Introduction:The no-reflow phenomenon is a major complication in patients with acute coronary syndrome undergoing percutaneous coronary intervention, significantly impacting prognosis. Endothelial dysfunction and systemic inflammation are central to its pathogenesis. Aim:This study aimed to evaluate the predictive value of the endothelial stress ratio - a novel composite index incorporating fibrinogen, albumin, C-reactive protein, and lymphocyte count - for the occurrence of the no-reflow phenomenon in patients with acute coronary syndrome. Material and methods:This retrospective study included 1256 patients with acute coronary syndrome treated with percutaneous coronary intervention. Clinical and procedural data, including Killip class, presentation type, and angiographic findings such as infarct-related artery, multivessel disease, and pre-procedural Thrombolysis in Myocardial Infarction flow, were evaluated. The endothelial stress ratio was calculated using pre-procedural blood samples. To address multicollinearity, two separate multivariate logistic regression models were constructed: Model 1 included the fibrinogen-to-albumin ratio, while Model 2 evaluated the independent predictive value of the endothelial stress ratio alongside clinical variables. Results:The no-reflow phenomenon occurred in 73 (5.8%) patients. Patients with no-reflow had significantly higher endothelial stress ratio values (138 (102-198) versus 72 (49-104), p < 0.001). In multivariate analysis, the endothelial stress ratio was the strongest independent predictor of no-reflow (Model 2, odds ratio: 1.48, 95% confidence interval: 1.21-1.82, p < 0.001). Receiver operating characteristic analysis demonstrated a strong discriminative performance, with an area under the curve of 0.82 (p < 0.001). Conclusions:The endothelial stress ratio is a novel, independent biomarker for predicting no-reflow. Incorporating this ratio into pre-procedural assessment may help identify high-risk patients and guide therapeutic strategies.
Introduction:Branched thoracic endovascular aortic repair (bTEVAR) is a method enabling the treatment of complex aortic arch pathologies in patients who are not eligible for open surgery. This single-center study evaluated the medium-term results of aortic arch pathology treatment using the bTEVAR method. Aim:To evaluate the technical feasibility, safety and mid-term outcomes of bTEVAR technique for complex aortic arch pathologies in non-urgent patients. Material and methods:The study included 15 patients treated with double- and triple-branched stent grafts based on specific criteria. Treatment evaluation was performed using computed tomography angiography. Technical success, perioperative complications, and follow-up results were assessed. Results:Technical success was achieved in 12 (80%) patients. Within 30 days after the procedure, 1 (6.7%) death and 2 (13.3%) strokes, 1 of which was non-disabling, were observed. During the follow-up period, which averaged 15.6 months (median: 10 months, range: 0-47 months), endoleaks were observed in 3 patients, 2 of whom required reintervention. Three patients required further treatment due to progression of aortic pathology. No retrograde type A dissection, stent-graft-induced new entry, or stent-graft infection was observed. Conclusions:The bTEVAR technique using double- and triple-branched stent grafts in the treatment of patients with aortic arch pathology is a relatively effective method that prevents arch degeneration and offers acceptable medium-term results. This method can only be used by experienced vascular units due to the high risk of neurological complications and postoperative mortality.
Introduction:Optical coherence tomography-derived fractional flow reserve (FFR-OCT), computed as virtual flow reserve, combines anatomical and functional lesion assessment without pressure-wire manipulation or pharmacological hyperemia. Its output may depend on accurate lumen delineation and side-branch recognition. Aim:To assess the agreement between operator-reviewed FFR-OCT and wire-based FFR in routine practice, and the effect of manual segmentation correction. Material and methods:We analyzed 14 consecutive patients (19 vessels) undergoing wire-based FFR followed by OCT-guided percutaneous coronary intervention (PCI). OCT pullbacks were processed with Ultreon 3.0 software; automated FFR-OCT values were reviewed by an experienced operator with manual correction of lumen and side-branch segmentation. Comparison used Pearson's correlation, Bland-Altman analysis, and concordance in ischemia classification at the 0.80 threshold. Results:Wire-based FFR was 0.79 ±0.10. In 13 vessels with both values, automated FFR-OCT increased from 0.68 ±0.16 to 0.75 ±0.11 after operator review (mean paired difference +0.064; Wilcoxon p = 0.016). Across 19 vessels, operator-reviewed FFR-OCT (0.76 ±0.10) correlated moderately with wire-based FFR (r = 0.614, 95% CI: 0.222-0.835; p = 0.005; bias +0.025, 95% limits of agreement -0.153 to +0.203). Classification was concordant in 15 of 19 vessels; 4 were discordant (21.1%, 95% CI: 6.1-45.6%). Conclusions:Manual review of segmentation substantially changed the automated FFR-OCT result. Although operator-reviewed FFR-OCT was associated with wire-based FFR, agreement near the 0.80 threshold was imperfect. FFR-OCT may aid PCI planning but does not yet appear interchangeable with pressure-wire physiology. Larger prospective studies with prespecified, blinded image analysis are warranted.
Introduction:There is a lack of scientific evidence regarding the association between the ACEF score and the prediction of coronary slow flow (CSF). Aim:To investigate the relationship between the ACEF score and CSF. Material and methods:This retrospective, single-center study enrolled 257 patients who underwent elective coronary angiography between January 2024 and August 2025. Patients were stratified into two groups: the CSF group (n = 121) and the normal coronary flow (NCF) group (n = 136). Receiver operating characteristic (ROC) curve analysis evaluated the accuracy of the ACEF score, glycated hemoglobin (HbA1c), and low-density lipoprotein cholesterol (LDL-C) in predicting CSF. The incremental value of the ACEF score relative to its components was assessed using C-statistics, IDI, and NRI. Logistic regression was conducted to evaluate independent predictors of CSF presence. The model included sex, hypertension, peripheral artery disease, atrial fibrillation, hemoglobin, white blood cell count, platelet count, HbA1c, triglycerides, LDL-C, high-density lipoprotein cholesterol (HDL-C), and the ACEF score. Results:In ROC analysis, the cut-off value of the ACEF risk score was 0.94, with 81% sensitivity and 53% specificity for predicting CSF (AUC = 0.763, 95% CI: 0.706-0.821). For HbA1c, the optimal cut-off value was 5.44%, with a sensitivity of 70% and a specificity of 52% to predict CSF (AUC = 0.610, 95% CI: 0.538-0.682). The risk of CSF increased by 28% for every 0.1-unit increase in the ACEF score (OR per 0.1-unit increase: 1.278, 95% CI: 1.168-1.396). The ACEF score demonstrated superior discrimination (AUC: 0.763 vs. 0.729, p = 0.018) and significant incremental predictive value (IDI = 0.052, p < 0.001) compared to its individual components. Conclusions:This study suggests that the ACEF score is closely associated with the presence of CSF, independent of its individual components. The discriminatory ability of the ACEF score was superior to that of HbA1c in patients with CSF.
Cardiac hypertrophy, characterized by an increase in the size of cardiac myocytes, is an adaptive response to increased workload on the cardiac tissue following physiological stimuli, such as exercise, and pathological conditions, such as hypertension or valvular heart disease. Typically, physiological hypertrophy induced by various exercise modalities leads to beneficial adaptations, such as improved contractile function and increased oxidative capacity. Understanding the molecular mechanisms underlying physiological cardiac hypertrophy is crucial for developing targeted therapeutic strategies. This review provides a comprehensive overview of current knowledge of physiological cardiac hypertrophy, with a particular focus on adaptations induced by various exercise modalities. We delved into the potential cellular and molecular pathways involved in physiological hypertrophy including IGF1/PI3K/AKT, angiotensin2, hepatocyte growth factor, platelet-derived growth factor. MAPK/ERK cascade, calcineurin, Neurogelin2 and downstream transcriptional factors such as HAND2, GATA4, MEF2, NKX2.5, TBX5, NFAT, c/EBPβ, CITED4, PHLPP, as well as the role of microRNAs (miRNAs) like miR-222 and miR-17 in mediating these adaptations. Furthermore, we used comparative tables to illustrate the differential effects of endurance, high-intensity interval training (HIIT), and resistance training on structural, molecular, and functional cardiac parameters, as markers of physiological hypertrophy. We also presented pathway-specific percentage changes observed across different exercise training modalities to highlight key differences. The discussion integrated these findings to explore translational perspectives and to offer the most beneficial exercise training schedules that induce physiological hypertrophy.
Introduction:CREST-2 comprised two parallel observer-blinded randomised controlled trials evaluating carotid revascularisation (carotid artery stenting - CAS, or carotid endarterectomy - CEA) plus intensive medical management (IMM; supervised pharmacologic therapy and risk factor control and coached lifestyle modification) versus IMM alone in patients with asymptomatic ≥ 70% carotid stenosis. Each trial carried an independent IMM control arm. The primary endpoint (peri-procedural stroke/death or ipsilateral ischaemic stroke thereafter by 4 years) occurred, in the CAS trial, in 2.8% vs. 6.0% (IMM + CAS vs. IMM; p = 0.02). The effect of CEA did not reach significance; 3.7% vs. 5.3% (IMM + CEA vs. IMM; p = 0.24). Aim:To test the hypothesis that the divergent control-arm event rates - rather than true differential efficacy of the interventional treatments - could underlie the CAS efficacy and CEA failure in CREST-2, we used a single combined control group as a balanced reference for both interventional treatment arms. Material and methods:An Aggregated Control Group of IMM-only (n = 1,252) was formed by merging the CREST-2 IMM control arms patient data and outcomes. Kaplan-Meier analysis was performed for the CAS and CEA treatment vs. the Aggregated Control Group, consistent with the trial statistical methodology (intent-to-treat). Results:In the Aggregated Control Group, the primary endpoint occurred in 5.65% of patients (95% CI: 4.47-7.12). Absolute risk reduction with CAS + IMM (n = 616) was 2.85% (relative risk reduction 50.4%; number-needed-to-treat 35, p = 0.0089). Absolute risk reduction with CEA + IMM (n = 617) was 1.95% (p = 0.0871, a maintained lack of statistical significance). Conclusions:Aggregated Control Group analysis of CREST-2, minimising control arms biases, confirmed CAS efficacy (50.4% relative risk reduction) and maintained failure of CEA in primary prevention of ipsilateral stroke in patients with asymptomatic carotid stenosis under intensive medical management. This refutes control-arm disparity as an explanation for the divergent outcomes with CAS vs. CEA.
