Pub Date : 2026-01-13DOI: 10.1016/j.cpcardiol.2026.103261
Joseph S Spindler, Robert J Henning
The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to more than 600 million people in 2023. Atherosclerotic vascular disease results not only from lipid accumulation within the arterial walls but also from acute and chronic inflammatory changes in response to arterial endothelial injury. Inflammation together with cytokines, chemokines, and acute-phase reactants play a pivotal role in atherosclerotic vascular plaque formation, progression, rupture, and thrombogenesis that lead to an acute coronary syndrome (ACS) or stroke. In addition, individuals who have previously sustained an ACS frequently have evidence of residual arterial inflammation as indicated by increased blood concentrations of the inflammatory biomarker C-reactive protein (CRP). As a consequence, chronic arterial inflammatory disease contributes to more than 15% of all global deaths from myocardial infarction, cerebral vascular events (transient ischemic attacks or strokes), and peripheral vascular disease. This Review Article discusses the important mechanisms by which inflammation contributes to the initiation and progression of coronary artery atherosclerosis, the biologic measurements which indicate arterial inflammation in individuals, the diagnostic techniques useful in the detection of arterial inflammation and atherosclerosis, and the clinical studies that have been performed and are currently being performed to limit the contributions of acute and chronic inflammation to the morbidity and mortality from coronary artery atherosclerosis.
{"title":"THE CRITICAL ROLE OF INFLAMMATION IN ATHEROSCLEROTIC CORONARY ARTERY HEART DISEASE.","authors":"Joseph S Spindler, Robert J Henning","doi":"10.1016/j.cpcardiol.2026.103261","DOIUrl":"https://doi.org/10.1016/j.cpcardiol.2026.103261","url":null,"abstract":"<p><p>The global burden of atherosclerotic cardiovascular disease has risen from 271 million people in 1990 to more than 600 million people in 2023. Atherosclerotic vascular disease results not only from lipid accumulation within the arterial walls but also from acute and chronic inflammatory changes in response to arterial endothelial injury. Inflammation together with cytokines, chemokines, and acute-phase reactants play a pivotal role in atherosclerotic vascular plaque formation, progression, rupture, and thrombogenesis that lead to an acute coronary syndrome (ACS) or stroke. In addition, individuals who have previously sustained an ACS frequently have evidence of residual arterial inflammation as indicated by increased blood concentrations of the inflammatory biomarker C-reactive protein (CRP). As a consequence, chronic arterial inflammatory disease contributes to more than 15% of all global deaths from myocardial infarction, cerebral vascular events (transient ischemic attacks or strokes), and peripheral vascular disease. This Review Article discusses the important mechanisms by which inflammation contributes to the initiation and progression of coronary artery atherosclerosis, the biologic measurements which indicate arterial inflammation in individuals, the diagnostic techniques useful in the detection of arterial inflammation and atherosclerosis, and the clinical studies that have been performed and are currently being performed to limit the contributions of acute and chronic inflammation to the morbidity and mortality from coronary artery atherosclerosis.</p>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":" ","pages":"103261"},"PeriodicalIF":3.3,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145991650","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}
Pub Date : 2026-01-01Epub Date: 2025-10-28DOI: 10.1016/j.cpcardiol.2025.103206
Dina Abushanab , Daoud Al-Badriyeh , Rawan F. Al Froukh , Rasha Kaddoura , Mohammed Abdelaal , Clara Marquina , Jazeel Abdulmajeed , Palli Valapila Abdulrouf , Shaban Mohamed , Zanfina Ademi
Background
Cardiovascular diseases (CVD) are a great public health challenge in Qatar, with significant impacts on long-term population health and societal costs.
Objective
We aimed to forecast the health and economic burden of the CVD in Qatar from 2024 to 2033, from both healthcare and societal perspective.
Methods
A validated two-stage dynamic model was structured, spanning a 10-year period and targeting individuals aged 40-79. The CVD incidents (i.e., myocardial infarction [MI], stroke) were estimated using the 2013 Pooled Cohort Equation, while recurrent events were obtained from the global REACH registry. The model outcomes included fatal and non-fatal MI and stroke, years of life lived, quality-adjusted life years (QALYs), total direct costs, and total productivity loss costs. Utility and cost inputs were derived from published sources. Outcomes were discounted at a rate of 3 % per annum. Calibration and validation were performed to ensure model accuracy. A multivariate sensitivity analysis was also conducted.
Results
By 2033, there will be 271,260 non-fatal MI events (95 % confidence interval [CI] 271,249-271,277), 258,892 non-fatal strokes (95 %CI 258,858-259,094), and 20,413 CVD deaths (95 %CI 20,405-20,429). The cumulative years of life lived and QALYs were 13,806,845 (95 % CI 13,802,149-13,811,541) and 10,655,665 (95 %CI 10,652,720-10,658,611), respectively. The direct costs were QAR71.14 (95 %CI QAR70.62-71.66) billion, and the productivity loss costs were estimated to surpass QAR108.12 (95 %CI QAR106.88-109.36) billion. The exchange rates used were based on 2024 values (1QAR=0.27US$).
Conclusions
This study offers valuable insights into the projected burden of CVD in Qatar, highlighting the need for effective preventive strategies to reduce risk.
{"title":"The next decade of cardiovascular disease burden in Qatar, a gulf cooperation council country: Projections from 2024 to 2033","authors":"Dina Abushanab , Daoud Al-Badriyeh , Rawan F. Al Froukh , Rasha Kaddoura , Mohammed Abdelaal , Clara Marquina , Jazeel Abdulmajeed , Palli Valapila Abdulrouf , Shaban Mohamed , Zanfina Ademi","doi":"10.1016/j.cpcardiol.2025.103206","DOIUrl":"10.1016/j.cpcardiol.2025.103206","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular diseases (CVD) are a great public health challenge in Qatar, with significant impacts on long-term population health and societal costs.</div></div><div><h3>Objective</h3><div>We aimed to forecast the health and economic burden of the CVD in Qatar from 2024 to 2033, from both healthcare and societal perspective.</div></div><div><h3>Methods</h3><div>A validated two-stage dynamic model was structured, spanning a 10-year period and targeting individuals aged 40-79. The CVD incidents (i.e., myocardial infarction [MI], stroke) were estimated using the 2013 Pooled Cohort Equation, while recurrent events were obtained from the global REACH registry. The model outcomes included fatal and non-fatal MI and stroke, years of life lived, quality-adjusted life years (QALYs), total direct costs, and total productivity loss costs. Utility and cost inputs were derived from published sources. Outcomes were discounted at a rate of 3 % per annum. Calibration and validation were performed to ensure model accuracy. A multivariate sensitivity analysis was also conducted.</div></div><div><h3>Results</h3><div>By 2033, there will be 271,260 non-fatal MI events (95 % confidence interval [CI] 271,249-271,277), 258,892 non-fatal strokes (95 %CI 258,858-259,094), and 20,413 CVD deaths (95 %CI 20,405-20,429). The cumulative years of life lived and QALYs were 13,806,845 (95 % CI 13,802,149-13,811,541) and 10,655,665 (95 %CI 10,652,720-10,658,611), respectively. The direct costs were QAR71.14 (95 %CI QAR70.62-71.66) billion, and the productivity loss costs were estimated to surpass QAR108.12 (95 %CI QAR106.88-109.36) billion. The exchange rates used were based on 2024 values (1QAR=0.27US$).</div></div><div><h3>Conclusions</h3><div>This study offers valuable insights into the projected burden of CVD in Qatar, highlighting the need for effective preventive strategies to reduce risk.</div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103206"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410514","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}
Pub Date : 2026-01-01Epub Date: 2025-10-28DOI: 10.1016/j.cpcardiol.2025.103205
Andrea Grillo , Sandro Lepidi , Massimo Puato
Atherosclerotic renal artery stenosis (ARAS) represents a common manifestation of systemic atherosclerosis and remains an underrecognized cause of secondary hypertension, chronic kidney disease, and cardiovascular morbidity. Although often clinically silent, progressive narrowing of the renal artery may result in renovascular hypertension, ischemic nephropathy, or cardiac destabilization syndromes such as recurrent pulmonary edema. The pathophysiology of ARAS extends beyond simple flow limitation, involving renin–angiotensin–aldosterone system activation, oxidative stress, microvascular rarefaction, and parenchymal fibrosis, thereby explaining the limited reversibility of renal damage after revascularization.
Over the past decades, management strategies have evolved considerably. While initial enthusiasm for surgical or endovascular revascularization was supported by observational reports of improved blood pressure and renal function, randomized controlled trials—including ASTRAL and CORAL—failed to demonstrate a consistent benefit of stenting over optimal medical therapy in unselected patients. These findings have shifted current practice toward medical therapy as the cornerstone of management, integrating renin–angiotensin system inhibitors, statins, antiplatelet agents, and, more recently, SGLT2 inhibitors.
Nevertheless, accumulating evidence indicates that specific high-risk subsets—patients with resistant hypertension, recurrent pulmonary edema, or progressive ischemic nephropathy—may derive meaningful clinical benefit from timely revascularization. In the post-CORAL era, the central challenge is therefore accurate patient selection to identify the small group in whom revascularization remains appropriate, leveraging advanced imaging, physiological indices, and risk stratification.
{"title":"Atherosclerotic renal artery stenosis in the post-CORAL Trial Era. A narrative review","authors":"Andrea Grillo , Sandro Lepidi , Massimo Puato","doi":"10.1016/j.cpcardiol.2025.103205","DOIUrl":"10.1016/j.cpcardiol.2025.103205","url":null,"abstract":"<div><div>Atherosclerotic renal artery stenosis (ARAS) represents a common manifestation of systemic atherosclerosis and remains an underrecognized cause of secondary hypertension, chronic kidney disease, and cardiovascular morbidity. Although often clinically silent, progressive narrowing of the renal artery may result in renovascular hypertension, ischemic nephropathy, or cardiac destabilization syndromes such as recurrent pulmonary edema. The pathophysiology of ARAS extends beyond simple flow limitation, involving renin–angiotensin–aldosterone system activation, oxidative stress, microvascular rarefaction, and parenchymal fibrosis, thereby explaining the limited reversibility of renal damage after revascularization.</div><div>Over the past decades, management strategies have evolved considerably. While initial enthusiasm for surgical or endovascular revascularization was supported by observational reports of improved blood pressure and renal function, randomized controlled trials—including ASTRAL and CORAL—failed to demonstrate a consistent benefit of stenting over optimal medical therapy in unselected patients. These findings have shifted current practice toward medical therapy as the cornerstone of management, integrating renin–angiotensin system inhibitors, statins, antiplatelet agents, and, more recently, SGLT2 inhibitors.</div><div>Nevertheless, accumulating evidence indicates that specific high-risk subsets—patients with resistant hypertension, recurrent pulmonary edema, or progressive ischemic nephropathy—may derive meaningful clinical benefit from timely revascularization. In the post-CORAL era, the central challenge is therefore accurate patient selection to identify the small group in whom revascularization remains appropriate, leveraging advanced imaging, physiological indices, and risk stratification.</div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103205"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145410471","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}
Pub Date : 2026-01-01Epub Date: 2025-11-14DOI: 10.1016/j.cpcardiol.2025.103210
Nicolaas P. Pronk PhD , Ross Arena PhD , Colin Woodard MA, FRGS
{"title":"The GLP-1 RA Era - A positive disruptor to the ecological framework of population health","authors":"Nicolaas P. Pronk PhD , Ross Arena PhD , Colin Woodard MA, FRGS","doi":"10.1016/j.cpcardiol.2025.103210","DOIUrl":"10.1016/j.cpcardiol.2025.103210","url":null,"abstract":"","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103210"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145535046","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}
Pulmonary arterial hypertension (PAH) creates a prothrombotic environment that may result in in situ pulmonary arterial thrombosis (PAT), a subtype that can resemble pulmonary embolism and chronic thromboembolic pulmonary hypertension (CTEPH) but requires different management.
Methods
We conducted a narrative review of epidemiology, mechanisms, diagnostic differentiation, imaging (CT pulmonary angiography [CTPA], ventilation–perfusion [V/Q] scanning, echocardiography), and treatment of in situ PAT, and incorporated an institutional retrospective series (screened 2020–2025).
Results
In situ PAT typically appears on CTPA as central or wall-adherent thrombi within markedly dilated proximal pulmonary arteries, often without stenosis. Early V/Q scanning is useful to rule out CTEPH; non-segmental or mottled perfusion favors Group 1 PAH. Caliber metrics (PA diameter, PA/Ao) and RV strain indices (RV/LV, TAPSE) support but do not by themselves establish the diagnosis. Of 364 PAH patients screened, 7 (1.9 %) met imaging criteria for in situ PAT; mean age 42 years, 71 % female, 43 % congenital heart disease. All had PA ≥30 mm and RV/LV ≥1; 71 % had aneurysmal PA ≥40 mm; 71 % had negative DVT Doppler. Functional and hemodynamic impairment was substantial.
Conclusions
A stepwise workflow—DVT assessment, V/Q to exclude CTEPH, and targeted CTPA morphology interpreted with hemodynamics—facilitates accurate classification of in situ PAT and avoids misdirected CTEPH interventions. Therapy should begin with PAH-targeted treatment; anticoagulation should be individualized according to phenotype, bleeding risk, and clinical course.
背景：肺动脉高压（PAH）产生血栓前环境，可能导致原位肺动脉血栓形成（PAT），这是一种类似于肺栓塞和慢性血栓栓塞性肺动脉高压（CTEPH）的亚型，但需要不同的治疗。方法：我们对原位PAT的流行病学、机制、诊断鉴别、影像学（CT肺血管造影[CTPA]、通气灌注[V/Q]扫描、超声心动图）和治疗进行了叙述性回顾，并纳入了一个机构回顾性系列（筛选2020-2025年）。结果：原位PAT通常在CTPA上表现为明显扩张的肺动脉近端中心或壁贴血栓，通常无狭窄。早期V/Q扫描有助于排除CTEPH；非节段性或斑驳灌注有利于1组PAH。口径指标（PA直径，PA/Ao）和RV应变指标（RV/LV， TAPSE）支持但不能单独确定诊断。在筛选的364例PAH患者中，7例（1.9%）符合原位PAT的影像学标准；平均年龄42岁，71%为女性，43%为先天性心脏病。PA≥30 mm, RV/LV≥1；动脉瘤样PA≥40 mm占71%；71% DVT多普勒阴性。功能和血流动力学损伤是实质性的。结论：分步工作流程——dvt评估、排除CTEPH的V/Q和用血流动力学解释的靶向CTPA形态学——有助于准确分类原位PAT，避免错误的CTEPH干预。治疗应从针对多环芳烃的治疗开始；抗凝治疗应根据表型、出血风险和临床病程进行个体化治疗。
{"title":"In situ pulmonary arterial thrombosis in pulmonary arterial hypertension: Diagnostic differentiation, imaging criteria, and management—A narrative review with an institutional case-series snapshot","authors":"María-José Bravo-Vásquez M.D. , Guillermo Cueto-Robledo M.D. , Ernesto Roldan-Valadez M.D., M.Sc., D.Sc. , Dulce-Iliana Navarro-Vergara M.D., M.Sc. , Luis-Eugenio Graniel-Palafox M.D. , Jonathan Ruiz-Ruiz M.D. , Nicolai Gonzalez-Stoylov M.D. , Erick-Mauricio Garcia-Luna M.D.","doi":"10.1016/j.cpcardiol.2025.103209","DOIUrl":"10.1016/j.cpcardiol.2025.103209","url":null,"abstract":"<div><h3>Background</h3><div>Pulmonary arterial hypertension (PAH) creates a prothrombotic environment that may result in in situ pulmonary arterial thrombosis (PAT), a subtype that can resemble pulmonary embolism and chronic thromboembolic pulmonary hypertension (CTEPH) but requires different management.</div></div><div><h3>Methods</h3><div>We conducted a narrative review of epidemiology, mechanisms, diagnostic differentiation, imaging (CT pulmonary angiography [CTPA], ventilation–perfusion [V/Q] scanning, echocardiography), and treatment of in situ PAT, and incorporated an institutional retrospective series (screened 2020–2025).</div></div><div><h3>Results</h3><div>In situ PAT typically appears on CTPA as central or wall-adherent thrombi within markedly dilated proximal pulmonary arteries, often without stenosis. Early V/Q scanning is useful to rule out CTEPH; non-segmental or mottled perfusion favors Group 1 PAH. Caliber metrics (PA diameter, PA/Ao) and RV strain indices (RV/LV, TAPSE) support but do not by themselves establish the diagnosis. Of 364 PAH patients screened, 7 (1.9 %) met imaging criteria for in situ PAT; mean age 42 years, 71 % female, 43 % congenital heart disease. All had PA ≥30 mm and RV/LV ≥1; 71 % had aneurysmal PA ≥40 mm; 71 % had negative DVT Doppler. Functional and hemodynamic impairment was substantial.</div></div><div><h3>Conclusions</h3><div>A stepwise workflow—DVT assessment, V/Q to exclude CTEPH, and targeted CTPA morphology interpreted with hemodynamics—facilitates accurate classification of in situ PAT and avoids misdirected CTEPH interventions. Therapy should begin with PAH-targeted treatment; anticoagulation should be individualized according to phenotype, bleeding risk, and clinical course.</div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103209"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534990","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}
Pub Date : 2026-01-01Epub Date: 2025-11-28DOI: 10.1016/S0146-2806(25)00243-9
{"title":"Information for Readers","authors":"","doi":"10.1016/S0146-2806(25)00243-9","DOIUrl":"10.1016/S0146-2806(25)00243-9","url":null,"abstract":"","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103224"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145693810","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}
Heart failure with preserved ejection fraction (HFpEF) remains a major clinical challenge, particularly among obese individuals. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), originally indicated for type 2 diabetes, have demonstrated potential cardiovascular benefits, including weight loss and anti-inflammatory effects. However, their efficacy in HFpEF remains uncertain. We conducted a systematic review and meta-analysis to evaluate the effects of GLP-1 RAs in obese patients with HFpEF.
Methods
We systematically searched PubMed, Embase, and Cochrane databases for randomized controlled trials (RCTs) and propensity score-matched cohort studies comparing GLP-1 RAs with placebo or standard care in obese HFpEF populations. The primary endpoints of this meta-analysis were as follows: (1) any HF event; (2) Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS); and (3) Six-minute walk test (6MWT) distance. A random-effects model was used to pool effect estimates.
Results
Five studies (4 RCTs, 1 propensity-matched cohort) comprising 5,561 patients met inclusion criteria. GLP-1 RAs significantly reduced HF events (HR: 0.50; 95 % CI: 0.36–0.70; p < 0.0001; I² = 29.5 %). Treatment was also associated with improvements in KCCQ-CSS (MD: 7.38 points; 95 % CI: 5.51–9.26; p < 0.0001; I² = 0 %), 6MWT distance (MD: 17.60 m; 95 % CI: 11.86–23.35; p < 0.0001; I² = 0 %) and weight loss (MD: -9.56 kg; 95 % CI: -12.71 to -6.41; p < 0.0001; I² = 95 %). Trends toward reduced CV and all-cause mortality were observed, though not statistically significant.
Conclusion
GLP-1 RAs are associated with reductions in HF events and meaningful improvements in quality of life and functional capacity in obese patients with HFpEF. These findings highlight their potential as a therapeutic strategy in this high-risk population.
{"title":"Efficacy of GLP-1 receptor agonists in obese patients with heart failure with preserved ejection fraction: A systematic review and meta-analysis of randomized trials and propensity score-matched cohorts","authors":"Giulia Caldeira Gaelzer MD , Alonzo Armani Prata , Luís Gustavo Rizzolli , Luisalice Mendes Afonso MD , Gustavo Lenci Marques MD, PhD, CCK, FACC","doi":"10.1016/j.cpcardiol.2025.103194","DOIUrl":"10.1016/j.cpcardiol.2025.103194","url":null,"abstract":"<div><h3>Background</h3><div>Heart failure with preserved ejection fraction (HFpEF) remains a major clinical challenge, particularly among obese individuals. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), originally indicated for type 2 diabetes, have demonstrated potential cardiovascular benefits, including weight loss and anti-inflammatory effects. However, their efficacy in HFpEF remains uncertain. We conducted a systematic review and meta-analysis to evaluate the effects of GLP-1 RAs in obese patients with HFpEF.</div></div><div><h3>Methods</h3><div>We systematically searched PubMed, Embase, and Cochrane databases for randomized controlled trials (RCTs) and propensity score-matched cohort studies comparing GLP-1 RAs with placebo or standard care in obese HFpEF populations. The primary endpoints of this meta-analysis were as follows: (1) any HF event; (2) Kansas City Cardiomyopathy Questionnaire Overall Summary Score (KCCQ-OSS); and (3) Six-minute walk test (6MWT) distance. A random-effects model was used to pool effect estimates.</div></div><div><h3>Results</h3><div>Five studies (4 RCTs, 1 propensity-matched cohort) comprising 5,561 patients met inclusion criteria. GLP-1 RAs significantly reduced HF events (HR: 0.50; 95 % CI: 0.36–0.70; p < 0.0001; I² = 29.5 %). Treatment was also associated with improvements in KCCQ-CSS (MD: 7.38 points; 95 % CI: 5.51–9.26; p < 0.0001; I² = 0 %), 6MWT distance (MD: 17.60 m; 95 % CI: 11.86–23.35; p < 0.0001; I² = 0 %) and weight loss (MD: -9.56 kg; 95 % CI: -12.71 to -6.41; p < 0.0001; I² = 95 %). Trends toward reduced CV and all-cause mortality were observed, though not statistically significant.</div></div><div><h3>Conclusion</h3><div>GLP-1 RAs are associated with reductions in HF events and meaningful improvements in quality of life and functional capacity in obese patients with HFpEF. These findings highlight their potential as a therapeutic strategy in this high-risk population.</div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103194"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145423333","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}
Pub Date : 2026-01-01Epub Date: 2025-10-19DOI: 10.1016/j.cpcardiol.2025.103193
Rogelio Robledo-Nolasco M.D. , Elias Noel Andrade-Cuellar M.D. , Juan Carlos Solis-Gómez M.D., M.Sc. , Saul Yair Guillot-Castillo M.D. , Jose Javier Ik Yahalcab Zamora-Diaz M.D. , Rocio Aceves-Millan M.D. , Andrea Paulina Maldonado-Tenesaca M.D. , Maria Alejandra Monroy-Jimenez M.D. , Ivan Alejandro Elizalde-Uribe M.D. , Daniel Torres Peynado , Rodrigo Bonilla-Figueroa M.D. , Kevin Josué Acevedo-Gómez M.D.
Background
Progressive atrial myopathy marked by fibrotic remodelling drives the transition from paroxysmal to persistent atrial fibrillation (AF), yet the temporal dynamics of fibrosis within persistent AF remain poorly defined.
Objective
To quantify dense scar and borderline fibrotic zones using high-density electro-anatomic mapping (HD-EAM) in patients with persistent AF, and to compare fibrotic burden between early persistent (>7 days–<3 months) and persistent (≥3 months–<1 year) AF.
Methods
Retrospectively analysed 78 consecutive patients (59 ± 15 years, 59 % men) undergoing first-time pulmonary vein isolation for persistent AF. Atrial voltage maps (CARTO 3 CONFIDENSE™) acquired in sinus rhythm classified tissue as healthy (>0.5 mV), borderline (0.3–0.5 mV), or dense scar (<0.2 mV). Echocardiographic left atrial diameter (LAD) and volume (LAV) were compared with mapping data. The primary endpoint was dense scar point count; secondary endpoints included AF/atrial tachycardia recurrence and correlation between imaging modalities.
Results
Twenty-two patients had early persistent and 56 persistent AF. Mapping resolution was similar (5 193 ± 459 vs 5 399 ± 601 points, p = 0.83). Dense scar points were significantly higher in persistent AF (2 807 ± 336 vs 1 634 ± 236; p < 0.001). LAD and LAV from HD-EAM correlated moderately with echocardiography (r = 0.45 and 0.48; both p < 0.01) but did not differ between groups. After 7.2 ± 3.7 months, recurrence occurred in 16 % of persistent versus 8 % of early persistent AF (p = 0.11).
Conclusions
Fibrotic burden increases markedly after three months of uninterrupted AF despite stable atrial size. HD-EAM enables intra-procedural quantification of atrial myopathy and may guide personalised ablation strategies.
{"title":"Atrial myopathy in persistent atrial fibrillation: Three-dimensional quantification of atrial fibrosis by high-density electro-anatomic mapping and its association with arrhythmia duration","authors":"Rogelio Robledo-Nolasco M.D. , Elias Noel Andrade-Cuellar M.D. , Juan Carlos Solis-Gómez M.D., M.Sc. , Saul Yair Guillot-Castillo M.D. , Jose Javier Ik Yahalcab Zamora-Diaz M.D. , Rocio Aceves-Millan M.D. , Andrea Paulina Maldonado-Tenesaca M.D. , Maria Alejandra Monroy-Jimenez M.D. , Ivan Alejandro Elizalde-Uribe M.D. , Daniel Torres Peynado , Rodrigo Bonilla-Figueroa M.D. , Kevin Josué Acevedo-Gómez M.D.","doi":"10.1016/j.cpcardiol.2025.103193","DOIUrl":"10.1016/j.cpcardiol.2025.103193","url":null,"abstract":"<div><h3>Background</h3><div>Progressive atrial myopathy marked by fibrotic remodelling drives the transition from paroxysmal to persistent atrial fibrillation (AF), yet the temporal dynamics of fibrosis within persistent AF remain poorly defined.</div></div><div><h3>Objective</h3><div>To quantify dense scar and borderline fibrotic zones using high-density electro-anatomic mapping (HD-EAM) in patients with persistent AF, and to compare fibrotic burden between early persistent (>7 days–<3 months) and persistent (≥3 months–<1 year) AF.</div></div><div><h3>Methods</h3><div>Retrospectively analysed 78 consecutive patients (59 ± 15 years, 59 % men) undergoing first-time pulmonary vein isolation for persistent AF. Atrial voltage maps (CARTO 3 CONFIDENSE™) acquired in sinus rhythm classified tissue as healthy (>0.5 mV), borderline (0.3–0.5 mV), or dense scar (<0.2 mV). Echocardiographic left atrial diameter (LAD) and volume (LAV) were compared with mapping data. The primary endpoint was dense scar point count; secondary endpoints included AF/atrial tachycardia recurrence and correlation between imaging modalities.</div></div><div><h3>Results</h3><div>Twenty-two patients had early persistent and 56 persistent AF. Mapping resolution was similar (5 193 ± 459 vs 5 399 ± 601 points, <em>p</em> = 0.83). Dense scar points were significantly higher in persistent AF (2 807 ± 336 vs 1 634 ± 236; <em>p</em> < 0.001). LAD and LAV from HD-EAM correlated moderately with echocardiography (r = 0.45 and 0.48; both <em>p</em> < 0.01) but did not differ between groups. After 7.2 ± 3.7 months, recurrence occurred in 16 % of persistent versus 8 % of early persistent AF (<em>p</em> = 0.11).</div></div><div><h3>Conclusions</h3><div>Fibrotic burden increases markedly after three months of uninterrupted AF despite stable atrial size. HD-EAM enables intra-procedural quantification of atrial myopathy and may guide personalised ablation strategies.</div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"51 1","pages":"Article 103193"},"PeriodicalIF":3.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145349924","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}
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