Search Results (1,359)

Background: Heart failure with reduced ejection fraction (HFrEF) may be caused by various factors. The etiology of HFrEF may influence prognosis and further management. Objectives: In this study we aimed to assess differences between ischemic and non-ischemic etiology in the context of clinical features, hemodynamic evaluation, and left ventricular (LV) and left atrial (LA) remodeling in a selected cohort of patients referred for device implantation. Methods: This prospective single-center study included 86 patients with HFrEF in sinus rhythm, without a history of atrial fibrillation, referred for ICD or CRT implantation. All patients underwent comprehensive echocardiography, electrocardiography, impedance cardiography and laboratory testing. This was a cross-sectional analysis without clinical follow-up. The pre-specified question was whether the two etiological groups differed in LV remodeling and LA function. All regression analyses were exploratory. Guideline-directed medical therapy was recorded in all patients. Results: Among 86 patients, 58 had ischemic and 28 had non-ischemic HFrEF. Patients with ischemic etiology were older, had worse renal function, and had higher N-terminal pro–B-type natriuretic peptide levels. They also exhibited lower left ventricular mass index (LVMI), left atrial reservoir strain (LASr), left atrial emptying fraction (LAEF), and higher left atrial stiffness index (LASI). Among myocardial work parameters, only global wasted work (GWW) differed significantly, with higher values in the non-ischemic group. Patients with ischemic HFrEF also had a higher Heather index (HI) in impedance cardiography. The two groups did not differ in guideline-directed medical therapy. In univariable logistic regression, older age, lower LVMI, reduced LASr and LAEF, higher LASI, higher HI, and lower eGFR were associated with ischemic HFrEF etiology. In the multivariable model, older age, lower LVMI, and reduced LASr remained independently associated with ischemic HFrEF (area under the ROC curve 0.82). Conclusions: Patients with ischemic and non-ischemic HFrEF referred for device implantation differ in LV remodeling and LA function. The between-group differences were small in absolute terms, with widely overlapping distributions, and the study was not designed to test whether echocardiography can replace established methods of establishing HFrEF etiology. These exploratory findings are hypothesis-generating and require confirmation in larger, independent cohorts. Full article

Systolic anterior motion (SAM) of the mitral valve remains a clinically relevant complication after mitral valve repair and may result in dynamic left ventricular outflow tract (LVOT) obstruction, SAM-associated mitral regurgitation, and hemodynamic instability. Despite advances in surgical techniques and perioperative imaging, SAM remains an important cause of difficult separation from cardiopulmonary bypass and postoperative circulatory compromise. The development of SAM is multifactorial and results from the interaction between mitral valve anatomy, ventricular geometry, surgical repair characteristics, and perioperative hemodynamic conditions. Contemporary evidence has identified several echocardiographic predictors, including excessive posterior leaflet height, elongated anterior leaflets, reduced coaptation–septal distance, a narrow mitro–aortic angle, basal septal hypertrophy, and small hyperdynamic left ventricles. Recognition of these risk factors facilitates perioperative risk assessment and pre-repair surgical planning. Transesophageal echocardiography plays a pivotal role throughout the perioperative period, enabling risk assessment before repair, early diagnosis after cardiopulmonary bypass, and guidance of therapeutic interventions. Initial treatment is based on preload optimization, afterload augmentation, withdrawal of inotropic stimulation, and heart rate control, whereas refractory cases may require surgical revision. This narrative review summarizes the current understanding of SAM after mitral valve repair, focusing on pathophysiological mechanisms, echocardiographic predictors, surgical prevention and perioperative management, with particular emphasis on the practical role of cardiac anesthesiologists and mitral valve surgeons. Full article

Molecular mechanisms underlying the progression from compensated eccentric hypertrophy to heart failure in chronic aortic regurgitation (AR) remain poorly understood. We investigated associated transcriptional changes induced by chronic volume overload in an experimental model of severe AR. AR was induced in male Wistar rats (n = 10) by retrograde aortic valve perforation and compared with age-matched control rats (n = 8). Sixty days after surgery, cardiac remodeling was evaluated by echocardiography, invasive hemodynamics and myocardial gene-expression profiling using RT-qPCR. Chronic AR induced marked left ventricular dilatation and systolic dysfunction, consistent with decompensated eccentric hypertrophy. These functional alterations were accompanied by coordinated transcriptional changes involving pathways related to apoptosis, oxidative balance, metabolic regulation and calcium handling. AR hearts exhibited an increased BAX/BCL2 ratio, together with reduced SOD2 and increased GPX1 expression, suggesting a transcriptional profile consistent with activation of pro-apoptotic and antioxidant responses. Metabolic remodeling was characterized by decreased AMPKα1, PPARγ and GLUT4 expression, together with increased OLR1 and 15-LOX. KLK10 expression was increased. Reduced SERCA2A expression was observed, consistent with transcriptional alterations involving calcium-handling pathways. Chronic AR is associated with marked structural and functional cardiac remodeling accompanied by coordinated transcriptional alterations across multiple pathways implicated in myocardial dysfunction. This provides potential molecular pathways for further investigation. Full article

Background/Objectives: Cardiac autonomic modulation, as assessed by heart rate variability (HRV), is a key indicator of physiological status. Although aging has traditionally been associated with reduced variability, morphological characteristics may be its main correlates. This study aimed to identify phenotypes of suppressed vagal modulation in women using a machine learning approach, specifically by correcting for HRV’s intrinsic mathematical dependence on heart rate (HR). Methods: Seventy-five women (30–69 years old) were recruited during fitness center enrollment. To control for hormonal fluctuations, the younger cohort (30–49 years old) was assessed during the follicular phase, whereas the older cohort (50–69 years old) was postmenopausal. Electrocardiogram data for HRV, bioimpedance, and anthropometric measurements were collected. Intrinsic vagal modulation was isolated by adjusting root mean square of successive differences (RMSSD) for the mean R–R interval (RMSSD_adj). The machine learning pipeline used LASSO for feature selection and multivariate logistic regression to identify suppressed vagal phenotypes (RMSSD_adj ≤ 0.0232). Model stability was verified using 1000 bootstrap iterations, and a cumulative Z-score index (ISCA) was used to characterize the morphologic–hemodynamic burden. Results: LASSO identified central adiposity, measured by the waist-to-hip ratio, as the primary independent correlate of suppressed vagal phenotypes (RMSSD_adj ≤ 0.0232). The model achieved an area under the curve (AUC)–ROC of 0.633 (95% CI: 0.490–0.771) with high specificity (0.900) and sensitivity of 0.360. No significant differences in intrinsic vagal modulation were observed between age cohorts (p > 0.05). However, women classified as having a high morphologic–hemodynamic burden (high-overload ISCA) exhibited a significantly higher resting heart rate, averaging 8.3 bpm more than the low-overload group (p < 0.05), reflecting a higher physiological demand in this phenotype. Conclusions: The autonomic status of women is characterized more accurately by morphological phenotypes than by chronological age. Integrated kinanthropometric monitoring is essential for identifying reduced autonomic resilience regardless of birth year. Full article

Background: Sodium-glucose cotransporter 2 (SGLT2) inhibitors, originally developed as glucose-lowering agents for type 2 diabetes mellitus, have been shown in large, randomized trials to improve clinical outcomes in heart failure (HF) across the ejection fraction (EF) spectrum. The imaging-derived and hemodynamic changes that accompany these benefits remain incompletely characterized, and it is not known whether the patterns of cardiac remodeling observed differ between HF with reduced ejection fraction (HFrEF, left ventricular ejection fraction [LVEF] ≤ 40%) and HF with preserved ejection fraction (HFpEF, LVEF ≥ 50%). This systematic review synthesized randomized evidence on the effects of SGLT2 inhibitors on cardiac remodeling parameters and described the patterns observed in each phenotype. Methods: PubMed/MEDLINE, Scopus and Embase were searched for randomized controlled trials (RCTs) published between February 2016 and March 2026. Eligible studies enrolled adults with chronic HF receiving an SGLT2 inhibitor, included a non-SGLT2-inhibitor comparator and assessed cardiac structure, function or loading by echocardiography, cardiac magnetic resonance (CMR) or cardiac catheterization over at least three months. Risk of bias was assessed with Cochrane RoB 2, separately for each outcome domain and targeting the effect of assignment to intervention, and certainty of evidence with GRADE, separately by phenotype and imaging modality. A structured narrative synthesis following Synthesis Without Meta-analysis (SWiM) guidance that prioritized the direction, magnitude and precision of randomized between-group treatment effects was performed. Results: Fourteen publications from thirteen unique RCTs (1232 participants) were included: four trials enrolled HFrEF (LVEF ≤ 40%), five enrolled mixed reduced and mildly reduced EF cohorts (LVEF < 50% or 35–49%), four enrolled HFpEF (LVEF ≥ 50%) and one enrolled a mixed ejection-fraction population. No trial enrolled an exclusively HFmrEF population. In reduced EF, the direction of effect on LV volumes favored SGLT2 inhibition in four of eight trials reporting volumes, but the estimates were not compatible in magnitude, and the one adequately powered trial at low risk of bias (EFFORT) was neutral; the largest volumetric estimates came from EMPA-TROPISM, which published no adjusted between-group estimate. The only prespecified, adjusted and confidence-interval-bearing volumetric estimates were those of SUGAR-DM-HF (left ventricular end-systolic volume index −6.0 mL/m², 95% CI −10.8 to −1.2; end-diastolic volume index −8.2 mL/m², 95% CI −13.7 to −2.6). The global longitudinal strain improved in the trial with blinded core-laboratory reading (EFFORT −1.44%, 95% CI −2.42 to −0.46), but effect sizes in the open-label trials without stated reader blinding were two to three times larger, and the CMR-derived strain was unchanged. In HFpEF, volumes, EF, mass and strain were unchanged throughout. The most secure finding of the review was invasive: in CAMEO-DAPA, dapagliflozin reduced pulmonary capillary wedge pressure at rest by 3.5 mmHg (95% CI −6.6 to −0.4) and at peak exercise by 5.7 mmHg (95% CI −10.8 to −0.7). NT-proBNP results were directionally inconsistent, and the trials in which NT-proBNP was a prespecified primary endpoint (Empire HF, CANDLE) were neutral. Certainty of evidence was very low for 18 of 20 evidence profiles and low for the remaining two. Conclusions: Randomized imaging and hemodynamic studies suggest phenotype-related differences in the cardiac remodeling associated with SGLT2 inhibitor therapy. In studies enrolling patients with reduced EF, treatment was associated predominantly with reverse remodeling of left ventricular volumes and modest improvements in myocardial function, whereas in preserved EF, the observed changes were mainly confined to filling pressures and diastolic function, with no consistent evidence of left ventricular volumetric remodeling. Given the limited number of studies, substantial heterogeneity, and the overall low certainty of evidence, these findings should be considered hypothesis-generating and warrant confirmation in adequately powered phenotype-specific mechanistic trials. Full article

Pulmonary hypertension (PH) frequently complicates heart failure with reduced ejection fraction (HFrEF) and worsens prognosis. Right heart catheterization (RHC) remains the diagnostic gold standard, but natriuretic peptides may help identify patients requiring invasive assessment. We retrospectively analyzed 563 HFrEF patients who underwent RHC. Patients with and without PH were compared. Associations between B-type natriuretic peptide (BNP), N-terminal pro-B-type natriuretic peptide (NT-proBNP) and RHC parameters were assessed using correlations, restricted cubic splines, logistic regression and receiver operating characteristic (ROC) curves. PH was present in 443 patients (78.7%). Of the study group, 87 (15.5%) were females and 476 (84.5%) were males, the median age was 55 years and the median ejection fraction was 20%. Patients with PH had significantly higher BNP (p < 0.001), NT-proBNP (p < 0.001), New York Heart Association (NYHA) class (p < 0.001) and lower ejection fraction (p < 0.001). Increase in PH risk (p < 0.001), mean pulmonary artery pressure (p < 0.001), pulmonary vascular resistance (PVR) (p < 0.001) and pulmonary arterial wedge pressure (p < 0.001) and decrease in cardiac index (p < 0.001) were associated with an increase in BNP up to approximately 500 pg/mL and NT-proBNP up to approximately 3000 pg/mL. BNP and NT-proBNP were independent predictors of PH and PVR > 5 Wood units. BNP and NT-proBNP predicted PH with area under the curve (AUC) 0.798 and 0.727, respectively, while prediction of PVR > 5 Wood units (AUC 0.661 and 0.664, respectively) or cardiac index < 2.0 L/min/m² was less accurate (AUC 0.607 and 0.623, respectively). Measurement of plasma natriuretic peptides may support PH screening in HFrEF, but their limited ability to detect severe precapillary component confirms RHC as the definitive tool for hemodynamic phenotyping. Full article

Background/Objectives: Single atrium is a rare congenital heart defect typically repaired in infancy. Unrepaired adults with pregnancy face high risk, and postpartum repair with delayed sternal closure (DSC) has rarely been reported. Methods: We present a 33-year-old multiparous woman who presented at 30 weeks + 1 day of gestation with progressive dyspnea. Transthoracic echocardiography (TTE) revealed a single atrium with a common atrioventricular valve and an estimated pulmonary artery systolic pressure (PASP) of 47 mmHg. The multidisciplinary team advised early cesarean section, which was performed at 30 weeks + 3 days of gestation, but postpartum symptoms persisted. Six months later, the patient underwent surgical correction. The procedure was converted from right subaxillary mini-thoracotomy to median sternotomy due to intraoperative aortic dissection, which was repaired. The single atrium was partitioned using a bovine pericardial patch. Due to myocardial edema and hemodynamic instability, the sternum was left open and closed on postoperative day 4. She required 8 days of mechanical ventilation and 13 days of intensive care, and was discharged on day 27. Results: Surgical repair was successful, and at the 6-month postoperative follow-up, she had achieved NYHA class I functional status, with an estimated PASP of 40 mmHg and a well-positioned baffle with no residual shunt. Conclusions: This case demonstrates that multidisciplinary collaboration is essential for pregnant patients with unrepaired congenital heart disease, postpartum surgical correction is feasible with careful perioperative planning, and DSC is a safe strategy for managing hemodynamic instability in complex cardiac cases. Full article

Transseptal puncture constitutes the foundational step required for left atrial access, serving as the critical gateway for pulmonary vein isolation, left-sided electrophysiological ablations, and percutaneous structural heart interventions. Although fluoroscopically guided transseptal puncture demonstrates high technical success rates alongside low reported complication rates, procedural training historically relies on unstructured apprenticeship models where overlooked mechanical nuances generate the majority of periprocedural adverse events. Methodological execution demands precise interatrial septal mapping, preprocedural left atrial thrombus screening, systemic anticoagulation, and rigorous hardware de-airing protocols. Real-time imaging using transesophageal or intracardiac echocardiography enhances fluoroscopic landmarks, facilitating precise localized puncture at the thin fossa ovalis while safeguarding adjacent anatomical structures such as the aortic root, posterior left atrial wall, and pericardial space. Modern auxiliary technologies, including radiofrequency crossing devices, provide systematic escalation strategies for fibrotic or altered septal substrates. Left atrial access must be unequivocally confirmed before dilator or sheath advancement using appropriate imaging, hemodynamic, or other procedural confirmation methods according to the technique employed. Ultimate procedural safety and operator competence depend on maintaining rigorous multi-modality confirmation protocols rather than relying on technical improvisation. Full article

Background: Chronic coronary syndrome (CCS) is a major source of morbidity and healthcare utilization, and a substantial proportion of patients continue to experience angina despite contemporary revascularization and guideline-directed medical therapy. Trimetazidine, a metabolic anti-ischemic agent that does not affect heart rate or blood pressure, has been used for decades as a non-hemodynamic add-on. Its position in international guidelines, however, has shifted. We aimed to synthesize current evidence on the clinical efficacy, safety, and guideline status of trimetazidine in CCS and coronary artery disease (CAD) and to delineate clinical circumstances in which a symptom-directed trial may be considered. Methods: We performed a structured narrative review of randomized controlled trials, network and conventional meta-analyses, and large observational studies indexed in PubMed/MEDLINE, Embase, and the Cochrane Library between January 1990 and March 2026. Reference lists of eligible articles, international clinical practice guidelines, and regulatory communications from European and national agencies were also examined. Results: Across pooled analyses, trimetazidine modestly but reproducibly improved exercise tolerance and reduced angina frequency and short-acting nitrate use, with efficacy comparable to other non–heart-rate-lowering antianginal agents. Improvements in left ventricular function were reported in small, single-center studies in ischemic cardiomyopathy and selected high-risk subgroups; however, these findings have not been validated in contemporary large-scale trials, and their clinical significance against modern guideline-directed therapy is unknown. The ATPCI trial confirmed safety but showed no reduction in major adverse cardiovascular events after percutaneous coronary intervention. Rare extrapyramidal effects prompted the 2012 European Medicines Agency referral and several prescribing restrictions. Conclusions: Trimetazidine remains a reasonable symptom-directed adjunct for residual angina in carefully selected CCS patients, particularly those in whom further hemodynamic up-titration is limited or poorly tolerated. The 2024 ESC class IIb recommendation may partly reflect a broader emphasis on prognostic benefit, although the neutral post-PCI outcome evidence and regulatory safety restrictions also support a more cautious position. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) and heart failure (HF) frequently coexist within a shared cardiometabolic environment, yet their mitochondrial abnormalities are stage- and phenotype-dependent rather than uniform. In MASLD, mitochondrial adaptation evolves from increased oxidative metabolism in early steatosis toward impaired respiratory flexibility, oxidative stress, and defective quality control with disease progression, whereas the failing myocardium develops reduced energetic reserve and altered substrate utilization. These organ-specific disturbances can modify mitochondria-linked metabolites, mitochondrial damage-associated molecular patterns, stress-responsive endocrine mediators, and extracellular vesicle-associated mitochondrial cargo. However, similar mitochondrial abnormalities or circulating signals in the liver and heart do not by themselves establish direct inter-organ communication. This review distinguishes shared systemic drivers and organ-intrinsic mitochondrial stress from source-resolved cardio-hepatic signaling, highlighting hepatic ketogenesis, fibroblast growth factor 21 (FGF21), mitochondrial DNA (mtDNA)-dependent inflammatory pathways, and extracellular vesicle-mediated cargo transfer as mechanistically distinct examples with different levels of evidence. We further discuss biomarker limitations, HF-related hemodynamic liver injury, and therapeutic strategies ranging from established cardiometabolic unloading to emerging mitochondria-centered interventions. A stage-, phenotype-, and source-resolved framework may improve interpretation of mitochondrial signals and guide future mechanistic and translational studies in the MASLD–HF overlap. Full article

Background: Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction. ¹⁸F-FDG PET/MRI may reveal metabolic alterations in the pulmonary parenchyma and vasculature. We investigated pulmonary FDG uptake in PAH versus healthy controls and its associations with hemodynamics, RV function, and clinical outcomes. Methods: Twenty-eight stable PAH patients and 12 age-matched healthy controls underwent ¹⁸F-FDG PET/MRI. Standardized uptake values (SUVs) were measured in lung parenchyma and proximal pulmonary arteries. Hemodynamic parameters were obtained via right heart catheterization; RV–PA coupling was assessed as stroke volume/end-systolic volume (SV/ESV). Twenty PAH patients underwent follow-up imaging after targeted therapy. Clinical endpoints (CEPs: death, hospitalization, disease progression) were analyzed by Kaplan–Meier and Cox regression. Results: PAH patients showed markedly elevated lung parenchymal SUV (0.405 [0.338–0.533] vs. 0.225 [0.207–0.273], p < 0.001) and proximal PA SUV (3.46 [1.95–6.89] vs. 1.48 [1.15–1.65], p < 0.001). The two metrics were uncorrelated (r = +0.105, p = 0.595). SUV PA Proximal correlated with mPAP (r = +0.551) and PVR (r = +0.517), while SUV Lung showed no hemodynamic correlations. After 24 months of therapy, RV–PA coupling improved significantly (p = 0.037); lung SUV showed a non-significant trend toward reduction (Δ = −0.10, p = 0.128). Sixteen CEPs occurred; impaired RV–PA coupling (HR = 0.04, p = 0.002), elevated mPAP (HR = 1.08, p < 0.001), and reduced RVEF (HR = 0.91, p < 0.001) were strong univariable predictors. Neither SUV metric retained independent prognostic value in multivariable analysis. Conclusions: Pulmonary parenchymal and proximal PA FDG uptake are markedly elevated in PAH. However, neither metric independently predicts hemodynamic severity or clinical outcomes, limiting their current role as reliable prognostic surrogates. Full article

The heart–kidney axis has emerged as a central framework for understanding the bidirectional interactions that drive cardiorenal syndrome and broader cardiovascular–kidney–metabolic (CKM) disease. However, existing interpretations have often emphasized hemodynamic and neurohormonal mechanisms without fully integrating the growing evidence for endocrine, inflammatory, and metabolic mediators that coordinate injury across organs. This Review was therefore undertaken to provide an updated and clinically relevant synthesis of the physiological basis of heart–kidney communication, the mechanisms underlying its disruption, and the therapeutic implications of these insights. To achieve this aim, we performed a systematic narrative review of the literature using PubMed, Embase, Web of Science, and Scopus for studies, supplemented by manual screening of reference lists. Priority was given to original studies, large cohort analyses, randomized controlled trials, meta-analyses, and authoritative reviews. We integrated evidence spanning physiological regulation, maladaptive signaling pathways, emerging mediators, experimental models, and evolving treatment strategies. The reviewed evidence indicates that heart–kidney crosstalk is driven not only by altered perfusion and venous congestion, but also by sustained activation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic nervous system (SNS), inflammation, oxidative stress, mitochondrial dysfunction, anemia, uremic toxins, and disordered mineral metabolism. Among novel mediators, fibroblast growth factor 23 (FGF23) emerges as a major bone-derived, chronic kidney disease (CKD)-associated endocrine mediator linking renal injury to cardiac hypertrophy, fibrosis, calcium mishandling, and diastolic dysfunction, whereas Klotho appears to exert counter-regulatory protective effects. Heart-derived natriuretic peptides, including atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), remain important modulators of renal blood flow, natriuresis, and volume homeostasis. We further highlight the translational relevance of newer biomarkers and therapies, including sodium–glucose cotransporter 2 inhibitors (SGLT2is), glucagon-like peptide-1 receptor agonists (GLP-1 receptor agonists), and mineralocorticoid receptor antagonists (MRAs), which may help address cardiac and renal dysfunction in parallel. Overall, this Review supports a revised conceptual model in which the heart–kidney axis is governed by multidirectional hemodynamic, neurohormonal, immune, and endocrine signaling networks. A more integrated understanding of these mechanisms may improve biomarker discovery, refine risk stratification, and promote therapies that target both organs simultaneously. Full article

Background/Objectives: Atrial fibrillation (AF) and heart failure with reduced ejection fraction (HFrEF) frequently coexist and are linked by shared risk factors and pathophysiological mechanisms. Their association is consistently related to worse clinical outcomes. This narrative review summarizes current evidence regarding the epidemiology, pathophysiology, management strategies, and prognosis of patients with AF and HFrEF. Methods: This is a narrative review based on published randomized trials, registries, and observational studies evaluating the interaction between AF and HFrEF, with a focus on therapeutic strategies including rate and rhythm control, catheter ablation, stroke prevention, and guideline-directed medical therapy. Results: AF and HFrEF have a bidirectional relationship, with each condition promoting the development and progression of the other. AF contributes to hemodynamic impairment and adverse remodeling, while HFrEF promotes atrial structural and electrical changes. Management remains complex. Rate control is commonly achieved with beta-blockers and digoxin, while rhythm control is limited by the safety profile of antiarrhythmic drugs. Catheter ablation has shown improvements in left ventricular function and, in selected patients, reductions in hospitalizations and mortality, although results are not consistent across all trials. Guideline-directed medical therapy improves outcomes in HFrEF, but its interaction with AF varies across drug classes. Stroke risk is significantly increased, requiring appropriate anticoagulation. Patients with AF and HFrEF have an increased risk of mortality, hospitalization, and adverse clinical events compared with those with either condition alone, although the extent to which these outcomes are attributable to AF itself, HF severity, or the associated comorbidity burden remains uncertain. Conclusions: The coexistence of AF and HFrEF identifies a high-risk population with complex management and unfavorable outcomes. While advances in rhythm control and heart failure therapies have improved selected outcomes, optimal treatment strategies and their impact on long-term prognosis remain incompletely defined. Full article

Ephedrine is used as a vasopressor in cats, but the hemodynamic effects of intravenous (IV) administration have not been characterized. This study evaluated the hemodynamic effects of IV ephedrine in 10 cats that developed hypotension during anesthesia. Cats received either saline (SE) or atropine (AE) before ephedrine for hypotension (mean arterial pressure < 60 mmHg). Hemodynamic variables were analyzed using a linear mixed-effects model. No significant differences were observed between groups in the response rate (defined as mean arterial pressure ≥ 65 mmHg after ephedrine administration; SE, 70%; AE, 80%) or the duration of the pressor response (SE, 4 [1–10] min; AE, 3 [1–5] min). A significant main effect of ephedrine administration was identified for the systemic vascular resistance index, with increases observed in both groups, reaching statistical significance in the AE group. Significant interaction effects were observed for heart rate and cardiac index, both of which increased significantly in the AE group. These findings indicate that the pressor effect of IV ephedrine in anesthetized hypotensive cats is mediated primarily by increasing systemic vascular resistance index. Ephedrine provides a rapid and reliable pressor response and may be considered an early treatment option for anesthesia-induced hypotension in cats. Full article

Background/Objectives: Raghib syndrome is a rare congenital heart disease where the left superior vena cava (LSVC) drains into the left atrium in addition to an absent coronary sinus and an atrial septal defect. This condition can lead to hemodynamic impairment and ultimately put the patient at a high risk of stroke. While computational flow modeling enables predictive understanding of the heart hemodynamic, augmented reality (AR) provides a deeper understanding of complex anatomic geometries. This study shows the case of a 53-year-old woman with Raghib syndrome in whom preoperative planning was supported by the integration of computational fluid dynamics (CFD) and AR. Methods: Three-dimensional (3D) anatomical models were segmented from CT imaging and used to perform CFD simulations of pre- and post-operative hemodynamics, quantifying the left-to-right shunt and confirming restoration of normal intracardiac flow after surgical repair. Results: The AR application developed allowed surgeons to visualize and manipulate holographic cardiac models, enabling accurate assessment of LSVC length, vessels distances and septal defect geometry using HoloLens 2 headsets. Conclusions: This work demonstrates the feasibility and adds value of the immersive approach coupled with quantitative in silico flow analysis for preoperative planning of complex congenital heart disease. Full article