Search Results (1,552)

The design of intravascular ultrasound (IVUS) catheters involves inherently coupled acoustic, hemodynamic, and structural requirements. Existing design strategies, which often rely on empirical geometric refinement or single-physics optimization, are limited in their ability to simultaneously ensure acoustic transmission efficiency, flow compatibility, and mechanical reliability. A multiphysics topology optimization method for the integrated design of IVUS catheters under acoustic–fluid–structure interactions is proposed in this paper. A density-based design variable is introduced to characterize the material distribution within the design domain, and consistent interpolation schemes are employed to relate this variable to the effective acoustic properties in the Helmholtz equation, the Brinkman penalization coefficient in the incompressible Navier–Stokes equations, and the elastic stiffness tensor in the structural equilibrium equation. The optimization problem is formulated as a normalized multi-objective minimization of acoustic transmission loss, flow resistance, and structural compliance, subject to constraints on material volume, received acoustic energy, wall shear stress, and structural displacement. Density filtering and smooth Heaviside projection are incorporated to regularize the design field and promote well-defined material boundaries. An adjoint sensitivity formulation is further developed to enable efficient gradient evaluation for the coupled system. Compared with the initial design, the average acoustic transmission efficiency has increased by $59.01\%$, the shear stress has decreased by $53.87\%$, and the stiffness matching rate has reached $98.27\%$. The objective function converged after 35 iterations, demonstrating the numerical stability of the proposed acoustic–fluid–structure topology optimization framework. Full article

Lactate was traditionally considered a metabolic by-product of anaerobic glycolysis, mainly associated with tissue hypoxia and muscle fatigue. However, increasing evidence has redefined lactate as a multifunctional metabolic intermediate and signaling molecule involved in exercise-induced systemic adaptations. During physical activity, circulating lactate levels rise markedly when skeletal muscle production exceeds systemic clearance, allowing lactate to act as an exercise-responsive metabolite, or exerkine, and as a mediator of cardiometabolic adaptation. In the cardiovascular system, lactate serves not only as an efficient substrate for myocardial energy production but also as a regulator of vascular tone, endothelial function, angiogenesis, inflammation, and cardiac remodeling. These effects occur through receptor-dependent and receptor-independent mechanisms, including activation of hydroxycarboxylic acid receptor 1 (HCAR1/GPR81), modulation of intracellular redox balance, and histone or non-histone protein lactylation. This review summarizes current evidence on lactate in cardiovascular physiology and disease, focusing on myocardial lactate metabolism, HCAR1/GPR81 signaling, protein lactylation, extracellular vesicle communication, gut microbiota interactions, and therapeutic implications in heart failure, atherosclerosis, and diabetic cardiomyopathy. Although lactate is also produced under resting, postprandial, and pathological conditions, exercise is characterized by the amplitude and kinetics of lactatemia, coordinated hormonal and hemodynamic responses, and transient high-concentration signaling. These features support exercise-derived lactate as a context-dependent cardiovascular exerkine. Full article

Background: Laparoscopic cholecystectomy is the gold standard for gallbladder disease but is often associated with significant postoperative pain. Opioid analgesia is effective and is the mainstay of treatment. However, opioids are limited by multiple adverse effects such as nausea and respiratory depression. Esketamine is an NMDA receptor antagonist that has emerged as a potential analgesic adjunct. This systematic review and meta-analysis aims to evaluate the efficacy and safety of perioperative esketamine for patients undergoing laparoscopic cholecystectomy. Methods: We conducted a systematic review and meta-analysis of randomized controlled trials comparing perioperative esketamine with control regimens in adults undergoing laparoscopic cholecystectomy. Five databases were searched from inception to 25 August 2025. Random-effects meta-analyses were performed for pain, hemodynamic, recovery, and safety outcomes. Results: Six randomized controlled trials including 569 patients were eligible. Esketamine was associated with lower pain scores at rest and during movement, although neither were statistically significant. No significant clinical differences were observed in mean arterial pressure or heart rate changes during surgery or after surgery. However, esketamine significantly shortened wake-up time (MD = −3.55 min, 95% CI [−6.09 to −1.02]), improved postoperative sleep quality (MD = −5.78, 95% CI [−6.80 to −4.76]), and reduced PONV (RR = 0.47, 95% CI [0.24 to 0.92]) and respiratory depression (RR = 0.18, 95% CI [0.03 to 0.98]). Conclusions: Esketamine improved selected recovery and safety outcomes but did not significantly reduce hemodynamic parameters, postoperative pain or rescue analgesia. Larger high-quality trials are needed to confirm its role in laparoscopic cholecystectomy. Full article

Diabetic kidney disease (DKD) represents the single most common etiology of chronic kidney disease and end stage kidney disease globally, a burden that continues to expand in direct proportion to the worldwide growth of the diabetes epidemic. The pathogenesis of DKD is multifactorial, involving metabolic, hemodynamic, inflammatory, and fibrotic pathways. Among these, aldosterone has emerged as a key mediator of kidney injury, extending beyond its traditional role in sodium balance and blood pressure regulation. Through activation of both MR-dependent transcriptional processes and MR-independent signaling cascades, aldosterone drives a coordinated pattern of renal injury encompassing oxidative stress generation, endothelial dysfunction, podocyte damage, inflammatory cell recruitment, and progressive interstitial fibrosis. Current therapies targeting the renin–angiotensin–aldosterone system (RAAS), including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor antagonists, have significantly improved outcomes in DKD. Despite these advances, a considerable degree of residual cardiovascular and renal risk persists, attributable in part to the incomplete attenuation of aldosterone activity and the well-characterized phenomenon of aldosterone escape under sustained RAAS blockade. Aldosterone synthase inhibitors (ASIs) represent a mechanistically distinct therapeutic approach that targets aldosterone overproduction at its enzymatic source, potentially addressing both MR-dependent and independent pathways. Early clinical trials evaluating the efficacy of ASIs have demonstrated promising effects on blood pressure and albuminuria. This review summarizes the role of aldosterone in DKD pathogenesis, evaluates current therapeutic approaches, and discusses emerging evidence supporting ASIs as a potential addition to the evolving treatment landscape. Full article

Background and Objectives: Right heart failure is a life-threatening complication of pulmonary hypertension (PH), with limited treatment options. Although recombinant human brain natriuretic peptide (rhBNP) is widely used in left heart failure, its effectiveness in right heart failure associated with varying groups of PH (Groups 1, 2, and 4) is unknown. Materials and Methods: 763 patients with varying groups of PH (PH Groups 1, 2, and 4) were enrolled and received both conventional therapy and rhBNP treatment. Therapeutic efficacy and adverse event incidence were evaluated among the PH groups. Results: Significant reductions in variables reflecting cardiac congestion, including NT-proBNP, total bilirubin, and body weight, were observed in all PH subgroups (all p < 0.001). The median percentage changes were −47% (IQR −76 to −24), −21% (IQR −33 to −1), and −3% (IQR −7 to −1), respectively. Alanine transaminase levels presented a decreasing trend (p < 0.001), whereas creatinine levels remained unchanged (p > 0.05), with consistent trends across PH subgroups. The hemodynamic response was heterogeneous, with marked decreases in the mean arterial pressure in Groups 1 and 4 (p < 0.001) but not in Group 2. Improvement in dyspnea and edema of the lower limbs was observed in 49.9% and 66.6% of cases, respectively. The overall incidence of adverse events was 0.66%, with 0.26% (2/763) being serious, all of which were in Group 1 PH. Conclusions: Findings from this exploratory analysis indicated that rhBNP treatment was associated with favorable changes in congestive status and clinical symptoms across different PH subgroups, as well as stable end-organ function. Of note, all patients received comprehensive conventional background therapy; thus, these improvements cannot be exclusively attributed to rhBNP alone. Given the observed hemodynamic fluctuations, close blood pressure monitoring should be considered throughout the treatment course, particularly for patients in Groups 1 and 4, and most notably for high-risk PAH patients (Group 1 PH). Full article

Background and Objectives: Pulmonary sequestration (PS) is a rare congenital lung anomaly with anomalous systemic arterial supply. Surgical resection is the standard treatment, but some children have contraindications. Endovascular embolization (EE) is an established alternative; published pediatric experience is limited, particularly in neonates. We report a two-centre experience with extended follow-up and quantitative hemodynamic data. Methods: Six pediatric patients (five male; median age 6 months, range 11 days to 4 years and 8 months) underwent EE for PS at two centres in Gdańsk, Poland, between 2020 and 2025. Contraindications to surgery were severe pulmonary arterial hypertension, high-output cardiac failure, low body weight with comorbidity, complex extralobar anatomy or refused parental consent. Procedures were performed under general anesthesia via right common femoral arterial access; device strategy was tailored to vessel anatomy. Results: Technical success was 100% with no procedural complications. Median feeding-artery diameter was 3.4 mm (range 2.1 to 5.3 mm). An Amplatzer-family vascular plug was used in five patients (83.3%), pushable platinum coils in two (33.3%) and Onyx-18 in one (16.7%); two had hybrid combinations and one underwent planned staged two-step embolization. Median procedural duration was 51 min. At median follow-up of 50 months (range 11 to 68), all patients showed sequester regression on imaging. Reverse cardiac remodelling occurred within five weeks in the patient with pre-procedural left ventricular dilation (Z-score +2.45 returning to normal); systolic pulmonary artery pressure fell from 35 to 40 to 17 mmHg within six weeks in the neonate treated at 11 days of life for high-output cardiac failure. No patient required surgical resection. Conclusions: Endovascular embolization is safe and effective in pediatric patients with pulmonary sequestration and contraindications to surgery, including neonates with comorbidity. Documented reverse cardiac remodelling and rapid hemodynamic improvement support its use in selected cases. Full article

Background/Objectives: Spontaneous intracranial hypotension (SIH) is caused by spinal cerebrospinal fluid (CSF) leakage and is typically diagnosed by clinical presentation and characteristic MRI signs; however, objective tools for monitoring physiological changes and treatment response remain limited. Cine phase-contrast MRI (PC-MRI) enables noninvasive quantification of aqueductal CSF dynamics, yet reliable analysis is challenging since the cerebral aqueduct is extremely small and susceptible to low contrast, partial volume effects, and ROI-dependent measurement variability—particularly in SIH where CSF pulsatility is often reduced. Methods: We propose an end-to-end automated framework that integrates (1) a cascade localization–segmentation strategy, consisting of Tiny YOLOv4 detection followed by MultiResUNet segmentation on a YOLOv4-derived cropped ROI; (2) physiology-informed pulsatility-based segmentation (PUBS) to refine anatomical masks into functional flow ROIs; and (3) one-dimensional convolutional neural networks (1D-CNNs) to extract exploratory waveform morphology features from 32-phase cardiac-cycle velocity waveforms. The study includes 39 participants, yielding 59 cine PC-MRI examinations: 11 controls, 28 Pre-treatment SIH scans and 20 Post-treatment Recovery scans. Results: The cascade model significantly improves segmentation robustness compared with a full-image baseline, achieving higher Dice scores and markedly lower boundary errors across cohorts (e.g., Pre-treatment SIH HD95: 1.66 ± 0.74 px vs. 15.37 ± 44.98 px). PUBS refinement reduces quantification deviation from expert manual references in SIH (mean relative error: 7.4% to 5.6%) and improves diagnostic performance for multiple hemodynamic parameters (e.g., downward mean flow AUC: 0.747 to 0.792). For waveform morphology analysis, the end-to-end 1D-CNN classifier was evaluated using repeated-seed participant-level grouped LOOCV. The repeated-seed ensemble prediction showed modest out-of-sample discrimination between Normal controls and Pre-treatment SIH scans, with an AUC of 0.646, a bootstrap 95% confidence interval of 0.455–0.826, and a permutation-test p-value of 0.072. Separately, exploratory analysis of the final baseline-trained 1D-CNN latent space showed marked, apparent Normal-versus-SIH separability and an intermediate recovery distribution in PCA space, suggesting that aqueductal waveform morphology may encode SIH-related physiological information. Conclusions: These findings suggest that SIH-related information may be reflected not only in flow magnitude but also in aqueductal CSF waveform morphology. However, the modest and statistically non-significant out-of-sample performance of the end-to-end 1D-CNN classifier indicates that morphology-based AI features should currently be regarded as exploratory biomarker candidates rather than validated stand-alone diagnostic tools. Larger independent cohorts are required to confirm their reproducibility, physiological meaning, and clinical utility. Full article

Pulmonary hypertension (PH) is a progressive, multifactorial syndrome characterized by elevated pulmonary arterial pressure and right heart dysfunction, associated with significant morbidity, impaired quality of life, and poor prognosis. Advances in classification, hemodynamic definitions, and targeted pharmacotherapies have improved understanding and management, yet therapeutic challenges persist across the five World Health Organization groups of PH. Historically, exercise was discouraged due to concerns about adverse hemodynamic effects, but growing evidence has suggested that structured, supervised training is safe and beneficial. Randomized trials and meta-analyses show improvements in six-minute walk distance, peak oxygen uptake, right ventricular function, ventilatory efficiency, and health-related quality of life, with a low incidence of adverse events. Physiological adaptations include favorable cardiac remodeling, enhanced endothelial function, improved skeletal and respiratory muscle performance, and improved neurohormonal activity. Despite this evidence, barriers such as patient fears, limited clinical expertise, and restricted access to specialized rehabilitation programs hinder widespread implementation. Current guidelines recommend supervised exercise as part of pulmonary rehabilitation for patients with stable PH, supporting its role as an adjunct to pharmacotherapy. This descriptive review briefly summarizes the pathophysiology of PH, phenotype-related differences and current therapeutic approaches, and the beneficial adaptations to exercise training, with the aim of informing exercise specialists and supporting safer, more effective integration of exercise-based rehabilitation into patient care. Full article

Background/Objectives: Myocardial microcirculatory dysfunction is a critical pathological feature of cardiovascular diseases, closely associated with inflammation, oxidative stress, and excessive neutrophil activation. Neutrophil extracellular traps (NETs) serve as crucial mediators of myocardial microvascular inflammatory injury. Dalbergia odorifera volatile oil (DOVO) demonstrates anti-inflammatory and antioxidant properties; however, its protective role against myocardial microcirculatory damage and its regulatory effect on NET formation remain inadequately characterized. This study investigates the protective effects of DOVO on myocardial microcirculatory disturbances and elucidates the underlying mechanisms related to NETs. Methods: A rat model of myocardial microcirculatory dysfunction was established through polyethylene microsphere injection, and an in vitro neutrophil inflammation model was generated using differentiated HL-60 cells. DOVO was administered at various doses both in vivo and in vitro, and hemodynamics, inflammatory cytokines, oxidative stress, and NET-related markers, including MPO and CitH3, were analyzed. Results: DOVO dose-dependently ameliorated microcirculatory impairment, hemodynamic disorders, inflammation, and oxidative stress in rats, significantly suppressing NET formation. In differentiated HL-60 cells, DOVO similarly reduced inflammatory gene expression and inhibited LPS-induced NETs production by downregulating MPO and CitH3. Conclusions: DOVO suggests a protective effect against myocardial microcirculatory injury by inhibiting oxidative stress, inflammatory responses, and subsequent NET formation. These findings elucidate a novel mechanism by which DOVO alleviates microcirculation-related cardiac damage and provide a theoretical basis for its application in cardiovascular injury. Full article

Background: Endothelial dysfunction and renal injury are emerging as a common feature of long COVID, especially in those with hypertension. It is not yet well characterised whether SARS-CoV-2 infection exacerbates podocyte dysfunction, fibrotic signalling and renal hemodynamic remodelling, over and above the effects of hypertension alone and there are no reliable early biomarkers in this population. Methods: We conducted a comparative cross-sectional study with prospective 6-month treatment response follow-up in 120 adult patients (aged 30–60 years) with essential hypertension (Stage I, II or III; n = 40 per stage), at Bukhara Regional Multidisciplinary Hospital. Each stage subgroup was further divided into post-COVID (3–6 months after recovery; n = 20) and non-COVID (n = 20) strata. Patients with diabetes, known chronic kidney disease, previous myocardial infarction or stroke and other major comorbidities were excluded. Serum cystatin-C, creatinine, aldosterone, TGF-β1 and VEGF-A; urinary nephrin and microalbumin; cystatin-C-derived eGFR (CKD-EPI) and oral protein-loaded renal functional reserve (RFR); and renal Doppler indices (Vps, Ved, RI, PI) of the main, segmental and interlobar arteries were assessed before and after 6 months of guideline-based renin–angiotensin–aldosterone system (RAAS) blockade (enalapril 5–10 mg or azilsartan 40–80 mg, ±eplerenone). Comparisons were made by Student’s t-test—associations by Pearson correlation. Results: At baseline, post-COVID hypertensive patients exhibited consistently higher endothelial–podocyte injury markers than non-COVID counterparts. Urinary nephrin was elevated across all stages (Stage I: 126.5 ± 9.1 vs. 91.9 ± 8.3 pg/mL, p < 0.01; Stage III: 203.3 ± 11.2 vs. 164.5 ± 9.7 pg/mL, p < 0.05), as were VEGF-A (Stage III: 286.1 ± 16.4 vs. 223.2 ± 12.6 pg/mL, p < 0.01) and TGF-β1 (Stage III: 186.4 ± 10.1 pg/mL, 1.3-fold higher; p < 0.01). The detection of microalbuminuria was 100% in Stage III post-COVID patients and 85% in non-COVID controls. The post-COVID groups had selective loss of renal functional reserve (7.8 ± 1.1% in Stage III compared to 12.5 ± 1.6% in non-COVID controls, p < 0.001). Nephrinuria correlated strongly with RFR (r = −0.824, p < 0.001), eGFR (r = −0.797, p < 0.001) and aldosterone (r = 0.613, p < 0.001). Six months of RAAS blockade reduced nephrinuria, microalbuminuria and TGF-β1 in both arms but the magnitude of biomarker reduction appeared smaller in the post-COVID group, particularly in Stage III. Conclusions: Long COVID appears to be associated with persistent endothelial dysfunction and podocyte injury in hypertensive patients. These results indicate that nephrinuria, VEGF-A, TGF-β1 and renal functional reserve are potential exploratory markers of endothelial and renal abnormalities in hypertensive patients following COVID-19. Before clinical utility can be determined, larger studies with multivariable modelling, diagnostic-performance analyses and correction for multiple testing are needed. The differences in biomarker response between groups observed in this study need to be confirmed in larger prospective studies with multivariable modelling and formal interaction analyses. Full article

Background/Objectives: Hemodynamic disturbances in sepsis and septic shock arise from the vasoactive effects of inflammatory mediators involved in the immune response. Relaxin-1 is a pleiotropic hormone associated with inflammation, angiogenesis, tissue repair, and vasodilation. This study aimed to investigate the changes in relaxin-1 levels in septic shock and to evaluate their association with mortality. Methods: This prospective observational study was conducted in a Level II intensive care unit. Demographic characteristics, vital signs, APACHE II and SOFA scores, comorbidities, and routine laboratory parameters were recorded at admission and at 48 h. Serum relaxin-1 levels were measured at both time points and analyzed in relation to survival status. Binary logistic regression was additionally performed to evaluate variables associated with mortality in a multivariable framework. Results: A total of 48 patients with sepsis and septic shock were included (54.2% female; mean age 73.4 ± 14.7 years). Overall mortality was 33.3%. Relaxin-1 levels significantly increased from baseline (11.25 ± 4.85 pg/mL) to 48 h (12.64 ± 4.81 pg/mL) (p = 0.047). Baseline relaxin-1 levels were significantly higher in non-survivors compared to survivors (14.62 ± 4.47 pg/mL vs. 11.65 ± 4.73 pg/mL, p = 0.043). Conclusions: Elevated Relaxin-1 levels were associated with mortality in patients with sepsis and septic shock. The observed increase in Relaxin-1 during early follow-up suggests a potential link with the underlying pathophysiological processes. Although Relaxin-1 was associated with mortality, its independent prognostic value could not be established in multivariable analysis due to the limited sample size. Larger, adequately powered multicenter studies are required to confirm these findings. Full article

Kidney transplantation is the treatment of choice for end-stage renal disease, although delayed graft function remains a frequent early complication with important clinical implications. Because early graft recovery depends on adequate perfusion, careful perioperative volume assessment and hemodynamic optimization are essential. Conventional markers such as interdialytic weight gain and estimated dry weight provide only indirect information on intravascular volume and may lead to pre-transplant misclassification of volume status. Complementary tools, including bioimpedance, natriuretic peptides, and congestion-focused ultrasound, may improve characterization of fluid distribution and hemodynamic stress, but none reliably define effective graft perfusion. Pressure-based parameters remain central to perioperative management; however, mean arterial pressure reflects systemic perfusion pressure and may be preserved despite reduced renal blood flow. Central venous pressure is an imprecise surrogate of intravascular volume and fluid responsiveness, with inconsistent associations with clinical outcomes across studies. In this context, flow-guided strategies based on dynamic indices of fluid responsiveness provide a more direct assessment of circulatory adequacy and have been associated, in selected studies, with improved early graft outcomes. Overall, the evidence supports a multimodal approach integrating volume assessment tools with pressure- and flow-oriented monitoring to optimize graft perfusion and early transplant outcomes. Full article

Background: Obesity is an independent and major risk factor for cardiovascular diseases. However, the presence of common comorbidities such as diabetes and hypertension makes it difficult to understand the direct impact of obesity on the myocardium. The aim of this study is to evaluate the isolated effects of weight loss achieved after bariatric surgery on left ventricular (LV) geometry and diastolic functions in individuals with the “Metabolically Healthy Obese” (MHO) phenotype. Materials and Methods: The study included 28 patients (Surgical Group) who underwent Laparoscopic Sleeve Gastrectomy (LSG) between January 2022 and December 2025, had a preoperative Body Mass Index (BMI) > 40 kg/m², and had no known cardiovascular or metabolic diseases. The control group consisted of 25 age- and gender-matched metabolically healthy morbidly obese patients who had not undergone surgery. Demographic and echocardiographic data of all participants were analyzed at baseline and at 6 months. Results: Weight Loss: In the surgical group, BMI decreased from 46.21 kg/m² to 37.11 kg/m² at the 6th month, while no significant change was observed in the control group. Cardiac Structure: In the surgical group, Left Ventricular Mass Index was significantly decreased from 51.11 g/m² to 44.57 g/m². Cardiac Function: The E/A ratio, an indicator of diastolic function, increased significantly from 1.19 to 1.34 in the surgical group, indicating notable improvement. No clinically meaningful change in systolic function was detected. Metabolic Parameters: The surgical group exhibited marked improvements in glucose and lipid profiles (decrease in Total Cholesterol, increase in HDL). Conclusions: The study demonstrates that bariatric surgery, independent of metabolic comorbidities, directly provides “reverse remodeling” of cardiac structure and improves function through reduction of adipose tissue and alleviation of hemodynamic load. These results support the effectiveness of surgery in reducing cardiovascular risk and preserving cardiac structure even in morbidly obese patients without comorbidities. Full article

Background/Objectives: Strict hemodynamic stability is critical during supratentorial craniotomy. This systematic review and meta-analysis aimed to evaluate the efficacy of magnesium sulfate (MgSO₄) as a multimodal adjuvant on intraoperative hemodynamics, opioid consumption, and biomarker outcomes in this setting. Methods: We systematically searched PubMed, Scopus, EBSCO, and the Cochrane Library for randomized controlled trials (RCTs) comparing perioperative MgSO₄ administration to placebo or standard care in adult patients undergoing elective supratentorial craniotomy. Results: Meta-analysis of nine included RCTs using a random-effects model demonstrated that MgSO₄ significantly reduced intraoperative mean arterial pressure (mean difference [MD]: −4.65 mmHg; 95% confidence interval [CI]: −7.76 to −1.55; p = 0.0033; I² = 73.6%). Furthermore, MgSO₄ administration significantly lowered postoperative serum S100B levels (standardized MD [SMD]: −0.81; 95% CI: −1.24 to −0.38; p = 0.0002, I² = 0.0%), indicating mitigated cellular neural damage, and decreased perioperative fentanyl consumption (standardized MD: −1.01; 95% CI: −1.45 to −0.57; p < 0.0001; I² = 0.0%). Intraoperative blood loss volume did not differ significantly between groups (MD: −85.03 mL; 95% CI: −331.42 to 161.37; p = 0.4952; I² = 92.5%). Conclusions: MgSO₄ is a safe and effective multimodal adjuvant for supratentorial craniotomy, providing significant hemodynamic stability, opioid-sparing effects, and preliminary biochemical evidence suggestive of neuroprotection without compromising intraoperative hemostasis. Full article

Background: New Zealand blackcurrant (NZBC) is an anthocyanin-rich supplement with reported ergogenic effects in endurance exercise; however, its effects in resistance-trained adults remain largely unexplored. Objective: This study aimed to examine whether seven days of low- or high-dose NZBC supplementation improves resistance exercise performance, anaerobic capacity, and cognitive function in resistance-trained adults. Methods: Twenty resistance-trained adults completed a randomized, double-blind, placebo-controlled crossover trial with four conditions: no-capsule control (CON), placebo (PL), low-dose blackcurrant (LDBC; 250 mg·day⁻¹), and high-dose blackcurrant (HDBC; 600 mg·day⁻¹), each for seven days. Outcomes included bench press and leg press 1RM, total lifting volume, Tendo-derived bench press power, 30 s Wingate performance, Stroop Color–Word Test scores, readiness, perceived exertion, hemodynamic responses, and adverse events. Results: LDBC and HDBC increased bench press 1RM versus CON and PL, with increases versus CON of +3.33 kg (ES = 0.72; p = 0.005) and +2.34 kg (ES = 0.49; p = 0.041), respectively. Leg press 1RM was higher in PL, LDBC, and HDBC versus CON, with the largest effects observed for LDBC (+37.2 kg, ES = 1.33; p < 0.001) and HDBC (+25.8 kg, ES = 1.11; p < 0.001). Leg press total lifting volume was substantially higher with LDBC (+2627 kg, ES = 1.56; p < 0.001) and HDBC (+1025 kg, ES = 0.74; p = 0.004) versus CON. Bench press volume showed no significant overall treatment effect (p > 0.05). For Tendo-derived power, HDBC exceeded PL for peak (+79.5 W; p = 0.006) and mean power (+46.2 W; p = 0.026). Wingate outcomes did not differ across conditions (all p > 0.05). LDBC exceeded PL on Stroop Color, Color–Word, and total scores (all p < 0.05); HDBC exceeded PL on Color–Word only. Hemodynamic responses and adverse events were comparable across all conditions. Conclusions: Short-term NZBC supplementation improved selected resistance-exercise and cognitive outcomes, with the strongest evidence observed for outcomes that exceeded both CON and PL. The PL response relative to CON suggests that non-specific capsule, expectancy, repeated testing, or period effects may have contributed to some of the lower-body improvements; therefore, placebo-controlled contrasts should be emphasized when interpreting NZBC-specific efficacy. Wingate performance was unaffected, and both doses were well tolerated over the short-term supplementation period. Full article