AngiologyPub Date : 2026-10-12DOI: 10.1177/00033197261494448
Luca Galassi, Federica Facchinetti, Carlo Banfi
{"title":"Beyond Patency: Patient-Centered Outcomes and the Proposed Accountability Gap in Chronic Limb-Threatening Ischemia.","authors":"Luca Galassi, Federica Facchinetti, Carlo Banfi","doi":"10.1177/00033197261494448","DOIUrl":"https://doi.org/10.1177/00033197261494448","url":null,"abstract":"<p><p>Chronic limb-threatening ischemia (CLTI) carries 1-year mortality of 20% to 25%, comparable with many solid-organ malignancies. Technically successful revascularization, defined by anatomical patency, does not reliably deliver pain relief, restored function, or sustained quality of life. This narrative review synthesizes landmark randomized trials (BEST-CLI, BASIL-1, BASIL-2) and current European and United States guidelines, grading every claim with a scheme in which population indirectness downgrades design strength. We examine 4 domains of morbidity persisting after anatomically successful revascularization: mechanistically heterogeneous pain; functional and quality-of-life decline; psychological burden; and sustained health care use, including chronic opioid use (approximately 35%), unhealed wounds at 1 year (10%-32%), and unplanned 30-day readmission (approximately 25%). No patient-reported outcome measure has been validated specifically for CLTI or used as a co-primary trial endpoint. We propose an accountability gap: the under-measured transfer of unresolved morbidity from vascular services to primary care. We state it as a falsifiable prediction about the discrimination of patency rather than prevalence, with a pre-specified effect size, explicit treatment of death as a competing risk, and a core outcome battery justified against COSMIN criteria. Patient co-production is the indispensable next step.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261494448"},"PeriodicalIF":2.7,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-12DOI: 10.1177/00033197261491116
Hülya Yıldırım, Miraç Tonyalı, Mücahit Taşdemir
{"title":"Early Ulnar Artery Occlusion and Recanalization After Coronary Angiography via Distal Ulnar Access: A Doppler-Followed Case Series.","authors":"Hülya Yıldırım, Miraç Tonyalı, Mücahit Taşdemir","doi":"10.1177/00033197261491116","DOIUrl":"https://doi.org/10.1177/00033197261491116","url":null,"abstract":"<p><p>This single-center retrospective case series assessed early ulnar artery patency by Doppler ultrasonography (DUS) after coronary angiography via distal ulnar access (DUA), described flow evolution in patients with follow-up, and reported access-related complications. Thirty-eight consecutive patients with a day-3 DUS after coronary angiography via DUA between September 2023 and March 2024 were included. All procedures were performed by 1 operator using a short 6F sheath and 5000 IU intra-arterial heparin. Flow was categorized as thrombosis/no flow, monophasic, or triphasic; the primary endpoint was day-3 non-triphasic flow, and month-1 and month-3 DUS were selective. Mean age was 58.8 ± 10.1 years and 47.4% were male; 21.1% underwent same-session percutaneous coronary intervention. On day 3, thrombosis/no flow occurred in 18.4% (7/38), monophasic flow in 5.3% (2/38), and triphasic flow in 76.3% (29/38); non-triphasic flow was 23.7% (9/38). Month-1 DUS (n = 35) showed no thrombosis/no flow and 94.3% triphasic flow; month-3 DUS (n = 4) was triphasic in all. No clinically relevant hematoma, neuropathy, hand ischemia, or functional impairment was documented. After coronary angiography via DUA, day-3 non-triphasic flow occurred in 23.7%; selective follow-up suggested recanalization without major clinical complications, but limits generalizability.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261491116"},"PeriodicalIF":2.7,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164432","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-12DOI: 10.1177/00033197261491118
Ahmed Hassanein, Humam Emad Rajha, Mohammed Abdel Hamid, Ibrahim E Hashem, Rafif Mahmood Al Saady, Shona Pedersen
{"title":"Apolipoprotein A (ApoA) in Cardiovascular Disorders: Connections and Insights.","authors":"Ahmed Hassanein, Humam Emad Rajha, Mohammed Abdel Hamid, Ibrahim E Hashem, Rafif Mahmood Al Saady, Shona Pedersen","doi":"10.1177/00033197261491118","DOIUrl":"https://doi.org/10.1177/00033197261491118","url":null,"abstract":"<p><p>Apolipoprotein A (ApoA) family members-ApoA-I, ApoA-II, ApoA-IV, and ApoA-V-play important roles in the vasculature that extend beyond lipid transport to regulate lipid-immune crosstalk, vascular homeostasis, and triglyceride metabolism. ApoA-I mediates reverse cholesterol transport, yet its cardioprotective capacity depends on functional integrity rather than HDL-cholesterol levels alone. ApoA-II, ApoA-IV, and ApoA-V exhibit context-dependent roles ranging from enhancing cholesterol efflux and triglyceride clearance to modulating inflammation, oxidative stress, endothelial activation, and thrombosis. Post-translational modifications such as oxidation, glycation, and citrullination within inflammatory milieus can convert protective ApoA proteins into dysfunctional or proinflammatory mediators. Genetic variations within APOA gene clusters have clarified the causal contribution of triglyceride-rich lipoproteins to atherosclerotic risk, shifting emphasis from HDL quantity toward lipoprotein quality and remnant cholesterol burden. In this comprehensive review, we synthesize structural, genetic, mechanistic, and clinical evidence to evaluate the position of the 4 ApoA proteins as context-dependent modulators of cardiovascular disease. We highlight the dualistic nature of their actions and examine failed clinical trials of ApoA-I infusions and mimetic peptides. We conclude by discussing how shifting focus from HDL quantity toward lipoprotein quality and preservation of ApoA functional integrity may inform more precise approaches to residual cardiovascular risk and triglyceride-driven atherogenesis.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261491118"},"PeriodicalIF":2.7,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-08DOI: 10.1177/00033197261495224
Hongxiao Lv, Wentao Yu
{"title":"Interpreting Sex- and Age-Specific Associations Between the TC/HDL-C Ratio and Carotid Plaque.","authors":"Hongxiao Lv, Wentao Yu","doi":"10.1177/00033197261495224","DOIUrl":"https://doi.org/10.1177/00033197261495224","url":null,"abstract":"","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261495224"},"PeriodicalIF":2.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Asprosin as a Molecular Switch in Epicardial Adipose Tissue Remodeling and Cardiometabolic Disease: New Insights.","authors":"Nandhakumar Prasath, Kadalangudi Aravaanan Arul Senghor, Vellore Mohanakrishnan Vinodhini, Sabapathi Surya Prakash, Thoddi Ramamurthy Muralidharan","doi":"10.1177/00033197261492072","DOIUrl":"https://doi.org/10.1177/00033197261492072","url":null,"abstract":"<p><p>Epicardial adipose tissue (EAT) is a specialized visceral fat depot that directly interfaces with the myocardium. Under physiological conditions, EAT exhibits a beige-like thermogenic phenotype with enhanced angiogenesis and an anti-inflammatory secretome, contributing to cardioprotection. However, metabolic stress associated with obesity and type 2 diabetes mellitus disrupts this homeostasis, promoting EAT whitening, vascular dysfunction, hypoxia, fibrosis, and chronic inflammation, ultimately leading to adverse cardiovascular outcomes. Asprosin, a recently characterized fasting-induced adipokine, is an important regulator of systemic glucose metabolism, appetite, and insulin resistance. Experimental evidence suggests that asprosin suppresses adipose browning by downregulating thermogenic pathways while promoting adipogenesis and lipid accumulation. This review proposes an integrated asprosin-EAT whitening-angiogenesis axis as a conceptual framework linking EAT dysfunction and cardiovascular disease. Asprosin may contribute to phenotypic remodeling of epicardial adipose tissue through mechanisms involving impaired adipose browning, altered angiogenesis, and vascular dysfunction. Further investigation of the local and paracrine actions of asprosin within EAT is required to determine its potential as a biomarker and therapeutic target for cardiometabolic disease.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261492072"},"PeriodicalIF":2.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-07DOI: 10.1177/00033197261494019
Nadire Işık Erol Algül, Muhammed Erzurum, Mehmet Ali Felekoğlu, Mehmet Emre Özerdem, Nail Burak Özbeyaz, Engin Algül
{"title":"Prognostic Value of the CALLY Index in Predicting Contrast-Associated Acute Kidney Injury in Patients With Acute Coronary Syndrome.","authors":"Nadire Işık Erol Algül, Muhammed Erzurum, Mehmet Ali Felekoğlu, Mehmet Emre Özerdem, Nail Burak Özbeyaz, Engin Algül","doi":"10.1177/00033197261494019","DOIUrl":"https://doi.org/10.1177/00033197261494019","url":null,"abstract":"<p><p>Contrast-associated acute kidney injury (CA-AKI) is a serious complication associated with increased morbidity and mortality in patients with acute coronary syndrome (ACS) undergoing coronary angiography. The C-reactive protein-albumin-lymphocyte (CALLY) index is a novel biomarker reflecting inflammatory and nutritional status. This retrospective study evaluated the prognostic value of the CALLY index calculated at hospital admission for predicting CA-AKI in 1516 patients with ACS. CA-AKI developed in 267 patients (17.6%). Patients who developed CA-AKI had significantly lower CALLY index values (0.35 ± 0.16 vs 0.84 ± 0.30; <i>P</i> < .001). In separate multivariable logistic regression analyses adjusted for baseline clinical and procedural confounders, the CALLY index emerged as an independent predictor of CA-AKI (Odds ratio [OR] 0.592 per 0.1-unit increase; 95% CI 0.525-0.668; <i>P</i> < .001). Receiver operating characteristic curve analysis demonstrated good discriminatory capacity for the CALLY index (Area Under the Curve [AUC] = 0.822), significantly outperforming conventional clinical scores and other inflammatory indices (DeLong test <i>P</i> < .001). Furthermore, adding the CALLY index to the Mehran risk score significantly improved reclassification metrics (Net Reclassification Improvement [NRI] = 14.2%, Integrated Discrimination Improvement [IDI] = 0.048; <i>P</i> < .001). The CALLY index serves as a simple, practical, and effective score for early CA-AKI risk stratification in ACS.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261494019"},"PeriodicalIF":2.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-07DOI: 10.1177/00033197261496390
Xinghao Liu
{"title":"Letter: The CALLY Index for In-Hospital Mortality in Elderly ACS: Value Revisited and Length-of-Stay Bias.","authors":"Xinghao Liu","doi":"10.1177/00033197261496390","DOIUrl":"https://doi.org/10.1177/00033197261496390","url":null,"abstract":"","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"33197261496390"},"PeriodicalIF":2.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Artificial Intelligence and Machine Learning for Risk Prediction of Abdominal Aortic Aneurysm Growth and Rupture.","authors":"Jia Guo, Fabien Lareyre, Regent Lee, Martin Teraa, Hervé Delingette, Juliette Raffort","doi":"10.1177/00033197251379127","DOIUrl":"10.1177/00033197251379127","url":null,"abstract":"<p><p>Artificial intelligence (AI) and machine learning (ML) are emerging tools in the management of abdominal aortic aneurysms (AAA). They have offered new tools to develop advanced imaging analysis and prediction models. This narrative review summarizes studies exploring AI/ML models to evaluate the risk of AAA growth and rupture. We provide an overview and critical analysis on methodology used, identify current limits and propose future directions for research and implementation in surgical practice.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"1091-1097"},"PeriodicalIF":2.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
AngiologyPub Date : 2026-10-01Epub Date: 2025-11-20DOI: 10.1177/00033197251393619
Ankit Agrawal, Danny Rayes, Larisa G Tereshchenko, Umesh Bhagat, Ahmad Safdar, Aro Daniela Arockiam, Akiva Rosenzveig, Elio Haroun, Rahul Gupta, Pulkit Chaudhury, Venu Menon, Brian Griffin, Tom Kai Ming Wang
{"title":"Contemporary Trends, Outcomes, and Novel Risk Score for Spontaneous Coronary Artery Dissection: A Nationwide Analysis.","authors":"Ankit Agrawal, Danny Rayes, Larisa G Tereshchenko, Umesh Bhagat, Ahmad Safdar, Aro Daniela Arockiam, Akiva Rosenzveig, Elio Haroun, Rahul Gupta, Pulkit Chaudhury, Venu Menon, Brian Griffin, Tom Kai Ming Wang","doi":"10.1177/00033197251393619","DOIUrl":"10.1177/00033197251393619","url":null,"abstract":"<p><p>Spontaneous coronary artery dissection (SCAD) is an under-recognized cause of acute coronary syndrome (ACS). We reviewed the characteristics, predictors, and outcomes of SCAD using the National Inpatient Sample (NIS) database. ACS and SCAD patients were identified from the 2016 to 2020 NIS database. Multivariable logistic regression was performed to identify risk factors associated with SCAD and in-hospital mortality. A risk score model was developed using the 2016 to 2019 cohort and validated with 2020 data. Among 7 219 004 ACS hospitalizations, 30 770 (0.43%) had SCAD (mean age 59.6 years; 58.5% female). Compared with non-SCAD ACS patients, SCAD patients had higher rates of all-cause mortality (8.0% vs 6.0%), and acute stroke (3.2% vs 1.7%). History of percutaneous coronary intervention (3.63 [3.33-3.96]), coronary artery aneurysm (8.87 [5.75-13.70]), and fibromuscular dysplasia (90.50 [69.86-117.25]), all with <i>P</i> < .001, are the strongest predictors of SCAD. Five mortality risk predictors in our risk model were cardiogenic shock, extracorporeal membrane oxygenation, balloon pump, cardiac arrest, and acute kidney injury. The area under the curve for the development and validation datasets was 0.867 and 0.860, respectively. SCAD is a rare but serious form of ACS with distinct risk factors and outcomes. Our risk model may help in early identification and management.</p>","PeriodicalId":8264,"journal":{"name":"Angiology","volume":" ","pages":"1170-1179"},"PeriodicalIF":2.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145562120","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}