Search Results (141)

Post-occlusive reactive hyperemia (PORH) is a classical probe of microvascular function, yet its assessment remains largely based on amplitude-derived indices that do not capture the temporal organization of vascular regulation. Photoplethysmography (PPG), widely used in clinical and wearable technologies, offers a practical platform for nonlinear characterization of PORH. Twelve healthy adults underwent a standardized PORH protocol (10 min baseline, 5 min suprasystolic occlusion, 10 min reperfusion) with bilateral reflective green-light PPG. Pulse amplitude, detrended fluctuation analysis (global DFA α exponent), and multiscale entropy (Complexity Index, CI) were computed in 5 min epochs. Occlusion nearly abolished pulsatility in the test limb but produced only modest changes in fractal structure, as α decreased minimally despite near-zero flow. In contrast, CI showed a marked collapse, indicating loss of multiscale organization. During reperfusion, α exhibited a trend toward increased fractal persistence, whereas CI recovered only partially. Contralateral responses were small and detectable mainly through subtle reductions in α during occlusion and consistently higher CI compared with the test limb. These findings indicate that occlusion disrupts multiscale complexity without eliminating fractal persistence, whereas reperfusion restores correlation structure and only partially re-establishes dynamical richness. Overall, DFA and MSE reveal nonlinear features of PORH that are not captured by conventional amplitude-based metrics, extending the physiological interpretation of microvascular responses using widely available PPG technology. Full article

Background: Recent research has drawn attention to potential systemic inflammation in patients with inherited epidermal differentiation disorders (EDD)—rare genetic skin conditions that may contribute to vascular dysfunction. Objective: This study assessed selected vascular, inflammatory, and biochemical parameters in 20 patients with selected EDD and 20 matched healthy controls. Methods: Assessments included Doppler ultrasound, ankle-brachial index, intima-media thickness (IMT), and laboratory profiling focused on lipid metabolism and systemic inflammation. Results: EDD patients showed significantly lower LDL cholesterol and higher interleukin-17A (IL-17A) than controls. IMT values were similar across groups and disease types, but correlated positively with age, body weight, waist circumference, triglycerides, and glucose, and negatively with reactive lymphocytes. No link was found between IMT and self-reported cardiovascular symptoms. Conclusions: In patients with selected EDD, we observed a distinct biochemical profile characterized by lower LDL cholesterol and higher IL-17A concentrations, without accompanying structural arterial changes—carotid IMT and ABI did not differ from controls and remained stable at short-term follow-up. These alterations may reflect disease-specific disturbances of lipid and inflammatory homeostasis rather than classical atherosclerosis. Although they could be of theoretical relevance to long-term vascular health, no structural arterial abnormality was demonstrated. Longitudinal studies incorporating endothelial function testing are needed to clarify their significance. Full article

Background/Objectives. Pulmonary arterial hypertension (PAH) is a rare but severe disease which leads to right ventricular (RV) maladaptation, failure and death. Currently approved drugs have limited impact on disease progression. A multitarget strategy consisting of adenosine A₂B receptor activation and phosphodiesterase-4 (PDE4) inhibition, combined with human mesenchymal stromal cells (hMSCs) therapy, was tested in experimental PAH. The main objective was to determine whether the combination improved pulmonary hemodynamics, vascular remodeling, and RV function, given the limited disease-modifying effects of currently approved vasodilators. Methods. Vascular reactivity was assessed in isolated rat pulmonary artery rings exposed to the dual-target compound (LASSBio-1860) alone or in the presence of either ZM-241385 or MRS-1706. PAH was induced in male Wistar rats with monocrotaline (MCT, 60 mg·kg⁻¹) and confirmed by a decrease in pulmonary artery acceleration time to ejection time ratio (PAAT/TET). Animals were randomized to receive vehicle, hMSC (single i.v. dose, 1 × 10⁵ cells), LASSBio-1860 (62 mg·kg⁻¹·day⁻¹, p.o., 14 days), or their combination. Outcomes included PAAT/TET and RV cardiac output (RV-CO) by echocardiography, RV systolic pressure (RVSP) by direct puncture, Fulton index and RV wall thickness, lung histology (perivascular cell counts and wall thickness), and RV protein expression (TGF-β, CaMKII) by Western blot. Results. LASSBio-1860 produced endothelium-independent vasorelaxation of rat pulmonary arteries, consistent with A₂B agonism and PDE4 inhibition. In MCT-induced PAH, combination of LASSBio-1860 and hMSCs resulted in recovery of PAAT/TET and RV-CO, decrease in RVSP, RV hypertrophy, vascular inflammation and remodeling by downregulation of ventricular TGF-β and CaMKII. Conclusions. Combination of LASSBio-1860 with hMSC improved RV function, attenuated pulmonary hypertension, RV and vascular remodeling, and reduced inflammatory/proliferative signaling in MCT induced-PAH, supporting a promising multitarget therapeutic strategy for PAH. Full article

Background: Arterial stiffness is a major predictor of cardiovascular-related mortality in chronic kidney disease (CKD). While acrolein—an endogenous reactive aldehyde that accumulates with declining renal function—may be linked to vascular injury, its association with high peripheral arterial stiffness (HPAS) remains unclear. Methods: This cross-sectional study used the cardio-ankle vascular index (CAVI) to examine the association between serum acrolein levels and HPAS (CAVI ≥ 9.0) in 204 adults with non-dialysis CKD stages 3–5. Results: HPAS was identified in 90 patients (44.1%) and was associated with a higher prevalence of diabetes (p = 0.047), older age (p = 0.023), higher spot urine protein–creatinine ratio (UPCR, p = 0.046), higher serum fasting glucose (p = 0.041), higher interleukin-6 (p = 0.025), and higher acrolein (p = 0.008). In multivariable logistic regression analysis, serum acrolein (odds ratio, 1.015; 95% confidence interval, 1.002–1.028; p = 0.025), age (p = 0.010), and UPCR (p = 0.046) remained independently associated with HPAS. Log-transformed acrolein was positively correlated with bilateral CAVI (all p < 0.001) and log-transformed UPCR (p < 0.001) but negatively correlated with the estimated glomerular filtration rate (p = 0.001). Conclusions: Elevated serum acrolein is independently associated with HPAS in non-dialysis CKD stages 3–5. Full article

Background/Objectives: Bleomycin is an antineoplastic antibiotic used in the management of various malignancies. Nevertheless, its benefits are constrained by the development of pulmonary fibrosis. Amentoflavone, a biflavonoid, exhibits diverse pharmacological activities, including anti-inflammatory, antiviral, antioxidant, and antitumor effects, whereas alogliptin possesses antioxidant and anti-inflammatory properties. This study aimed to assess the potential protective effects of alogliptin and/or amentoflavone in a murine model of bleomycin-induced pulmonary fibrosis and to clarify the underlying mechanisms. Methods: Fifty male C57BL/6 mice were randomly divided into 5 equal groups: control, bleomycin, bleomycin + alogliptin, bleomycin + amentoflavone, and bleomycin + alogliptin + amentoflavone. The assessed endpoints included lung weight/body weight index, lung tissue fibrotic mediators, oxidative stress parameters, proinflammatory cytokines, and pyroptotic and autophagy mediators. Also, the bronchoalveolar lavage fluid (BALF) was evaluated for total and differential leukocytic counts and lactate dehydrogenase (LDH) activity. Moreover, vascular responses to potassium chloride, phenylephrine, and carbachol, together with tracheal responses to carbachol were determined. Lung tissues were further examined histopathologically and immunohistochemically. Results: Treatment with alogliptin and/or amentoflavone significantly decreased the lung weight/body weight index and BALF LDH activity, concomitant with mitigation of lung tissue oxidative stress parameters, fibrotic mediators, apoptosis, and pyroptosis with a significant augmentation of autophagy signals, alongside marked improvement in the lung architecture and vascular and airway reactivity compared with the bleomycin group. These effects were most pronounced with animals treated with the alogliptin/amentoflavone combination. Conclusions: These findings suggest that combined alogliptin and amentoflavone may constitute a promising strategy to prevent bleomycin-induced lung fibrosis. Full article

Background and Objectives: Endothelial dysfunction is essential in the development and progression of coronary artery disease (CAD) and its complications. Galectin-3 mediates inflammation and organ fibrosis and promotes endothelial dysfunction. Meanwhile, the vascular reactivity index (VRI) reflects endothelial function. The purpose of this research was to evaluate the association between serum galectin-3 levels and VRI in patients diagnosed with CAD. Materials and Methods: One hundred and eighteen patients with CAD were enrolled. Endothelial function was noninvasively evaluated using digital thermal monitoring, and VRIs were obtained. According to VRI values, patients were classified into good (≥2.0), intermediate (1.0–1.9), and poor (<1.0) subgroups. Galectin-3 levels were quantified using an enzyme-linked immunosorbent assay. Results: Patients with poor vascular reactivity were older in age (p = 0.028) and had higher serum total cholesterol (p = 0.003), low-density lipoprotein cholesterol (p = 0.005), and galectin-3 (p < 0.001) levels. Multivariable stepwise linear regression analysis revealed galectin-3 as an independently associated factor of lower VRIs (β = −0.488; p < 0.001). Logistic regression model confirmed that galectin-3 independently was associated with higher odds of vascular reactivity dysfunction (odds ratio, 1.120; 95% confidence interval, 1.016–1.235; p = 0.023) or poor vascular reactivity (odds ratio, 1.445; 95% confidence interval, 1.179–1.772; p < 0.001). Conclusions: Serum galectin-3 is independently associated with reduced VRIs and endothelial dysfunction in patients with CAD. Full article

p-Cresyl sulfate (PCS) is associated with endothelial injury and adverse cardiovascular outcomes. However, its association with endothelial function in patients on peritoneal dialysis (PD) remains unclear. In this cross-sectional study, 82 patients receiving PD were enrolled. Serum PCS concentrations were quantified using high-performance liquid chromatography–mass spectrometry. Endothelial function was evaluated by digital thermal monitoring (DTM), and vascular reactivity was stratified based on vascular reactivity index (VRI) values into good (>2.0), intermediate (1.0–1.9), and poor (<1.0). Overall, 46.3%, 43.9%, and 9.8% of participants had poor, intermediate, and good vascular reactivity, respectively. Poor reactivity was associated with a higher prevalence of diabetes (p = 0.018), old age (p < 0.001), higher waist circumference (p = 0.013), serum C-reactive protein levels (p = 0.010), and PCS levels (p < 0.001) and lower diastolic blood pressure (p = 0.032) and serum creatinine levels (p = 0.005). Higher serum log-transformed PCS levels were associated with reduced VRI after adjustment for covariates (p < 0.001). In multivariable models adjusted for potential confounders, PCS was independently associated with poor vascular reactivity (p = 0.029), with consistent findings observed across penalized regression analyses (all p < 0.001). An inverse relationship was observed between serum PCS levels and endothelial function in patients undergoing PD. Full article

Objective: This study examined age- and sex-specific correlates of arterial stiffness, assessed by the cardio–ankle vascular index (CAVI), in apparently healthy Chinese adults using an anthropometric–metabolic–inflammatory framework, and descriptively compared subgroup association patterns across these domains. Methods: In this cross-sectional study, 525 apparently healthy Chinese adults aged 20–78 years were included. Regression models with age-by-indicator interaction terms were used to test whether the age–CAVI association varied across anthropometric, metabolic, and inflammatory indicators. Sex-adjusted analyses were applied to the overall sample, sex-stratified analyses were used to characterize sex-specific patterns, and the Benjamini–Hochberg false discovery rate correction was applied for multiple interaction tests. Results: CAVI increased progressively with age, with a steeper age–CAVI association after 50 years (p < 0.05). Notably, females showed a transient midlife elevation. Association patterns appeared to differ by sex. In the sex-stratified interaction analyses, anthropometric signals were more prominent in men, particularly for height (p < 0.01), whereas metabolic-related interaction signals were more evident in women, with triglycerides providing the clearest corresponding signal and low-density lipoprotein cholesterol (LDL-C) showing a weaker accompanying pattern; the C-reactive protein (CRP)-related contrast was not retained after additional adjustment for blood pressure and smoking. Conclusions: CAVI increased with age, with a steeper rise after midlife and a transient midlife elevation in women. The association patterns across anthropometric, metabolic, and inflammatory indicators appeared to differ by sex, with signals from the anthropometric domain appearing more evident in men and metabolic-related signals appearing more evident in women. These findings suggest that age- and sex-specific interpretation of CAVI may be informative in preventive health check-up settings. Full article

The kidney and the brain share similarities in terms of structure and haemodynamic regime. The aim of the study was to assess a potential correlation of vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor receptor-1 (sFlt-1), and placental growth factor (PlGF) with biomarkers of podocyte damage, proximal tubular (PT) dysfunction, and endothelial dysfunction, as well as with cerebral vessels haemodynamic indices in neurologic asymptomatic type 2 DM patients. A cohort of 212 patients diagnosed with type 2 DM and 49 age- and gender-matched healthy controls were enrolled in the study. Parameters studied were urinary albumin/creatinine ratio (UACR), biomarkers of podocyte damage (synaptopodin, podocalyxin), PT dysfunction (kidney injury molecule-1-KIM-1, N-acetyl-β-(D)-glucosaminidase-NAG), endothelial dysfunction (P-selectin), VEGF, sFlt-1, and PlGF. The cerebrovascular hemodynamic indices evaluated were intima–media thickness (IMT) in the common carotid arteries (CCAs), the pulsatility index (PI), and the resistivity index (RI) in the internal carotid arteries (ICAs) and middle cerebral arteries (MCAs). Cerebrovascular reactivity (CVR) was assessed by the breath-holding index (BHI). In multivariable regression analysis, serum VEGF correlated directly with UACR, synaptopodin, NAG, serum P-selectin; serum sFlt-1 correlated directly with UACR, synaptopodin, podocalyxin, NAG, KIM-1; serum PlGF correlated negatively with eGFR and directly with UACR, synaptopodin, KIM-1. IMT-CCA correlated indirectly with eGFR and directly with UACR, serum P-selectin, and serum sFlt-1. The PI-ICAs correlated negatively with eGFR and positively with UACR, synaptopodin, serum P-selectin, and serum sFlt-1. The PI-MCAs correlated indirectly with eGFR and directly with synaptopodin, serum P-selectin, and serum sFlt-1. The RI-ICAs had a negative correlation with eGFR and a positive one with UACR, synaptopodin, NAG, KIM-1, urinary sFlt-1, and serum PlGF. The RI-MCAs displayed an indirect correlation with eGFR and a direct correlation with NAG, KIM-1, and serum sFlt-1. The BHT correlated directly with eGFR and negatively with serum P-selectin and serum PlGF. The study shows a significant association of VEGF, sFlt-1, and PlGF with biomarkers of podocyte injury, PT dysfunction, and endothelial dysfunction in early stages of DKD. These pro-angiogenic and anti-angiogenic factors correlated with cerebrovascular haemodynamic indices in neurologic asymptomatic type 2 DM, even in the normoalbuminuric stage of diabetic kidney disease. Full article

Background and Objectives: Cardiac Syndrome X (CSX), a clinical entity within the Ischaemia with Non-Obstructive Coronary Arteries (INOCA) spectrum, is increasingly recognised as an inflammatory and systemic vascular disorder. Remnant cholesterol (RC) and inflammation are emerging contributors to residual cardiovascular risk; however, their combined role in microvascular angina remains unclear. This study aimed to evaluate the association between the remnant cholesterol inflammation index (RCII), integrating RC and high-sensitivity C-reactive protein (hs-CRP), and the clinical presence of CSX. Methods: This single-centre, retrospective observational study included 392 individuals who underwent coronary angiography between January 2023 and January 2025. The study population comprised 197 patients diagnosed with CSX and 195 control subjects with normal coronary anatomy and no objective evidence of myocardial ischaemia. RC was calculated as total cholesterol minus the sum of LDL-C and HDL-C, and RCII was derived as RC × hs-CRP. Importantly, invasive microvascular testing (e.g., CFR or IMR) was not performed. Logistic regression analyses were performed to identify independent predictors of CSX, and receiver operating characteristic (ROC) curve analysis was used to evaluate diagnostic performance. Results: Patients with CSX exhibited significantly higher levels of hs-CRP, SII, and RCII compared with controls (all p < 0.001). In the multivariable logistic regression analysis, RCII demonstrated an independent association with CSX (odds ratio 1.095, 95% confidence interval 1.060–1.131; p < 0.001). ROC curve analysis showed that RCII provided moderate but significant discrimination for CSX (area under the curve [AUC] 0.765, 95% CI 0.695–0.795). Pairwise comparisons confirmed that RCII had a significantly higher AUC than RC, hs-CRP, or SII individually. Conclusions: Higher RCII levels appear to be significantly associated with the clinical diagnosis of CSX. By integrating atherogenic remnant cholesterol burden and systemic inflammation, RCII may serve as a valuable composite biomarker for identifying residual inflammatory lipid risk. Rather than acting as a definitive diagnostic tool, these findings warrant further validation in large-scale prospective cohort studies. Full article

Background and Objectives: Peripheral arterial disease (PAD) is highly prevalent in patients with end-stage renal disease and is associated with adverse cardiovascular outcomes. Although the ankle–brachial index (ABI) is widely used to identify PAD, it may not fully reflect the complex vascular pathophysiology in patients undergoing peritoneal dialysis (PD). Antibodies against oxidized low-density lipoprotein (anti-oxLDL Ab) have been implicated in atherogenesis; however, their clinical relevance in PD populations remains unclear. Materials and Methods: In this cross-sectional investigation, 90 patients receiving maintenance PD were included. PAD was defined by an ABI below 0.90, and serum anti-oxLDL antibody concentrations were quantified using an enzyme-linked immunosorbent assay. Results: Patients with PAD were older (p = 0.006), had a higher prevalence of diabetes (p = 0.010), and exhibited higher levels of triglycerides (p = 0.008), fasting glucose (p < 0.001), and C-reactive protein (CRP, p < 0.001), but lower anti-oxLDL Ab levels (p = 0.008). Multivariable logistic regression demonstrated that reduced anti-oxLDL Ab levels (per 10 mU/mL increase, odds ratio [OR]: 0.803, 95% confidence interval [CI]: 0.648–0.995, p = 0.045) and increased CRP levels (per 0.1 mg/dL increase, OR: 1.662, 95% CI: 1.152–2.398, p = 0.007) were independently associated with PAD, with consistent results across penalized regression models. Log-transformed anti-oxLDL Ab levels were positively correlated with both left and right ABI values (p = 0.005 and p = 0.017, respectively). Decision curve analysis indicated that the anti-oxLDL Ab-based model provided greater net benefit compared with the treat-all and treat-none strategies across a range of threshold probabilities. Conclusions: Reduced serum anti-oxLDL Ab levels are independently associated with PAD in patients undergoing PD. Serum anti-oxLDL Ab levels are positively associated with ABI values. These findings suggest that impaired immunity against oxidized LDL may contribute to vascular disease in PD patients. Full article

Insulin resistance (IR) promotes a prothrombotic milieu by enhancing platelet hyperactivity, oxidative stress, and endothelial dysfunction, driving both microvascular and macrovascular complications in type 2 diabetes. Our review synthesizes mechanistic evidence showing that insulin-resistant platelets exhibit increased basal activation, elevated sensitivity to agonists, and reduced responsiveness to inhibitory signals, with distinct pro-aggregatory subpopulations amplifying thrombotic risk. Molecular pathways underlying platelet hyperactivation include reactive oxygen species accumulation, advanced glycation end-product signaling, disrupted calcium homeostasis, and impaired nitric oxide/prostacyclin pathways. Clinically, these mechanisms contribute to heightened arterial thrombosis, coronary artery disease, stroke, and microvascular injury, including nephropathy and retinopathy. Nutritional interventions emerge as effective modulators of platelet function and vascular health. Diets such as the Mediterranean, DASH, low-glycemic-index, and plant-based regimens, alongside bioactive compounds—including omega-3 fatty acids, polyphenols, vitamins D, E, C, and minerals like magnesium and zinc—may reduce platelet aggregation, oxidative stress, and systemic inflammation while restoring endothelial function. Clinical and epidemiological evidence demonstrates improvements in flow-mediated dilation, arterial elasticity, and stabilization of atherosclerotic plaques following dietary interventions. Integrating whole-diet strategies with targeted nutrients provides synergistic benefits, suggesting that personalized nutritional approaches can mitigate IR-induced platelet hyperactivity and lower vascular risk. These findings highlight nutrition as a practical, evidence-based adjunct to pharmacotherapy for cardiovascular protection in insulin-resistant populations. Full article

Mild fasting hypertriglyceridemia is often accompanied by early insulin resistance and atherogenic dyslipidemia, making it an attractive target for pragmatic dietary prevention. This trial aims to determine whether substituting common cereal-based staples with functional low-glycemic index (low-GI) products improves the triglyceride–glucose (TyG) index in adults with fasting triglycerides >150 mg/dL. The GLOW study is an exploratory, randomized, double-blind, single-center crossover trial. Adults aged ≥18 years with fasting triglycerides >150 mg/dL and body mass index ≤30 kg/m² will be enrolled. Participants will follow a stabilized Mediterranean-style diet and will complete two 28-day intervention periods in random sequence: (i) functional low-GI Altograno^® pasta, pizza base and flatbread; and (ii) conventional standard wholegrain products. Intervention periods will be separated by a 28-day washout. Study foods will be consumed as fixed daily substitutions of usual staple servings (one bread portion and one pasta or pizza portion). The primary endpoint is the between-intervention difference in TyG response over each period, defined as the period-specific change from the corresponding period baseline to the end-of-period assessment. The primary analysis will compare end-of-period TyG between interventions while adjusting for the period-specific baseline value. Secondary endpoints include fasting triglycerides and glucose, atherogenic lipoproteins (non–high-density lipoprotein cholesterol and apolipoprotein B), inflammation (high-sensitivity C-reactive protein), endothelial reactivity assessed with the Endocheck^®/Vicorder^® system, and food acceptability. Safety endpoints include adverse event recording. Treatment effects will be estimated using linear mixed-effects models accounting for treatment, period and sequence, with prespecified carryover sensitivity analyses. A total of 40 participants will be recruited to generate feasibility data and effect size estimates. This protocol will provide crossover evidence on whether pragmatic, product-level low-GI staple substitution improves TyG and related cardiometabolic and vascular biomarkers in adults with suboptimal triglyceridemia, informing larger trials. Trial registration: ClinicalTrials.gov NCT07198789. Full article

Background: Dyspnea is a frequent complaint during pregnancy and is often considered a benign physiological finding; however, it may also reflect underlying subclinical cardiovascular alterations. Pregnancy-related vascular remodeling and low-grade systemic inflammation may contribute to changes in aortic elastic properties and inflammatory biomarkers, particularly in symptomatic women. Objective: This study aimed to compare aortic elastic properties and albumin-based inflammatory indices between dyspneic and asymptomatic third-trimester pregnant women. A secondary aim was to establish reference values for echocardiographic and biomarker parameters in dyspneic pregnancy. Methods: In this prospective observational study, third-trimester pregnant women (≥27 gestational weeks) presenting to the emergency department (ED) with dyspnea were consecutively enrolled and compared with age-matched asymptomatic pregnant controls. Demographic, laboratory, and echocardiographic data were recorded. Aortic strain, aortic distensibility, and aortic stiffness were calculated using transthoracic echocardiography. Albumin-based inflammatory indices, including the hemoglobin–albumin–lymphocyte–platelet (HALP) score, prognostic nutritional index (PNI), C-reactive protein-to-albumin ratio (CAR), and RDW-to-albumin ratio (RAR), were analyzed. Receiver operating characteristic (ROC) and correlation analyses were performed. Results: A total of 241 pregnant women were included (121 dyspneic, 120 controls). Demographic characteristics were comparable between groups. Dyspneic pregnant women exhibited significantly lower aortic strain and aortic distensibility and higher aortic stiffness compared with controls (for all p < 0.05). Among laboratory parameters, CAR levels were significantly elevated in the dyspneic group (p < 0.001), whereas HALP, PNI, and RAR did not differ significantly. After adjustment for potential confounders, differences in aortic elastic properties remained significant. CAR demonstrated moderate discriminative ability for dyspnea (AUC = 0.692), while aortic elastic parameters showed modest predictive performance. In combined prediction models incorporating CAR with echocardiographic parameters, discriminatory performance improved, with area under the curve values exceeding 0.70. Weak positive correlations were observed between PNI and aortic strain and distensibility. Conclusions: Dyspneic third-trimester pregnant women exhibit impaired aortic elastic properties and increased CAR levels, suggesting the presence of subclinical vascular and inflammatory alterations. Assessment of aortic elasticity and CAR may provide a simple and practical approach for early cardiovascular risk stratification in symptomatic pregnancy, particularly in ED settings. Further multicenter studies with longitudinal follow-up are warranted to clarify their prognostic significance. Full article

Objectives: This study aims to evaluate whether changes in perfusion index (PI) after the first deflation of the blood pressure cuff during remote ischemic conditioning (RIC) are associated with passive leg raising (PLR)-induced changes in stroke volume. In addition, we compared PI changes after cuff deflation during RIC between critically ill patients and healthy controls. Methods: This prospective, single-center study was conducted in a mixed ICU at a tertiary teaching hospital. Patients aged >18 years admitted to the ICU, monitored using calibrated pulse contour analysis, and scheduled for a PLR test as decided by the attending physicians were included. The PI was measured after blood pressure cuff deflations during RIC (3 cycles of brachial cuff inflation to 200 mmHg for 5 min, followed by instantaneous deflation to 0 mmHg for another 5 min) in the supine position after PLR. Preload responsiveness was defined as a ≥10% increase in the stroke volume index (SVI) during PLR. Data were compared with a healthy control group. Results: Thirty-three patients were included (median age 62; 45% in shock; 55% mechanically ventilated). When comparing critically ill patients with healthy volunteers, the maximum PI change (dPImax) and the time to reach it were higher in critically ill patients after the first and second cuff deflations (p < 0.05). However, after the third deflation, the difference was no longer significant. Following the first deflation, dPImax was significantly correlated with SVI changes during PLR (r = 0.63, p < 0.001). After the cuff was first deflated, we detected a PI cutoff with a positive SVI response (≥10%) during PLR, with a sensitivity of 64% and a specificity of 94% (area under the receiver operating characteristic curve 0.752; 95% CI, 0.564–0.940; p = 0.008). Conclusions: The maximum change in perfusion index following brachial blood pressure cuff deflation after five minutes of inflation may serve as a promising noninvasive bedside indicator of preload responsiveness in critically ill patients. Additionally, the observed normalization of PI kinetics during RIC suggests possible acute modulation of vascular reactivity, though further research is needed to confirm an association between PI changes and endothelial function. Full article