure gradient (HVPG) measurement and vPPG calculation were prospectively collected. The ideal‐state model (ISM; n = 44) was defined by sinusoidal PH without hepatic vein shunt or portal vein thrombosis, whereas those not conforming to the criteria were classified as non‐ISM (n = 26). Correlation analyses were conducted to determine the relationship between vPPG or its associated 3D hemodynamic parameters and HVPG. The diagnostic and predictive performance of vPPG and HVPG for cirrhotic‐related complications was evaluated using the receiver operating characteristic (ROC) curve and Kaplan–Meier analysis.In the ISM group, vPPG‐associated hemodynamic parameters including total branch cross‐sectional area (S2), average branch cross‐sectional area (S), and average portal vein model length (h) were correlated with HVPG (r = 0.592, 0.536, −0.497; all p < 0.001), whereas vPPG was strongly correlated with HVPG (r = 0.832, p < 0.001). In the non‐ISM group, vPPG, S2, S, and h were not related to HVPG (all p > 0.05). In the ISM group, both vPPG and HVPG showed significant diagnostic and predictive capabilities for cirrhosis‐related complications. While in the non‐ISM group, the diagnostic accuracy and predictive efficacy of vPPG surpassed those of HVPG.HVPG exhibited superior diagnostic and predictive efficacy for cirrhotic PH in the ISM, whereas vPPG showed enhanced performance in non‐ISM. [ABSTRACT FROM AUTHOR]

Background: Growing evidence suggests that for rodents, a substantial fraction of cerebrospinal fluid (CSF) drains by crossing the cribriform plate into the nasopharyngeal lymphatics, eventually reaching the cervical lymphatic vessels (CLVs). Disruption of this drainage pathway is associated with various neurological disorders. Methods: We employ a lumped parameter method to numerically model CSF drainage across the cribriform plate to CLVs. Our model uses intracranial pressure as an inlet pressure and central venous blood pressure as an outlet pressure. The model incorporates initial lymphatic vessels (modeling those in the nasal region) that absorb the CSF and collecting lymphatic vessels (modeling CLVs) to transport the CSF against an adverse pressure gradient. To determine unknown parameters such as wall stiffness and valve properties, we utilize a Monte Carlo approach and validate our simulation against recent in vivo experimental measurements. Results: Our parameter analysis reveals the physical characteristics of CLVs. Our results suggest that the stiffness of the vessel wall and the closing state of the valve are crucial for maintaining the vessel size and volume flow rate observed in vivo. We find that a decreased contraction amplitude and frequency leads to a reduction in volume flow rate, and we test the effects of varying the different pressures acting on the CLVs. Finally, we provide evidence that branching of initial lymphatic vessels may deviate from Murray's law to reduce sensitivity to elevated intracranial pressure. Conclusions: This is the first numerical study of CSF drainage through CLVs. Our comprehensive parameter analysis offers guidance for future numerical modeling of CLVs. This study also provides a foundation for understanding physiology of CSF drainage, helping guide future experimental studies aimed at identifying causal mechanisms of reduction in CLV transport and potential therapeutic approaches to enhance flow. [ABSTRACT FROM AUTHOR]

Introduction and Purpose: Varicose veins in the lower limbs are common, particularly among those with prolonged standing occupations, contributing to chronic venous insufficiency (CVI). CVI affects about 60% of adults, with varicose veins present in 25–33% of women and 10–20% of men, increasing with age. Understanding and addressing this condition is crucial as it impacts daily life and raises the risk of thrombosis. Effective treatments are essential to alleviate these health issues. State of Knowledge: Varicose veins result from a mix of genetic, hemodynamic, and vein wall factors. Family history plays a significant role, increasing susceptibility. Hemodynamic issues include malfunctioning venous valves and elevated venous pressure. Vein wall changes and thrombotic activity also contribute. Symptoms range from cosmetic concerns to pain and complications like venous ulcers. Understanding these factors is key for effective management. Conclusions: Surgical treatments like high ligation and stripping are standard but have drawbacks such as scarring and long recovery. Valvuloplasty addresses deep venous valve issues but is limited. Minimally invasive options, such as endovenous laser therapy and sclerotherapy, offer promising alternatives but with some recurrence risk. Compression therapies, including elastic stockings and pneumatic compression, aid recovery and symptom relief. Elastic bandage therapy is effective but requires precise application to avoid complications. Each method has pros and cons, underscoring the need for tailored treatment approaches. [ABSTRACT FROM AUTHOR]

The document discusses a study on right ventricular-pulmonary arterial (RV-PA) coupling dynamics and their impact on exercise capacity in patients with pulmonary hypertension (PH) during the 6-minute walk test (6MWT). The study found that maintaining RV-PA coupling during exercise is crucial for 6MWT performance in PH patients, with uncoupling leading to decreased exercise capacity. The research highlights the importance of contractile reserve and the potential impact of RV function on real-world exercise capacity in PH patients. The study acknowledges limitations, such as the small sample size and the use of a pressure-only method for calculating RV-PA coupling during the 6MWT. [Extracted from the article]

Recently intermittent negative pressure has emerged as a potential treatment in vascular disease and has similarities with established experimental interventions such as lower body negative pressure. The direct, local influences of either method upon intravascular pressure still require some clarification however, particularly in the immediate moments following onset. We investigated the acute intravascular pressure responses to intermittent cycles of negative pressure in the supine and sitting postures. Fifteen participants (6 female) received intermittent negative pressure cycles (-37 mmHg; 9.5-sec on, 7.5-sec off) upon the lower leg in both postures. Saphenous venous (n = 15), and dorsalis pedis artery pressure (n = 3) were recorded via pressure catheter, alongside beat-by-beat systemic cardiovascular parameters (heart rate and blood pressure; n = 15), from which the arteriovenous pressure gradient was ultimately derived. Negative pressure induced a transient reduction in local intravenous pressure (Supine: 14±3 mmHg to -18±6 mmHg, p<0.001; Sitting: 58±10 mmHg to 41±10 mmHg, p<0.001). Rate of venous pressure recovery during the negative pressure plateau phase was faster during sitting, than supine (1.94±0.72 vs. 1.06±0.69 mmHg·sec-1; p = 0.002). Local intraarterial pressure did not change. External negative pressure readily transmits to the superficial intravenous environment of the leg and transiently augments the arteriovenous pressure gradient. The greatest and most sustained effect was during the supine position. The augmented arteriovenous gradient might briefly produce Poiseuille-dependent haemodynamics before local autoregulatory mechanisms engage. These findings benefit understanding of the immediate in-vivo effects of negative pressure upon the local vasculature, and may partly account for the positive clinical effects of intermittent negative pressure treatments in vascular disease. [ABSTRACT FROM AUTHOR]

Introduction: Myocardial dissection is a rare complication of ischaemic heart disease. It occurs when a haematoma forms within the cardiac muscle, either due to an endocardial rupture or rupture of an intra-myocardial vessel. Higher ventricular wall tension and reduced myocardial tensile strength increase the risk of dissection. We describe a young male who developed a myocardial dissection following an ST elevation infarction. We explore the possible pathophysiological connection between myocardial dissection and his amphetamine use. Case presentation: A 37-year-old Sri Lankan patient presented with progressively worsening heart failure for two weeks. One month before the presentation, he had developed an ischaemic chest pain, for which he had not sought medical advice. He was abusing inhalational heroin, crystal methamphetamines and cigarette smoke daily for five years. On examination, the patient had a blood pressure of 90/60 mmHg and a pulse rate of 110 beats per minute. The cardiac apex was deviated. The jugular venous pressure was elevated, bilateral pitting ankle and pulmonary oedema were present. The ECG had Q-ST elevations in the lateral leads. Serum troponin was elevated. A transthoracic echocardiogram revealed a poorly functioning dilated left ventricle with a mass within the myocardial apex. Cardiac MRI established that the mass was an intra-myocardial haematoma. A coronary angiogram demonstrated a critical plaque stenosis at the mid left-anterior-descending artery with poor distal flow. The patient did not have HIV or infective endocarditis. We treated the patient with diuretics and guideline-directed medical therapy for heart failure with reduced ejection fraction. We did not attempt surgical repair as the dissection was non-expanding, and the patient was at a high risk of operative complications. Conclusions: Myocardial dissection with aneurysm formation is a rare complication of ischaemic heart disease. Methamphetamines enhance the risk of myocardial dissection by inducing myocardial inflammation, causing a dilated cardiomyopathy and increasing the left ventricular pressures. [ABSTRACT FROM AUTHOR]

Pituitary tumours are the second most common intracranial tumours. The anaesthetic management of pituitary tumours requires an in-depth understanding of the principles of neuroanaesthesia and pituitary disorders. Immaculate preanaesthetic evaluation, intraoperative management and postoperative care with interdisciplinary teamwork are essential for successful outcomes in surgeries for pituitary tumours. This case report discusses a 34-year-old female patient presenting for the management of a pituitary macroadenoma, illustrating the anaesthetic challenges faced in such cases. The presence of acromegaly, along with co-morbidities such as hypertension, necessitated a detailed anaesthetic management plan. The patient underwent thorough preanaesthetic evaluation and had a transnasal trans-sphenoidal tumour excision under general anaesthesia, following standard protocols for difficult airway management. The patient was intubated using a video laryngoscope and invasive blood pressure and central venous pressure monitoring were conducted. Following surgery, the patient was transferred to the neurosurgery intensive care unit and was subsequently discharged on the 10th postoperative day. [ABSTRACT FROM AUTHOR]

It is generally accepted that intraocular pressure (IOP) depends on the rate of aqueous humor production, system outflow resistance, and episcleral venous pressure. Therefore, control IOP values are expected to be within the strict and predictable limits in specific animal species, and there should be no vast differences between species. However, in the literature the control IOP values significantly vary (from potentially "hypotensive" to "hypertensive") within the same species, and especially between species depending on the measurement technique, head position in relation to the rest of the body, circadian rhythm, age, and topical and systemic drugs (anesthetics) applied. These variations make it difficult to compare different therapeutic approaches for intraocular hypertension, investigate the correlation between IOP and intracranial pressure, and determine target IOP values in glaucoma research. We recommend that different IOP physiology and pathophysiology studies take into account all the mentioned factors when describing IOP measurement methodology. [ABSTRACT FROM AUTHOR]

Postural fluid shifts may directly affect respiratory control via a complex interaction of baro‐ and chemo‐reflexes, and cerebral blood flow. Few data exist concerning the steady state ventilatory responses during head‐down tilt. We examined the cardiorespiratory responses during acute 50° head‐down tilt (HDT) in 18 healthy subjects (mean [SD] age 27 [10] years). Protocol 1 (n = 8, two female) was 50° HDT from 60° head‐up posture sustained for 10 min, while exposed to normoxia, normoxic hypercapnia (5% CO2), hypoxia (12% inspired O2) or hyperoxic hypercapnia (95% O2, 5% CO2). Protocol 2 (n = 10, four female) was 50° HDT from supine, sustained for 10 min, while breathing either medical air or normoxic hypercapnic (5% CO2) gas. Ventilation (V̇E${{\dot{V}}_E}$, pneumotachograph), end‐tidal O2 and CO2 concentration and blood pressure (Finapres) were measured continuously throughout each protocol. Middle cerebral artery blood flow velocity (MCAv; transcranial Doppler) was also measured during protocol 2. Ventilation increased significantly (P < 0.05) compared to baseline during HDT in both hyperoxic hypercapnia (protocol 1 by mean [SD] 139 [26]%) and normoxic hypercapnia (protocol 1 by mean [SD] 131 [21]% and protocol 2 by 129 [23]%), despite no change in PETCO2${{P}_{{\mathrm{ETC}}{{{\mathrm{O}}}_2}}}$ or PETO2${{P}_{{\mathrm{ET}}{{{\mathrm{O}}}_2}}}$ from baseline. No change in V̇E${{\dot{V}}_E}$ was observed during HDT with medical air or hypoxia, and there was no significant change in MCAv during HDT compared to baseline. The absence of change in cerebral blood flow leads us to postulate that the augmented ventilatory response during steep HDT may involve mechanisms related to cerebral venous pressure and venous outflow. What is the central question of this study?Postural fluid shifts affect respiratory control via complex interactions between baroreceptor and chemoreceptor reflexes, and cerebral blood flow. Few data exist concerning steady state ventilatory responses during head down tilt.What is the main finding and its importance?Acute 50° head‐down tilt augments the ventilatory response to steady state normoxic and hyperoxic hypercapnia possibly via mechanisms involving cerebral blood flow. These findings are relevant clinically during procedures performed in a steep head‐down position and microgravity environments where individuals are exposed to fluid shifts and elevated atmospheric CO2. [ABSTRACT FROM AUTHOR]

Background: Pediatric idiopathic intracranial hypertension (IIH) is a rare and challenging condition. As implied by the nomenclature, the etiologies remain unknown, and multiple etiologies are being investigated. In this study, we explored the potential role of increased systemic or cerebral venous pressure in the pathogenesis. Method: An observational cohort study following the STROBE guidelines, including prepubertal children with clinical symptoms and imaging findings consistent with IIH referred to the neurosurgical department, was conducted. The patients underwent a comprehensive diagnostic protocol, including MRI, continuous intracranial pressure (ICP) monitoring, and endovascular venography with venous pressure measurements. Results: The study included 11 consecutive patients (six boys and five girls) with an average age of 2.3 years, and an average BMI of 18.4. Among these, one patient was found to have venous stenosis with a gradient; the other 10 patients presented with normal intracranial anatomy. All patients exhibited elevated venous pressures, with an average superior sagittal sinus pressure of 18.9 mmHg, average internal jugular vein pressure of 17.0 mmHg, and average central venous pressure of 15.9 mmHg. Daytime ICP averaged 12.9 mmHg, whereas nighttime ICP averaged 17.2 mmHg with either A- or B-waves in 10 of the 11 patients. Despite pathological ICP, only three patients had papilledema. Conclusions: All patients had an increased systemic venous pressure, indicating a possible pathological factor for prepubertal IIH. Additionally, our findings show that young children often only partly meet the Friedman criteria due to a lack of papilledema, emphasizing the need for pediatric-specific diagnostic criteria. Further large-scale studies are needed to confirm these findings and to explore the underlying reasons for this increase in venous pressure and potential new treatment avenues. [ABSTRACT FROM AUTHOR]

Background/Objectives: Arteriovenous malformations (AVMs) are complex vascular anomalies that can present with significant complications, including intracranial hemorrhage. This report presents the case of a 36-year-old female with Prothrombin G20210A mutation-associated thrombophilia, highlighting its potential impact on AVM pathophysiology and management. Methods: The patient presented with a right paramedian intraparenchymal frontal hematoma, left hemiparesis, and seizures. Cerebral angiography identified a ruptured right parasagittal frontal AVM classified as Spetzler–Martin Grade II. A right interhemispheric frontal craniotomy was performed, enabling microsurgical resection of the AVM. Intraoperative findings included evacuation of a subcortical hematoma and excision of a 20 mm AVM nidus with arterial feeders from the A4 segment of the anterior cerebral artery and a single venous drainage into the superior sagittal sinus. Results: Postoperative recovery was favorable, with significant neurological improvement. The patient demonstrated resolution of hemiparesis and a marked reduction in seizure activity. The hypercoagulable state associated with Prothrombin G20210A mutation was identified as a contributing factor in the thrombosis of the AVM's draining vein, potentially leading to increased venous pressure, rupture, and hemorrhage. Conclusions: This case underscores the importance of recognizing thrombophilia in patients with AVMs for optimal surgical planning and complication management. Despite the challenges posed by the hypercoagulable condition, microsurgical resection proved to be a viable and effective treatment option. Further research is warranted to elucidate the relationship between thrombophilic disorders and AVMs to enhance patient management strategies and outcomes. [ABSTRACT FROM AUTHOR]

Background: Fontan circulation maintains an elevated venous pressure; this promotes venous and lymphatic congestion and may lead to late circuit failure. Our objective was to determine the association between thoracic lymphatic perfusion patterns assessed by magnetic resonance imaging and late Fontan failure. Methodology: A retrospective study was performed. We included patients who underwent the Fontan procedure between January 2005 and December 2019 and who were evaluated with lymphatic mapping using magnetic resonance imaging. Lymphatic abnormalities were classified into four types. The prevalence of late failure was determined, and logistic regression analysis was performed to establish the association between the variables of interest and the outcome. Results: Fifty-four patients were included with a mean age at surgery of 8.8 years ± 3.5 years; 42.6% (n = 23) were men. The most frequent diagnosis was tricuspid atresia (50%, n = 27), and the Fontan procedures were mainly performed using an extracardiac conduit (96.3%, n = 52). The prevalence of late Fontan failure was 35.2%. The lymphatic perfusion patterns observed were Type 1 in 25.9% (n = 14), Type 2 in 46.3% (n = 25), Type 3 in 25.9% (n = 14), and Type 4 in 1.8% (n = 1), with no differences in relation to late failure. (p = 0.42). The age at surgery was found to be a factor associated with the late Fontan failure (OR: 1.23; 95% CI: 1.02–1.48; p = 0.02). Conclusions: One-third of patients with Fontan circulation may experience late failure, not significantly associated with lymphatic changes, but when the total cavopulmonary connection is completed at an older age. [ABSTRACT FROM AUTHOR]

Objectives: This study is performed to determine the effects of fluid height, inner catheter diameter, and peripheral venous pressure on room-temperature intravenous fluid administration. Methods: We employed the Bernoulli equation, with frictional forces considered for volumetric analysis. Results: The results of this study demonstrate that infusion-set height, catheter size, fluid type, and blood pressure significantly affect flow rates. Under normotensive conditions, flow rates ranged from 58.2 to 10,743.18 cc/h, with the highest rates observed at a 1 m infusion-set height and larger catheters. Additionally, 6% hetastarch exhibited the lowest flow rates, while 0.9% normal saline showed the highest. Under hypertensive conditions, slightly higher infusion-set elevations were required for measurable flow rates, but they remained lower than those under normotensive conditions. Conclusion: This study investigates the mechanics of peripheral venous fluid therapy and provides foundational data for future nursing research on fluid management. [ABSTRACT FROM AUTHOR]

Portal inflow modulation has become standard practice in many transplant centers performing living donor liver transplantation. This is believed to counteract the deleterious effects of excess portal flow into a small-for-size graft. A splenectomy negates the contribution of the splenic vein flow completely and thereby substantially reduces portal inflow. Although it has been adopted as a standard strategy by many Japanese centers for inflow modulation, especially while using left hemiliver grafts, there is justifiable apprehension about its usage due to potential increases in morbidity. Described here is a splenectomy performed while using a modified right hemiliver graft with a graft to recipient weight ratio of 0.49. The challenges in decision making and reasons regarding how such a small graft might have worked without manifestations of small-for-size/flow syndrome are discussed. [ABSTRACT FROM AUTHOR]

Background and Objectives: Vascular access complications, particularly high venous pressure, pose significant challenges for hemodialysis patients undergoing hemodialysis. Limited research has focused on identifying predictive factors for invasive treatment. This study aimed to identify patients who might benefit from frequent monitoring and conservative management based on duplex ultrasound (DUS) evaluation. Materials and Methods: This retrospective study included 72 hemodialysis patients with high venous pressure who underwent DUS. Patients were divided into conservative (n = 26) and invasive treatment groups (n = 46). Key factors such as flow/pressure ratio, blood flow, and venous pressure were analyzed. Logistic regression was used to identify risk factors for invasive treatment, while receiver operating characteristic (ROC) analysis was performed to establish the optimal cutoff for the flow/pressure ratio. Results: Three months after the DUS, 3.85% of the conservative group experienced access failure, compared to 71.7% in the invasive group. The flow/pressure ratio was significantly lower in the invasive group (1.28 ± 0.26 vs. 1.47 ± 0.23, p < 0.05). A higher flow/pressure ratio (OR: 0.063, 95% CI: 0.004–0.932, p = 0.044) and the presence of tortuous veins (OR: 0.080, 95% CI: 0.007–0.897, p = 0.0405) were associated with a lower risk of invasive treatment. ROC analysis showed a flow/pressure ratio cutoff of 1.38 (AUC: 0.706, p = 0.004). Conclusions: Duplex ultrasound plays a crucial role in evaluating arterio-venous access in patients with high venous pressure. It provides a non-invasive assessment of vascular complications, helping avoid unnecessary invasive procedures. The flow/pressure ratio is significantly associated with the risk of invasive treatment, providing a valuable threshold for assessing risk and guiding clinical decision-making to optimize treatment strategies. [ABSTRACT FROM AUTHOR]

Background: Venous congestion is associated with adverse cardiovascular outcomes, necessitating accurate venous pressure assessment. Current methods, such as right heart catheterization (RHC), have limitations. Non-invasive techniques, including venous excess ultrasound (VExUS), inferior vena cava (IVC) assessment, and ultrasound-measured jugular venous pressure (uJVP), show promise but require validation in diverse populations. Aims: We aimed to assess the correlation between right atrial pressure (RAP) via RHC and non-invasive methods, including VExUS, IVC diameter with collapsibility index (CI) by American Society of Echocardiography (ASE) classification, and uJVP. Methods: In a prospective study involving 73 patients undergoing RHC, we evaluated the correlation between RAP and VExUS, IVC CI by ASE classification, and uJVP. We introduced and compared a modified VExUS grading system. Results: VExUS significantly correlated with RAP (p < 0.001), especially between VExUS grade 0 and grade 3. RAP significantly differed across IVC classifications by ASE (P < 0.001). VExUS grade 0 correlated with IVC class 1, and VExUS grade 3 correlated with IVC class 3. The modified VExUS grading system improved low and high RAP differentiation. uJVP exhibited a robust, highly significant positive correlation with invasively measured RAP (ρ = 0.67, P < 0.001). Conclusion: This study establishes a strong correlation between non-invasive ultrasound measurements (VExUS, IVC diameter with CI, and uJVP) and invasively measured RAP. These findings underscore the clinical potential of these non-invasive techniques in venous congestion assessment and patient risk stratification. [ABSTRACT FROM AUTHOR]

Background: Patients with cirrhosis and portal hypertension may have alterations in intestinal barrier resulting in increased susceptibility for infections. We investigated the effect of propranolol in gastrointestinal motility, permeability and bacterial overgrowth in cirrhosis. Methods: Patients with cirrhosis and esophageal varices were studied before and after a build-up dose of propranolol according to standard guidelines. Serum TNF-a, IL-6, IL-1b, LPS and bacterial DNA were measured before and during propranolol therapy. Oro-caecal transit time (OCTT) and bacterial overgrowth (BO) have been evaluated with H2 breath testing. Intestinal paracellular (IP), cellular passive non-carrier (ICNC), cellular passive carrier-mediated (ICCM), and gastric permeability (GP) were evaluated by measurement of lactulose, mannitol, D-xylose and sucrose respectively in urine, with high performance liquid chromatography (HPLC). Results: 35 patients with cirrhosis and portal hypertension with median age was 59.6 years (range 42–86) were included in the study. Twenty one had viral hepatitis and 25 were classified as having advanced cirrhosis (Child-Pugh B: 14 or C: 11). Median dose of administrated propranolol was 40 mg/day. After 7 days propranolol treatment BO was resolved in 15 out of 16 patients (93.7%, p = 0.0001) and OCTT was reduced significantly from 180 min to 139 min (SD 58.5, difference − 4 1 min, p = 0.0001). Serum IL-6 levels were reduced in 21/35 (60%) patients from 41.1 to 19 pg/ml (p = 0.01), TNF-a in 10/35 (28.5%) patients from 10.7 to 5.6 pg/ml (p = 0.007) and LPS in 20/35 (57%) from 7.1 to 5.2 mg/L (p = 0.1). No bacterial DNA was detected in serum of all patients either baseline or under propranolol treatment. IP was significantly reduced (0.2 to 0.16, p = 0.04) whereas ICNC (p = 0.9), ICCM (p = 0.4) and GP (p = 0.7) were not affected significantly. Intestinal Permeability (PI) index (Lactulose to Mannitol ratio) was significantly reduced (0.027 to 0.02, p = 0.03). Conclusion: In patients with cirrhosis and portal hypertension, propranolol use is associated with reduction in BO, increase in intestinal motility and amelioration in intestinal permeability. Moreover IL-6 and LPS levels are being decreased in the majority of patients under propranolol. [ABSTRACT FROM AUTHOR]

Recent discoveries have identified intrapulmonary bronchopulmonary anastomoses (IBAs) as a relatively common phenomenon forming intrapulmonary right‐to‐left shunts. This study hypothesizes that IBAs play a significant role in the pathophysiology of heart failure. We aim to investigate the impact of these intrapulmonary right‐to‐left shunts on pulmonary arterial and venous pressures in heart failure patients, utilizing mixed venous oxygen saturation (SvO₂) as a key measurement. This study included 237 patients with heart failure who underwent cardiac catheterization. The relationships between SvO₂ and pulmonary artery systolic pressure (sPAP), pulmonary artery wedge pressure (PAWP), and left ventricular end‐diastolic pressure (LVEDP) were examined using various statistical methods (single regression analysis, partial correlation analysis, structural equation modeling, and Bayesian estimation). All statistical methods that we performed showed that SvO₂ was significantly and negatively correlated with both sPAP and PAWP (p < 0.01, respectively). However, SvO₂ did not significantly correlate with LVEDP. These results suggest that a decrease in SvO₂ leads to an increase in PAWP and sPAP, while LVEDP is only passively influenced by PAWP. This phenomenon likely reflects the impact of an intrapulmonary right‐to‐left shunt caused by IBAs. The decrease in SvO₂ causes an increase in sPAP and may also cause an increase in PAWP via IBAs. [ABSTRACT FROM AUTHOR]

A variety of daily activities can intentionally or unintentionally cause the Valsalva manoeuvre, which induces a physiological response of elevated peripheral venous pressure. Studies have speculated that it may ultimately affect the choroidal anatomy. This is particularly important from a clinical point‐of‐view since patients occasionally hold their breath while undergoing macular optical coherence tomography (OCT). In this study, we systematically reviewed the literature to understand the impact of the Valsalva manoeuvre on the choroid and conducted meta‐analyses on the changes induced in the subfoveal choroidal thickness (SFCT) and the choroidal vascularity index (CVI). We searched 12 literature databases for studies in healthy participants undergoing Valsalva manoeuvre with choroidal OCT scans before and during the manoeuvre. Seven studies with a total of 444 eyes of 279 individuals were eligible for the review. The Valsalva manoeuvre led to a statistically significant but numerically small increase in the SFCT of 6.5 μm (95% CI: 1.6–11.4 μm; p = 0.01) and a statistically significant increase in the CVI of 1.48 (95% CI: 1.23–1.73; p = 0.0002). Thus, the Valsalva manoeuvre has a measurable impact on the choroid, and we recommend careful observation of how the patient sits and behaves behind the OCT scanner while scanning in order to allow accurate measurements of the choroid for diagnosis and monitoring. [ABSTRACT FROM AUTHOR]

Background Aim Study design Results Conclusion Relevance to Clinical Practice Regional citrate anticoagulation‐continuous renal replacement therapy (RCA‐CRRT) has a wide range of applications in clinical practice, but unplanned downtime due to RCA‐CRRT circuit coagulation is as high as 15.75%–66.70%.To build a nomogram model for predicting the lifespan circuits of RCA‐CRRT.A prospective observational cohort study was conducted in Sichuan, China. The collected clinical data from 404 RCA‐CRRT sessions involving 135 patients were utilized. The patients' basic information, laboratory indicators and RCA‐CRRT parameters were used as independent variables, and the survival status and survival time of RCA‐CRRT circuits were used as dependent variables. A Cox multivariate analysis was performed to build the nomogram model for predicting the lifespan of RCA‐CRRT circuits. The model was validated internally and externally.The median lifespan of RCA‐CRRT circuits was 28.0 (12.0–46.5) h, and the unplanned downtime rate was 23.76%. In the Cox multivariate analysis, venous pressure, haemoglobin, Sequential Organ Failure Assessment (SOFA), lactate, and blood transfusion were identified as statistically significant predictive factors for the lifespan of RCA‐CRRT circuits (p < .05). Subsequently, a nomogram model for predicting the lifespan of RCA‐CRRT circuits was developed. The AUC values for internal and external validation within the 12–72‐h timeframe ranged from 0.648 to 0.816 and 0.613 to 0.956, respectively. Both the calibration curve and clinical decision curve demonstrated the model's good performance.The nomogram model developed in this study demonstrates its efficacy in accurately predicting the lifespan circuits of RCA‐CRRT.Clinical nurses can use the prediction model to assess the lifespan of RCA‐CRRT circuits, so as to formulate a personalized RCA‐CRRT treatment plan for patients, thus reducing the unplanned downtime of RCA‐CRRT. [ABSTRACT FROM AUTHOR]

Background: The impact of continuous flow resulting from contemporary left ventricular assist devices (LVAD) on renal vascular physiology is unknown. Renal resistive index (RRI) reflects arterial compliance, as well as renal vascular resistance, contributed by afferent and efferent arteriolar tone, the renal interstitium as well as renal venous pressures. Methods: Prospective, single center study with renal Doppler evaluation at baseline (pre‐implant) and at 3‐months support. Outcomes assessed include need for post‐operative renal replacement therapy (RRT), worsening renal function (WRF) defined as persistent increase from pre‐implant KDIGO chronic kidney disease stage, right ventricular (RV) failure, and survival to transplantation. Results: Pre‐implant RRI did not predict cardiorenal outcomes including right heart failure, need for renal replacement therapy or worsening renal function. Post‐implant RRI was significantly lower than pre‐implant RRI, with a distinct Doppler waveform characteristic of continuous flow. Post‐implant renal end‐diastolic velocity, but not RRI, correlated strongly with LVAD flow (Spearman rho −0.99, p < 0.001), with trend toward correlation with mean arterial pressure (Spearman's rho 0.63, p = 0.129). There was a negative correlation between post‐implant RRI and mean pulmonary artery pressure (Spearman's rho −0.81, p = 0.049), likely driven by elevated pulmonary capillary wedge pressure (Spearman's rho −0.83, p = 0.058). Conclusion: The hemodynamic contributors to RRI in LVAD supported patients are complex. Higher mean pulmonary artery and pulmonary capillary wedge pressures seen in lower RRI may reflect a smaller difference in systolic and diastolic flow. Future simultaneous Doppler assessment of the LVAD outflow graft and RRI may help understand the hemodynamic interactions contributing to this index. [ABSTRACT FROM AUTHOR]

Background and Aims: The role of histamine in advanced chronic liver disease (ACLD) is poorly understood. We investigated plasma histamine levels across ACLD stages and their prognostic value. Methods: We included patients with evidence of ACLD, defined by portal hypertension (hepatic venous pressure gradient [HVPG] ≥6 mmHg) and/or a liver stiffness measurement by transient elastography ≥10 kPa, who underwent HVPG measurement between 2017 and 2020. Acute‐on‐chronic liver failure (ACLF) and/or liver‐related death were defined as composite endpoint. Results: Of 251 patients, 82.5% had clinically significant portal hypertension (median HVPG: 17 mmHg [interquartile range (IQR) 12–21]) and 135 patients (53.8%) were decompensated at baseline. Median plasma histamine was 8.5 nmol/L (IQR: 6.4–11.5), 37.1% of patients showed elevated values (>9.9 nmol/L). Histamine levels did not differ significantly across Child‐Turcotte‐Pugh (CTP) stages nor strata of model for end‐stage liver disease (MELD) or HVPG. Histamine levels correlated with markers of circulatory dysfunction (i.e. sodium, renin and aldosterone). During a median follow‐up of 29.2 months, 68 patients developed ACLF or liver‐related death. In univariate as well as in multivariate analysis (adjusting for age, sex, HVPG as well as either MELD, clinical stage, and serum albumin or CTP and serum sodium), elevated histamine levels remained associated with the composite endpoint. CTP‐based multivariate model adjusted sub‐distribution hazard ratio (asHR): 1.010 (95% CI: 1.004–1.021), p <.001; MELD‐based multivariate model asHR: 1.030 (95% CI: 1.017–1.040), p <.001. Conclusion: High levels of histamine were linked to circulatory dysfunction in ACLD patients and independently associated with increased risks of ACLF or liver‐related death. Further mechanistic studies on the link between histamine signalling and development of hyperdynamic circulation and ACLF are warranted. [ABSTRACT FROM AUTHOR]

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of advanced chronic liver disease (ACLD). Portal hypertension drives hepatic decompensation and is best diagnosed by hepatic venous pressure gradient (HVPG) measurement. Here, we investigate the prognostic value of HVPG in MASLD-related compensated ACLD (MASLD-cACLD). This European multicentre study included patients with MASLD-cACLD characterised by HVPG at baseline. Hepatic decompensation (variceal bleeding/ascites/hepatic encephalopathy) and liver-related mortality were considered the primary events of interest. A total of 340 patients with MASLD-cACLD (56.2% male; median age 62 [55-68] years, median MELD 8 [7-9], 71.2% with diabetes) were included. Clinically significant portal hypertension (CSPH: i.e. , HVPG ≥10 mmHg) was found in 209 patients (61.5%). During a median follow-up of 41.5 (27.5-65.8) months, 65 patients developed hepatic decompensation with a cumulative incidence of 10.0% after 2 years (2Y) and 30.7% after 5 years (5Y) in those with MASLD-cACLD with CSPH, compared to 2.4% after 2Y and 9.4% after 5Y in patients without CSPH. Variceal bleeding did not occur without CSPH. CSPH (subdistribution hazard ratio [SHR] 5.13; p < 0.001) was associated with an increased decompensation risk and a higher HVPG remained an independent risk factor in the multivariable model (adjusted SHR per mmHg: 1.12, p < 0.001). Liver-related mortality occurred in 37 patients at a cumulative incidence of 3.3% after 2Y and 21.4% after 5Y in CSPH. Without CSPH, the incidence after 5Y was 0.8%. Accordingly, a higher HVPG was also independently associated with a higher risk of liver-related death (adjusted SHR per mmHg: 1.20, p < 0.001). HVPG measurement is of high prognostic value in MASLD-cACLD. In patients with MASLD-cACLD without CSPH, the short-term risk of decompensation is very low and liver-related mortality is rare, while the presence of CSPH substantially increases the risk of both. While the incidence of compensated advanced chronic liver disease (cACLD) due to metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing worldwide, insights into the impact of clinically significant portal hypertension (CSPH) on the risk of liver-related events in MASLD-cACLD remain limited. Based on the findings of this European multicentre study including 340 MASLD-cACLD patients, we could show that increasing HVPG values and the presence of CSPH in particular were associated with a significantly higher risk of first hepatic decompensation and liver-related mortality. In contrast, the short-term incidence of decompensation in patients with MASLD-cACLD without CSPH was low and the risk of liver-mortality remained negligible. Thus, HVPG measurements can provide important prognostic information for individualised risk stratification in MASLD-cACLD and may help facilitate the study of novel and promising treatment possibilities for MASLD. [Display omitted] • HVPG measurement can identify patients with MASLD-cACLD at risk of liver-related events. • CSPH drives decompensation and liver-related death in MASLD-cACLD. • The risk of liver-related events in MASLD-cACLD without CSPH is low. • HVPG can facilitate risk-stratification and treatment decisions in MASLD-cACLD. [ABSTRACT FROM AUTHOR]

Aims: Adult congenital heart disease (ACHD) includes multiple disease states that predispose to pulmonary hypertension (PH). Haemodynamically, PH depends on abnormalities in three components: pulmonary blood flow (Qp), pulmonary vascular resistance (PVR) and pulmonary venous pressure (PVP). We sought to evaluate the prevalence and prognostic impact of individual haemodynamic abnormalities in ACHD. Methods and results: Retrospective study of ACHD patients undergoing cardiac catheterization at Mayo Clinic between 1999 and 2022 who were followed for the combined endpoint of death/heart transplantation. Among 1005 patients, 37% had mean pulmonary artery pressure (mPAP) ≥25 mmHg with more systemic ventricular disease, cyanotic disease and shunt lesions, highest N‐terminal pro‐B‐type natriuretic peptide and worse right heart remodelling/dysfunction. Among those with biventricular circulation, elevated PVP, PVR and mPAP were associated with prognosis, but not increased Qp >8 L/min. However, risk of death/transplant increased for PVR only at ≥3 Wood units (hazard ratio [HR] 3.00, 95% confidence interval [CI] 2.17–4.15; p < 0.0001) and for mPAP only at ≥25 mmHg (HR 3.15, 95% CI 2.17–4.58; p < 0.0001), not at current recommended lower cutpoints. Combined abnormalities in PVP and PVR were associated with worst outcome (HR 5.20, 95% CI 3.55–7.63; p < 0.0001) with intermediate risk with either abnormality (HR 2.11, 95% CI 1.46–3.04; p < 0.0001). Findings were consistent across type of biventricular ACHD. Only with the Fontan (univentricular) circulation was a lower mPAP threshold (20 mmHg) associated with adverse outcomes. Conclusions: Elevation of mPAP ≥25 mmHg in ACHD with a biventricular circulation is prognostically important regardless of disease phenotype, but milder PH of 21–25 mmHg is not associated with adverse outcome unless associated with Fontan circulation. Elevation in PVP >15 mmHg and PVR ≥3 Wood units were each individually associated with mortality with combined abnormalities associated with greatest risk. Categorizing PH in ACHD by haemodynamic mechanism (PVR, PVP or Qp) allows meaningful prognostication, and may allow more unified study of targeted therapies across heterogeneous disease states in ACHD. [ABSTRACT FROM AUTHOR]

Heart failure (HF) is a complex clinical syndrome characterized by the heart's inability to maintain sufficient circulation, leading to inadequate organ perfusion and fluid buildup. A thorough understanding of the molecular, biochemical, and hemodynamic interactions that underlie this condition is essential for improving its management and enhancing patient outcomes. Recent advancements in cardiovascular research have emphasized the critical role of microRNAs (miRNAs) as post-transcriptional regulators of gene expression, playing an important part in the development and progression of HF. This review aims to explore the contributions of miRNAs, systemic congestion markers, and traditional biomarkers to the pathophysiology of heart failure, with the objective of clarifying their prognostic value and potential clinical applications. Among the miRNAs studied, miR-30d, miR-126-3p, and miR-483-3p have been identified as key players in processes such as left ventricular remodeling, regulation of pulmonary artery pressure, and adaptation of the right ventricle. These findings underscore the importance of miRNAs in modulating the structural and functional changes seen in HF. Beyond the heart, HF affects multiple organ systems, including the kidneys and liver, with markers of dysfunction in these organs—such as worsening renal function and liver stiffness—being closely linked to increased morbidity and mortality. This highlights the interdependence of the heart and other organs, where systemic congestion, indicated by elevated venous pressures, exacerbates organ dysfunction. In this context, traditional biomarkers like natriuretic peptides and cardiac troponins remain vital tools in the diagnosis and management of HF. Natriuretic peptides reflect ventricular strain, while troponins are indicators of myocardial injury, both of which are critical for risk stratification and monitoring disease progression. Emerging diagnostic techniques, such as lung ultrasonography and advanced echocardiographic methods, offer new ways to assess hemodynamic status, further aiding therapeutic decision-making. These techniques, alongside established biomarkers, provide a more comprehensive approach to understanding the complexities of heart failure and managing its impact on patients. In conclusion, miRNAs, systemic congestion markers, and traditional biomarkers are indispensable for understanding HF pathophysiology and determining patient prognosis. The integration of novel diagnostic tools with existing biomarkers holds the promise of improved strategies for the management of heart failure. However, further research is needed to validate their prognostic value and refine their role in optimizing treatment outcomes. [ABSTRACT FROM AUTHOR]

PURPOSE Computed tomography (CT)-based body composition parameters and the hepatic venous pressure gradient (HVPG) are key characteristics in patients with liver cirrhosis. The present study aims to explore the correlation between CT-based body composition parameters and HVPG, as well as the difference in HVPG between patients with and patients without sarcopenia. METHODS A literature search for studies reporting the correlation between HVPG and CT-based body composition parameters published in English up to August 2023 in four databases, Embase, MEDLINE (via PubMed), Web of Science, and Cochrane Library, was conducted. The correlation coefficient between HVPG and CT-based body composition parameters was the primary outcome, and the difference in the HVPG value between the sarcopenia and non-sarcopenia groups was the secondary outcome. A meta-analysis was conducted using a random-effects models. The methodologic quality was assessed using the Quality Assessment of Diagnostic Studies instrument. RESULTS A total of 652 articles were identified, of which nine studies (n = 1,569) met the eligibility criteria. Among them, seven studies reported the primary outcome via the muscle index, five via the skeletal muscle index (SMI), two via the psoas-muscle-related index (PRI), and three via two adipose tissue indexes. A total of five studies reported the secondary outcome: four via SMI and one via PRI. No evidence of a significant correlation was determined between the various body composition parameters and the HVPG value, either in the muscle index or the adipose tissue index. Higher HVPG values were observed in patients with sarcopenia than in patients without sarcopenia [pooled standardized mean difference (SMD): 0.628 (-0.350, 1.606), P < 0.001; I² = 92.8%; P < 0.001] when an Asian sarcopenia definition was adopted. In contrast, when a Western cut-off value was applied, the HVPG value was higher in patients without sarcopenia than in patients with sarcopenia [pooled SMD: -0.201 (-0.366, -0.037), P = 0.016; I² = 0.00%; P = 0.785]. CONCLUSION No sufficient evidence regarding a correlation between the CT-based body composition and HVPG value was discovered. The difference in the HVPG value between the sarcopenia and non-sarcopenia groups was likely dependent on the sarcopenic cut-off value. [ABSTRACT FROM AUTHOR]

Background: Portal vein pressure (PVP) is crucial in the diagnosis, treatment monitoring, and prognosis of portal hypertension (PHT). At present, the hepatic venous pressure gradient (HVPG) and the portal vein pressure gradient (PPG) are the main approaches for portal pressure measurement. However, HVPG and PPG are limited in application due to invasive operations and high requirements for medical conditions. A more convenient way to measure portal pressure is demanded. Objectives: To detect whether the endoscopic variceal pressure (EVP) could predict the PVP. Design: This is a single-center retrospective study that detects whether the EVP could predict the PVP. Methods: Thirty-six patients were considered eligible for pre-emptive transjugular intrahepatic portosystemic shunt (TIPS) and were willing to accept the endoscopy-TIPS hybrid surgery (continuous operation within 24 h) from April 2023 to October 2023 retrospectively. EVP was measured in the procedure of the modified sandwich method. HVPG, PPG, and PVP were measured following TIPS operation. EVP was compared with HVPG, PPG, and PVP in groups divided by different sarin classifications and whether portal vein thrombosis (PVT) or not. Results: EVP was successfully measured and recorded in all. Totally, HVPG was lower than PPG, PPG was lower than PVP, and EVP manifested between PPG and PVP. In the PVT group, HVPG was lower than PPG, PPG was lower than EVP, and EVP manifested between PPG and PVP. In the non-PVT group, HVPG was lower than PPG, PPG was lower than PVP, and EVP manifested between PPG and PVP. In the gastroesophageal varices group, HVPG was lower than PPG, and PPG was lower than EVP. Conclusion: As a novel way for prediction, EVP measurement might be useful and convenient in PHT. Moreover, it might be closer to the PVP. [ABSTRACT FROM AUTHOR]

Background: Hepatic venous pressure gradient (HVPG) is considered the gold standard for diagnosing portal hypertension (PHT). Laparoscopic splenectomy plus esophagogastric devascularization (LSED) is an important surgery for treating PHT. However, the variation trend of HVPG after surgery is not clear. Moreover, whether HVPG can provide precise prognostic information for patients undergoing surgery remains to be further studied. This study aimed to investigate the independent prognostic value of HVPG in LSED. Methods: From January 2016 to March 2023, 135 patients with PHT underwent LSED at our hospital were retrospectively evaluated. We analyzed the correlations between clinical indicators and history of upper gastrointestinal bleeding (UGIB). Among them, 57 patients remeasured postoperative HVPG. We further investigated the postoperative alterations of HVPG and correlative factors, as well as the relationship between the HVPG and postoperative UGIB. Results: In this study, we found that 94 patients with preoperative UGIB (16.27 ± 5.73 mmHg) had a higher baseline HVPG than the other 41 patients without (14.02 ± 5.90 mmHg) (p = 0.04). The mean postoperative HVPG significantly decreased (-3.57 ± 8.09 mmHg, p = 0.001) compared to the baseline, and 66% of patients (38/57) experienced a decreased HVPG-response after surgery. The baseline HVPG and preoperative CTP class B were associated with the decreased HVPG-response (p<0.05). Additionally, patients with postoperative HVPG decreased>20% from baseline exhibited better recurrent hemorrhage-free survival rates than those without (log-rank, p = 0.013). Conclusion: We found that LSED led to a significantly decreased HVPG, and patients with postoperative HVPG decreased >20% obtained better UGIB-free survival benefits than those without. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: Non‐selective beta‐blockers (NSBB) are a well‐established treatment in patients with clinically significant portal hypertension. However, their potential role after insertion of a transjugular intrahepatic portosystemic shunt (TIPS) still needs to be determined. Of note, recent studies suggested that favourable anti‐inflammatory effects of NSBB might be independent from pressure reduction. This study aimed to evaluate whether NSBB‐treatment is associated with amelioration of systemic inflammation (SI), hepatic decompensation and survival after TIPS‐insertion. Methods: In a retrospective study comprising 305 consecutive patients, we investigated the impact of NSBB‐intake at TIPS‐placement on periinterventional cirrhosis‐associated complications and continued NSBB‐treatment after discharge on complications including hepatic decompensation and mortality during 1‐year follow‐up, employing multivariable competing‐risk‐analyses. In a prospective cohort including 45 patients, we performed a comprehensive analysis of SI analysing 48 soluble inflammatory markers (SIMs) at baseline plus 3 and 6 months after TIPS‐insertion. Results: Overall, 175 (57.4%) patients received NSBB‐therapy prior to TIPS‐insertion; upon discharge, this decreased to 131 (22.9%), with 36 (27.5%) discontinuing NSBB within 1‐year follow‐up. Neither NSBB‐therapy at TIPS‐insertion nor treatment‐continuation after discharge were associated with lower risks for hepatic decompensation, individual cirrhosis‐associated complications or mortality neither in the periinterventional period nor during follow‐up. Similarly, in the prospective cohort NSBB‐intake was not linked to lower levels or a more prominent change of WBC, CRP or any other SIM at any of the investigated time points. Conclusion: NSBB‐therapy at the time of TIPS‐insertion and its (dis‐)continuation afterwards seems to have no significant impact on SI, development of hepatic decompensation and survival. [ABSTRACT FROM AUTHOR]

Approximately half of pregnant women in India are anemic, representing over 7.5 million women. Few studies have assessed the relationship between multiple micronutrient deficiencies and anemia during pregnancy or the trajectory of hemoglobin (Hb) during pregnancy in low‐resource settings. We enrolled 200 pregnant women from the Maternal and Newborn Health (MNH) registry, a population‐based pregnancy and birth registry in Eastern Maharashtra, India to address these gaps. The women provided capillary (finger‐prick) and venous blood specimens at enrollment (<15 weeks), and a second capillary specimen in the 3rd trimester (>27 weeks). Capillary specimens were analyzed at the time of collection with a HemoCue Hb 201+; venous specimens were shipped on dry ice to a laboratory for cyanmethemoglobin assessment. In the 1st trimester, mean Hb concentration and anemia (Hb<11.0 g/dL) prevalence using capillary specimens were 10.9 ± 1.5 g/dL and 51.1%; mean Hb concentration using venous blood specimens was estimated to be 11.3 ± 1.3 g/dL and anemia prevalence was 37.5%. The prevalence of iron, vitamin B12 and folate deficiencies were 40%, 30% and 0%, respectively. Among women with anemia in the 1st trimester (venous blood), 56% had concurrent iron deficiency (inflammation‐adjusted serum ferritin <15 µg/L) indicating that their anemia may be amenable to iron supplementation. In total, 21% of women had ID and anemia, 19% ID in the absence of anemia, 16.5% anemia in the absence of ID and 43.5% had neither. By the 3rd trimester, mean Hb from capillary specimens had declined to 10.1 ± 1.35 g/dL and anemia prevalence increased to 70.7%, despite 99.4% mothers reporting receipt of iron‐folic acid (IFA) supplements during her current pregnancy, and 83.9% reporting IFA consumption the previous day. Significant predictors of anemia in the 1st trimester (both venous and capillary) included the number of weeks gestation at the time of Hb assessment and inflammation‐adjusted serum ferritin. For 3rd trimester anemia, significant predictors included 1st trimester height, BMI and IFA consumption during the 3rd trimester (but not 1st trimester micronutrient biomarkers), indicating that IFA supplementation over the course of pregnancy may have influenced micronutrient status and anemia risk. Our findings highlight the severity of the burden of anemia and micronutrient deficiencies in Eastern Maharashtra, but also highlight that in many cases, ID and anemia affect different individuals. Preventing and managing anemia in pregnancy in India will require strengthening both clinical and community‐based strategies targeting iron deficiency, as well as other causes of anemia. Key messages: Anemia, iron deficiency and vitamin B12 deficiency were all highly prevalent in pregnant women in Eastern Maharashtra, India. The prevalence of anemia increased over the course of pregnancy despite high reported rates of receipt (99.4%) and consumption of iron folic acid supplements (83.9% in the previous day).Measuring hemoglobin concentration from single‐drop capillary blood specimens (from finger pricks) with a point‐of‐care analyzer (i.e. HemoCue Hb 201+) resulted in lower concentration estimates (10.9 g/dL vs. 11.3 g/dL) and higher anemia prevalence (51.1% vs. 37.5%) in the 1st trimester of pregnancy than venous blood tested in a laboratory with the cyanmethemoglobin method.Addressing anemia during pregnancy in India, and other Low‐ and Middle‐income country settings, will require strengthening clinical and community‐based strategies addressing iron deficiency, but also other nutritional and non‐nutritional causes of anemia. When possible, hemoglobin assessment should be conducted on venous blood specimens. [ABSTRACT FROM AUTHOR]

Background and Aims: Nonselective beta‐blockers (NSBB) are the mainstay for treatment of portal hypertension (PH), but require caution in decompensated cirrhosis (DC) or acute‐on‐chronic liver failure (ACLF) with hypotension, hyponatremia, acute kidney injury (AKI) or type 2 hepatorenal syndrome (HRS). Midodrine is oral, rapidly acting, α1‐adrenergic agonist. We evaluated acute effects of midodrine on hepatic venous pressure gradient (HVPG) in DC and ACLF with contraindications to NSBB. Methods: Patients of DC (n = 30) with grade III ascites and serum sodium (Na) <130/systolic blood pressure (SBP) <90/type II HRS (group I) and ACLF patients (n = 30) with Na <130/SBP <90/AKI (group II) were included. HVPG was done at baseline and repeated 3 h after 10 mg midodrine. Primary outcome was HVPG response (reduction by >20% or to <12 mmHg). Results: In group I, midodrine significantly reduced HVPG (19.2 ± 4.6 to 17.8 ± 4.2, p =.02) and heart rate (HR) (86.3 ± 11.6 to 77.9 ± 13.1, p <.01) and increased mean arterial pressure (MAP) (74.1 ± 6.9 to 81.9 ± 6.6 mmHg, p <.01). In group II also, midodrine reduced HVPG (19.1 ± 4.1 to 17.0 ± 4.2) and HR (92.4 ± 13.7 to 84.6 ± 14.1) and increased MAP (85.4 ± 7.3 to 91.2 ± 7.6 mmHg), p <.01 for all. HVPG response was achieved in 3/30 (10%) in group I and 8/30 (26.7%) in group II. On logistic regression analysis, prerenal AKI (OR 11.04, 95% CI 1.83–66.18, p <.01) and increase in MAP (OR 1.22, 95% CI 1.03–1.43, p =.02) were independent predictors of response. Increase in MAP by 8.5 mmHg with midodrine had best cut‐off with AUROC of.76 for response. Conclusion: In decompensated cirrhosis and ACLF patients with contraindications to NSBB, midodrine is useful in decreasing HVPG. Dose of midodrine should be titrated to increase MAP atleast by 8.5 mmHg. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: Liver involvement is an increasingly recognised complication of common variable immunodeficiency (CVID). Nodular regenerative hyperplasia (NRH), a subgroup of porto‐sinusoidal vascular disorder, and manifestations of portal hypertension (PH) unrelated to cirrhosis are the most common findings. Nonetheless, the evolution of liver disease over time remains unknown. Methods: Retrospective review of patients followed at the National Institutes of Health with CVID‐related liver disease and liver biopsy from 1990 to 2020. Clinical, imaging and histological follow‐up were recorded as part of clinical research protocols. Results: Forty patients were included, with a median age of 37.5 years at initial biopsy, 73% presenting with clear evidence of NRH, and a median fibrosis stage of 1. At biopsy, median platelet count was 100 × 109/L, spleen size 19.5 cm, hepatic venous pressure gradient 9.5 mmHg and 37.5% of patients had signs of PH. Cumulative incidence of PH was 65% at 5 years. In a subgroup of 16 patients, a follow‐up liver biopsy, performed at a median time of 3 years after the index biopsy, revealed an increase in fibrosis by ≥2 stages in 31% of cases and an increase to an overall stage of 2.2 (p = 0.001). No clinical or histological factors were associated with progression of fibrosis. Conclusions: In this CVID cohort, NRH is the most common initial histological finding; however, unexpectedly fibrosis progresses over time in a subgroup of patients. A better understanding of the underlying causal process of liver disease CVID might lead to improved outcomes. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: Zinc and selenium are essential trace elements involved in important (patho)physiological processes. The prevalence and prognostic implications of zinc and selenium deficiency in patients with advanced chronic liver disease (ACLD) remain unknown. Methods: We determined serum zinc and selenium concentrations in 309 patients with ACLD undergoing hepatic venous pressure gradient (HVPG) measurement between 2019 and 2022. We evaluated the prevalence of zinc/selenium deficiency and assessed its association with severity of ACLD and liver‐related events (LRE, i.e. first/further hepatic decompensation/liver‐related death). Results: Among 309 ACLD patients (median: age: 57 [IQR: 50–64], MELD: 11 [IQR: 9–16], HVPG: 17 [IQR: 11–20]), 73% (227) and 63% (195) were deficient in zinc and selenium, respectively. Decompensated (dACLD) patients showed significantly lower serum zinc (median: 48 [IQR: 38–59] vs. compensated, cACLD: 65 [IQR: 54–78], p < 0.001) and selenium levels (median: 4.9 [IQR 4.0–6.2] vs. cACLD: 6.1 [IQR 5.1–7.3], p < 0.001). Significant correlations of zinc/selenium levels were found with MELD (zinc: ρ = −0.498, p < 0.001; selenium: ρ = −0.295, p < 0.001), HVPG (zinc: ρ = −0.400, p < 0.001; selenium: ρ = −0.157, p = 0.006) and liver disease‐driving mechanisms (IL6, bile‐acid homeostasis). On multivariable analysis, low zinc/selenium levels, age and MELD remained independently associated with LRE. Conclusion: Zinc and selenium deficiencies are common in ACLD patients especially with higher MELD and HVPG. Low zinc and selenium levels independently predicted hepatic decompensation and liver‐related death. The effect of zinc/selenium supplementation in ACLD should be investigated in future trials. [ABSTRACT FROM AUTHOR]

After Fontan operation, decreased venous capacitance and venoconstriction are adaptive mechanisms to maintain venous return and cardiac output. The consequent higher venous pressure may adversely impact end-organ function, exercise capacity and result in worse clinical outcomes. This pilot study evaluated the safety and effect of isosorbide dinitrate (ISDN), a venodilator, on exercise capacity, peripheral venous pressure (PVP), and liver stiffness in patients with Fontan circulation. In this prospective single-arm trial, 15 individuals with Fontan circulation were evaluated at baseline and after 4 weeks of therapeutic treatment with ISDN. Primary aims were to assess the safety of ISDN and the effect on maximal exercise. We also aimed to evaluate the effect of ISDN on ultrasound-assessed liver stiffness, markers of submaximal exercise, and PVP at rest and peak exercise. Repeated measures t-tests were used to assess change in variables of interest in response to ISDN. Mean age was 23.5 ± 9.2 years (range 11.2–39.0 years), and 10/15 (67%) were male. There was no statistically significant change in peak VO2 (1401 ± 428 to 1428 ± 436 mL/min, p = 0.128), but VO2 at the anaerobic threshold increased (1087 ± 313 to 1115 ± 302 mL/min, p = 0.03). ISDN was also associated with a lower peak exercise PVP (22.5 ± 4.5 to 20.6 ± 3.0 mmHg, p = 0.015). Liver stiffness was lower with ISDN, though the difference was not statistically significant (2.3 ± 0.4 to 2.1 ± 0.5 m/s, p = 0.079). Of the patients completing the trial, mild headache was common (67%), but there were no major adverse events. Treatment with ISDN for 4 weeks is well-tolerated in patients with a Fontan circulation. ISDN is associated with an increase in VO2 at anaerobic threshold, lower peak PVP, and a trend toward lower liver stiffness. Larger, longer duration studies will be necessary to define the impact of ISDN on clinical outcomes in the Fontan circulation. Clinical Trial Registration: URL: https://clinicaltrials.gov. Unique identifier: NCT04297241. [ABSTRACT FROM AUTHOR]

Objective: This study aims to evaluate the differences between The balloon catheter method and End-hole Catheter Method in measuring hepatic venous pressure gradient (HVPG) among cirrhosis patients. Methods: From October 2017 to January 2024, patients who underwent HVPG measurements using both methods were consecutively included. HVPGs obtained from both methods were compared with the portal vein pressure gradient (PPG) obtained via transjugular intrahepatic portosystemic shunt (TIPS) using paired comparisons. Additionally, the consistency and predictive ability for bleeding risk of the two methods, as well as the impact of intrahepatic veno-venous shunt (IHVS), were analyzed. Results: The study enrolled 145 patients, each of whom had HVPG measured by both methods. PPG was measured in 61 patients. There was a statistically significant difference between the PPGs and HVPGs measured by both the balloon catheter method and the end-hole catheter method (P < 0.001), with the HVPG mean values obtained by the end-hole catheter method being closer to the PPGs. In the non-IHVS group, no significant statistical difference was found between the two methods (P = 0.071). In contrast, the IHVS group showed a significant difference (P < 0.001), with a mean difference of 2.98 ± 4.03 mmHg. When IHVS was absent, the measurement results from the end-hole catheter method and the balloon catheter method were found to be highly correlated. The end-hole catheter method has a higher screening capability for patients at risk of bleeding compared to the balloon catheter method (75.90% vs. 72.86%). Conclusion: HVPG measurements using either the balloon catheter method or end-hole catheter method showed significant difference with the PPG. The end-hole catheter method has a higher screening capability for patients at risk of bleeding, and IHVS could lead to lower HVPG measurements with The balloon catheter method. [ABSTRACT FROM AUTHOR]

Backrground: Akkermansia muciniphila, a next-generation probiotic, is known as a cornerstone regulating the gut-organ axis in various diseases, but the underlying mechanism remains poorly understood. Here, we revealed the neuronal and antifibrotic effects of A. muciniphila on the gut-liver-brain axis in liver injury. Results: To investigate neurologic dysfunction and characteristic gut microbiotas, we performed a cirrhosis cohort (154 patients with or without hepatic encephalopathy) and a community cognition cohort (80 participants in one region for three years) and validated the existence of cognitive impairment in a 3,5-diethoxycarbonyl-1,4-dihydrocollidine-induced hepatic injury mouse model. The effects of the candidate strain on cognition were evaluated in animal models of liver injury. The expression of brain-derived neurotrophic factor (BDNF) and serotonin receptors was accessed in patients with fibrosis (100 patients) according to the fibrosis grade and hepatic venous pressure gradient. The proportion of A. muciniphila decreased in populations with hepatic encephalopathy and cognitive dysfunction. Tissue staining techniques confirmed gut-liver-brain damage in liver injury, with drastic expression of BDNF and serotonin in the gut and brain. The administration of A. muciniphila significantly reduced tissue damage and improved cognitive dysfunction and the expression of BDNF and serotonin. Isolated vagus nerve staining showed a recovery of serotonin expression without affecting the dopamine pathway. Conversely, in liver tissue, the inhibition of injury through the suppression of serotonin receptor (5-hydroxytryptamine 2A and 2B) expression was confirmed. The severity of liver injury was correlated with the abundance of serotonin, BDNF, and A. muciniphila. Conclusions: A. muciniphila, a next-generation probiotic, is a therapeutic candidate for alleviating the symptoms of liver fibrosis and cognitive impairment. [ABSTRACT FROM AUTHOR]

Background: Idiopathic intracranial hypertension (IIH) is a cause of chronic headaches that are probably driven by raised intracranial pressure (ICP). Cerebral venous sinus pressure is thought to play a role in the underlying pathology, but its relation with intracranial pressure requires further investigation. We aimed to evaluate the concordance between lumbar puncture opening pressure (LPOP) as indicator of the ICP and cerebral venous sinus pressure in patients investigated for IIH. Methods: In this case-series replication study, all patients with IIH suspicion and who underwent cerebral venous sinus pressure measurement followed immediately by LP opening pressure (LPOP) measurement were retrospectively included. Pearson's correlation and measurement agreement (Bland-Altman plots) between venous pressure and LPOP were analyzed. Results: 52 consecutive patients (46 women; median age, 31 years [IQR = 25–42]) were included. The mean pressure in the superior sagittal sinus (SSS) and in the torcular were 20.9mmHg (SD ± 7.3) and 20.8 mmHg (SD ± 6.8), respectively. The mean LPOP was 22mmHg (SD ± 6.4). Pressure measured in the transverse venous sinus, the torcular, and the SSS correlated with LPOP (p < 0.001). Bland-Altman plots showed that torcular pressure strongly agreed with LPOP (mean difference of 1.7mmHg). The limit of agreement (LOA) (mean difference ± 1.96SD) contained 98.1% of the differences between the two methods, confirming the concordance between the two measures. Torcular pressure and LPOP were consistent in patients with a trans-stenotic pressure gradient ≥ or < to 8 mmHg (mean difference: 1mmHg and 2.4mmHg, respectively), and for those with a LP OP ≥ or < to 18mmHg (mean difference: 1.8mmHg and 1.95mmHg, respectively). Conclusions: In patients investigated for IIH, the ICP measured at the LP is correlated and concordant with the torcular pressure. These results confirm previous findings and further corroborate the hypothesis that cerebral venous system plays a major role in CSF dynamics and ICP. [ABSTRACT FROM AUTHOR]

Simple Summary: The venoarteriolar reflex (VAR) consists of a local vasoconstriction occurring in response to an increase in venous transmural pressure. Its underlying mechanisms, including its impact on contralateral perfusion, still need clarification. In this study we assessed VAR in a group of healthy subjects by performing a unilateral limb dependency procedure. During dependency skin perfusion decreased significantly in both the dependent and the contralateral hands. Cutaneous sympathetic activity increased during dependency and upon returning to the initial position. These results corroborate previous reports that unilateral limb dependency impacts contralateral perfusion and suggest the participation of the sympathetic nervous system. This sympathetic activation seems to occur in response to the postural change itself and does not seem to be related to the VAR. The venoarteriolar reflex (VAR) is described as a vasoconstriction occurring in response to an increase in venous transmural pressure. Its underlying mechanisms are still not clarified, particularly the neural pathway that supposedly evokes this reflex. In addition, recent studies have shown that the postural maneuvers that evoke VAR also produce a decrease in contralateral perfusion, which is also poorly understood. Our study aimed to explore the contralateral response to unilateral upper limb dependency and its underlying mechanisms. Fifteen young, healthy subjects (24.1 ± 5.8 y.o.) participated in this study after giving informed consent. While seated, subjects remained for 7 min with both arms at heart level (baseline), after which a random hand was placed 40 cm below the heart level for 5 min (dependency) before resuming the initial position for another 7 min (recovery). Skin perfusion was assessed bilaterally with photoplethysmography, and electrodermal activity (EDA) was assessed in the contralateral hand. During hand dependency, perfusion decreased significantly in both limbs, although it was more pronounced in the dependent limb, corroborating previous reports that unilateral limb dependency evokes a decrease in contralateral perfusion. Transient EDA peaks were detected in the first seconds of the dependency and recovery phases. These results support the participation of the sympathetic nervous system as a mechanism regulating contralateral perfusion during unilateral limb dependency. This sympathetic activation is probably attributed to the postural changes themselves and is likely not related to the VAR. [ABSTRACT FROM AUTHOR]

Introduction: This study investigated the combination of venous stasis and inflammation in varicose vein development. Methods: The study included patients with primary varicose veins operated using high ligation and stripping of greater saphenous vein. All of them showed reflux at sapheno-femoral junction on preoperative Doppler ultrasound. Mesenteric veins from early or advanced gastric cancer specimens were used as control group. Inflammatory mediators expressed in the venous wall were measured via immunohistochemistry and compared between the two groups. Results: Thirty-five (59.3%) men and 24 women with a mean age of 52.8 years (range, 23–77 years) were included and 29 (49.2%) patients had edema or skin changes according to Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification and reporting standards for chronic venous disorders. The expression of interleukin 6 (IL-6) and transforming growth factor β1 (TGF-β1) in intima and those of IL-6 in media of greater saphenous veins increased, with statistically significant differences between the two groups (p < 0.001). IL-6 in media and TGF-β1 levels in intima were independent predictors of varicose veins (adjusted odds ratios 74.62 and 66.69, respectively). Conclusion: Elevated venous pressure represented by reflux on Doppler ultrasound and increased expression of inflammatory cytokines including IL-6 in media and TGF-β1 in intima are associated with the development of varicose veins. [ABSTRACT FROM AUTHOR]

Background: Cirrhosis patients often exhibit clinical symptoms such as right liver atrophy, portal hypertension, spleen enlargement and increased blood supply, which exhibit considerable variation between the left and right liver sections. These differences are hypothesized to stem from disparities in blood flow within the left and right portal vein (PV) branches. However, rigorous quantitative evidence remains scarce. Purpose: We mainly aim at quantitatively revealing the relationship between the blood flow rates of two PV branches and liver volumes, and providing quantitative evidence and theoretical support for the diagnosis and treatment of cirrhosis from the perspective of hemodynamics. Methods: Five cirrhotic patients and two healthy volunteers from Beijing Friendship Hospital are investigated. Their PV blood flow models are established based on computed tomography (CT) images and finite volume simulations. The volume of the left and right liver lobes are measured in 3‐matic. The distributions of blood source in the PV branches are tracked by streamline analysis. The blood flow rates are quantitatively counted by integrating the blood source velocities. Linear analysis is performed to build the relationship between liver volumes and PV blood flow distributions. Results: Streamline analysis reveals significant differences in blood distribution between the left and right PV branches. The majority of blood from the superior mesenteric vein (SMV) flowed into the right portal vein (RPV), while most blood from the splenic vein (SV) entered the left portal vein (LPV). The main PV pressure drop linearly increases with the SV blood velocity for all PV structures of patients and healthy volunteers. The flow rate ratio QRPV/QLPV demonstrates an increase in tandem with the volume ratio VR/VL, exhibiting a linear correlation with the Pearson correlation coefficient being 0.93. Conclusion: The differences in the blood distributions are consistent with the clinicians' knowledge and validate our simulations. We demonstrated a linear increase in PV pressure with elevated SV blood velocity. Additionally, the volumes of the left and right hepatic lobes exhibited a positive correlation with blood flow rates in the corresponding PV branches. [ABSTRACT FROM AUTHOR]

Purpose: This study is to investigate the increase in retinal venous pressure (RVP) induced by a stepwise increase in airway pressure (AirP) using the new IOPstim method, which is designed to artificially increase the intraocular pressure (IOP) and thus to stimulate vascular pulsation. Methods: Twenty-eight healthy subjects were examined in the left eye. The RVP was measured at baseline and at four different levels of AirP (10, 20, 30, and 40 mmHg) using the new IOPstim method: a half balloon of 8 mm diameter is inflated laterally to the cornea under observation of the central retinal vein. As soon as the vein pulsates at a certain AirP level, the IOP is measured with a commercially available tonometer, which then corresponds to the RVP. Results: Spontaneous venous pulsation was observed in all study participants. The mean RVP values at baseline and at the AirP levels of 10, 20, 30, and 40 mmHg were 17.6 ± 2.8 mmHg; 20.1 ± 3.0 mmHg; 22.1 ± 3.5 mmHg; 24.3 ± 3.7 mmHg, and 26.6 ± 4.2 mmHg, respectively. The mean RVP values of each AirP level were statistically significantly different from each other in pairwise comparison. In a linear mixed model, the effect of AirP on RVP was highly significant (p < 0.001). In the model, a 10-mmHg increase in AirP resulted in a linear increase in RVP of 2.2 mmHg. Conclusion: An increase in AirP was accompanied by a linear increase in RVP. The influence of AirP on RVP, and thus on retinal perfusion pressure during the Valsalva maneuver, is less than was assumed based on previous studies in which contact lens dynamometry was used. [ABSTRACT FROM AUTHOR]

The treatment of breast cancer has seen great success in the recent decade. With longer survivorship, more attention is paid to function and aesthetics as integral treatment components. However, breast cancer-related lymphedema (BCRL) remains a significant complication. Immediate lymphatic reconstruction is an emerging technique to reduce the risk of BCRL, the Lymphatic Microsurgical Preventive Healing Approach (LYMPHA) being the most widely used approach. Despite promising results, it is often difficult to find suitably sized recipient venules and perform the microanastomoses between mismatched vessels deep in the axilla. Moreover, high axillary venous pressure gradients and potential damage from radiotherapy may affect the long-term patency of the anastomoses. From an ergonomic point of view, performing lymphaticovenular anastomosis in the deep axilla may be challenging for the microsurgeon. In response to these limitations, we modified the technique by moving the lymphatic reconstruction distally—terming it distally based LYMPHA (dLYMPHA). A total of 113 patients underwent mastectomy with axillary clearance in our institution from 2018 to 2021. Of these, 26 underwent subsequent dLYMPHA (Group 2), whereas 87 did not (Group 1). In total, 17.2% (15 patients) and 3.84% (1 patient) developed BCRL in Groups 1 and 2, respectively (p = 0.018). Lymphatics and recipient venules suitable for anastomoses can be reliably found in the distal upper limb with better size match. A distal modification achieves a more favorable lymphaticovenular pressure gradient, vessel match, and ergonomics while ensuring a comparably low BCRL rate. [ABSTRACT FROM AUTHOR]

Background: Identification of hypoxaemia and hypercapnia is essential for the diagnosis and treatment of acute respiratory failure. While arterial blood gas (ABG) analysis is standard for PO2 and PCO2 measurement, venous blood gas (VBG) analysis is increasingly used as an alternative. Previous systematic reviews established that VBG reporting of PO2 and PCO2 is less accurate, but the impacts on clinical management and patient outcomes are unknown. Aims: This study aimed to systematically review available evidence of the clinical impacts of using ABGs or VBGs and examine the arteriovenous difference in blood gas parameters. Methods: A comprehensive search of the MEDLINE, Embase and Cochrane Library databases since inception was conducted. Included studies were prospective or cross‐sectional studies comparing peripheral ABG to peripheral VBG in adult non‐critical care inpatients presenting with respiratory symptoms. Results: Of 15 119 articles screened, 15 were included. No studies were found that examined clinical impacts resulting from using VBG compared to ABG. Included studies focused on the agreement between ABG and VBG measurements of pH, PO2, PCO2 and HCO3−. Due to the heterogeneity of the included studies, qualitative evidence synthesis was performed. While the arteriovenous difference in pH and HCO3− was generally predictable, the difference in PO2 and PCO2 was more significant and less predictable. Conclusions: Our study reinforces the notion that VBG is not comparable to ABG for physiological measurements. However, a key revelation from our research is the significant lack of data regarding the clinical implications of using VBG instead of ABG, a common scenario in clinical practice. This highlights a critical knowledge gap. [ABSTRACT FROM AUTHOR]