Previous studies have not fully explored the association between air pollutants and heart failure (HF) incidence in cancer participants, nor the role of genetic susceptibility. We aimed to assess air pollutants' impact on HF risk and their joint contribution with genetic susceptibility to incident HF in this group.
Methods
This study utilized data from the UK Biobank and included 50 923 cancer participants. The relationship between air pollutants and the onset of HF was examined using a Cox proportional hazards model. Furthermore, a polygenic risk score was constructed to evaluate the comprehensive impact of air pollutant exposure, genetic susceptibility, and their interactions on the risk of HF among cancer participants.
Results
The research results show that when comparing individuals in the lowest exposure quartile with those in the highest exposure quartile, the multivariate-adjusted HRs were 1.22 (1.07, 1.38) for PM10, 1.16 (1.03, 1.32) for PM2.5, 1.20 (1.06, 1.36) for NO2, and 1.26 (1.11, 1.43) for NOx. For the joint associations, cancer participants with both high genetic risk and elevated air pollutant exposure exhibited the highest risk of HF events. The risk estimates for the incidence of HF were 2.06 (1.52, 2.78) for PM10, 1.70 (1.27, 2.27) for PM2.5 1.77 (1.32, 2.37) for NO2, and 1.61 (1.21, 2.13) for NOx.
Conclusion
Our findings indicate that long-term combined exposure to multiple air pollutants, including PM2.5, PM10, NO2, and NOx, is associated with an elevated risk of new-onset HF in cancer patients, particularly among individuals with a high genetic predisposition to the disease.
{"title":"Joint Exposure to Multiple Air Pollutants, Genetic Susceptibility, and Risk of Heart Failure in Cancer Patients: A Prospective Study in UK Biobank","authors":"Xueqi Xiao, Yuting Yang, Binghua Zhang, Kaiyi Chi, Huijuan He, Liyu Guo, Long Pan, Yingyu Deng, Peipei Wang, Xin Lin, Kepeng Wei, Jianpeng Liang, Wenjuan Jiang, Meiting Jiao, Wangye Zhong, Peinan Tu, Linxuan Huang, Tianwang Guan, Gaobo Wu","doi":"10.1002/clc.70235","DOIUrl":"10.1002/clc.70235","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Previous studies have not fully explored the association between air pollutants and heart failure (HF) incidence in cancer participants, nor the role of genetic susceptibility. We aimed to assess air pollutants' impact on HF risk and their joint contribution with genetic susceptibility to incident HF in this group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This study utilized data from the UK Biobank and included 50 923 cancer participants. The relationship between air pollutants and the onset of HF was examined using a Cox proportional hazards model. Furthermore, a polygenic risk score was constructed to evaluate the comprehensive impact of air pollutant exposure, genetic susceptibility, and their interactions on the risk of HF among cancer participants.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The research results show that when comparing individuals in the lowest exposure quartile with those in the highest exposure quartile, the multivariate-adjusted HRs were 1.22 (1.07, 1.38) for PM<sub>10</sub>, 1.16 (1.03, 1.32) for PM<sub>2.5</sub>, 1.20 (1.06, 1.36) for NO<sub>2</sub>, and 1.26 (1.11, 1.43) for NO<sub>x</sub>. For the joint associations, cancer participants with both high genetic risk and elevated air pollutant exposure exhibited the highest risk of HF events. The risk estimates for the incidence of HF were 2.06 (1.52, 2.78) for PM<sub>10,</sub> 1.70 (1.27, 2.27) for PM<sub>2.5</sub> 1.77 (1.32, 2.37) for NO<sub>2</sub>, and 1.61 (1.21, 2.13) for NO<sub>x</sub>.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our findings indicate that long-term combined exposure to multiple air pollutants, including PM<sub>2.5</sub>, PM<sub>10</sub>, NO<sub>2</sub>, and NO<sub>x</sub>, is associated with an elevated risk of new-onset HF in cancer patients, particularly among individuals with a high genetic predisposition to the disease.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.70235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Volkan Kozluca, Irem Muge Akbulut, Turkan Seda Tan, Halil Gulyigit, Mehmet Emre Ozerdem, Tamer Sayin
Background
Heart failure (HF) is still an important disease with high mortality rates worldwide. HF treatment is also difficult due to different phenotypes. Diuretic response (DR) is one of the main differences across these subgroups. Novel urinary parameters are used for DR prediction. We sought to determine whether the MELD score could be used as an additional parameter for predicting the DR.
Methods
Eighty-one consecutive patients diagnosed with decompensated HF between June and October 2020 were included. The second hour urine sodium (UNa) level after the first intravenous diuretic administration and serum parameters were recorded. All patients underwent a comprehensive echocardiographic examination. MELD score derivatives were tested to assess the DR.
Results
A total of 81 patients (mean age: 66.4 ± 13.5; mean ejection fraction: 29.6 ± 12.7%) were divided into two groups according to UNa. 26 (32%) patients had poor DR. MELD Na score was independently associated with DR (OR = 0.88 [−0.21 to (−0.03)]; p = 0.008). Furthermore, MELD Na score was correlated with urinary sodium (r = −0.354; p = 0.004). Daily furosemide dose was higher (237.9 ± 204.7 vs. 129.3 ± 83.5 mg; p = 0.001) and length of hospital stay was longer (15.6 ± 10.8 vs. 8.5 ± 6.1 days; p < 0.01) in the low UNa group.
Conclusion
The MELD score derivative was associated with DR according to urinary sodium and may be used as an additional parameter to predict the DR.
背景：心力衰竭（HF）仍然是世界范围内死亡率高的重要疾病。由于不同的表型，HF治疗也很困难。利尿反应（DR）是这些亚组之间的主要差异之一。新的尿液参数被用于预测DR。我们试图确定MELD评分是否可以作为预测dr的附加参数。方法：纳入2020年6月至10月期间连续诊断为失代偿性HF的81例患者。记录第一次静脉利尿剂给药后第2小时尿钠（UNa）水平及血清参数。所有患者均行全面超声心动图检查。结果：81例患者（平均年龄：66.4±13.5岁，平均射血分数：29.6±12.7%）根据UNa分为两组。MELD Na评分与DR独立相关(OR = 0.88 [-0.21 ~ (-0.03)]；p = 0.008)。此外，MELD Na评分与尿钠相关（r = -0.354; p = 0.004）。每日速尿剂量较高（237.9±204.7 vs 129.3±83.5 mg, p = 0.001），住院时间较长（15.6±10.8 vs 8.5±6.1 d）； p结论：MELD评分衍生物与尿钠相关，可作为预测DR的附加参数。
{"title":"Diuretic Response Prediction With MELD Score in Heart Failure","authors":"Volkan Kozluca, Irem Muge Akbulut, Turkan Seda Tan, Halil Gulyigit, Mehmet Emre Ozerdem, Tamer Sayin","doi":"10.1002/clc.70245","DOIUrl":"10.1002/clc.70245","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Heart failure (HF) is still an important disease with high mortality rates worldwide. HF treatment is also difficult due to different phenotypes. Diuretic response (DR) is one of the main differences across these subgroups. Novel urinary parameters are used for DR prediction. We sought to determine whether the MELD score could be used as an additional parameter for predicting the DR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Eighty-one consecutive patients diagnosed with decompensated HF between June and October 2020 were included. The second hour urine sodium (UNa) level after the first intravenous diuretic administration and serum parameters were recorded. All patients underwent a comprehensive echocardiographic examination. MELD score derivatives were tested to assess the DR.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 81 patients (mean age: 66.4 ± 13.5; mean ejection fraction: 29.6 ± 12.7%) were divided into two groups according to UNa. 26 (32%) patients had poor DR. MELD Na score was independently associated with DR (OR = 0.88 [−0.21 to (−0.03)]; <i>p</i> = 0.008). Furthermore, MELD Na score was correlated with urinary sodium (<i>r</i> = −0.354; <i>p</i> = 0.004). Daily furosemide dose was higher (237.9 ± 204.7 vs. 129.3 ± 83.5 mg; <i>p</i> = 0.001) and length of hospital stay was longer (15.6 ± 10.8 vs. 8.5 ± 6.1 days; <i>p</i> < 0.01) in the low UNa group.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The MELD score derivative was associated with DR according to urinary sodium and may be used as an additional parameter to predict the DR.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12742049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I read with great interest the correspondence “GLP-1 and Dual GLP-1/GIP Receptor Agonists in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Systematic Review and Meta-Analysis” by Ahmed et al. examining the role of GLP-1 receptor agonists (GLP-1 RAs) and dual GLP-1/GIP receptor agonists in patients with heart failure with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF [1]). The authors should be acknowledged for their timely and rigorous synthesis of contemporary randomized data, contributing meaningfully to an important therapeutic gap in HFpEF. Despite these strengths, several limitations inherent to the available evidence deserve emphasis to appropriately contextualize the findings.
First, although all included studies were randomized, many HFpEF outcomes were obtained from post-hoc or secondary analyses of trials mainly designed for obesity, diabetes, or broad cardiovascular risk reduction (e.g., SELECT, FLOW, and EXSCEL). Such analyses are informative but are not well powered for HFpEF-specific endpoints and may be impacted by variations in heart-failure diagnosis and adjudication, thereby limiting causal inference despite randomization [2].
Second, care should be taken when interpreting the lack of a statistically significant effect on cardiovascular or all-cause mortality. The pooled analysis appears underpowered to identify mortality differences, given relatively short follow-up periods and low absolute numbers of deaths in several contributing trials, including SUMMIT. In HFpEF, mortality benefits often require longer follow-up and larger event numbers to become apparent [3, 4].
Third, the generalizability of these findings is limited by the obesity dominant nature of the study populations, with mean body-mass indices consistently above 34 kg/m². Since HFpEF is a heterogeneous syndrome, the observed benefits likely apply mainly to obesity-related or metabolically driven HFpEF. However, extrapolation to lean or non-metabolic HFpEF phenotypes should be undertaken cautiously [5, 6].
In summary, this meta-analysis provides valuable evidence that incretin-based therapies may be a promising adjunctive strategy for selected patients with HFpEF, especially those with obesity and metabolic dysfunction. However, the above limitations highlight the need for prospective, HFpEF-specific randomized trials with broader follow-up and diverse phenotypic representation to clarify the role of these agents across the HFpEF spectrum.
The author received no specific funding for this work.
The author has nothing to report.
The author declares no conflicts of interest.
No new data was created or generated in this work.
{"title":"Critical Evaluation of “GLP-1 and Dual GLP-1/GIP Receptor Agonists in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Systematic Review and Meta-Analysis”","authors":"Zubaida Bibi","doi":"10.1002/clc.70249","DOIUrl":"10.1002/clc.70249","url":null,"abstract":"<p>I read with great interest the correspondence “GLP-1 and Dual GLP-1/GIP Receptor Agonists in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Systematic Review and Meta-Analysis” by Ahmed et al. examining the role of GLP-1 receptor agonists (GLP-1 RAs) and dual GLP-1/GIP receptor agonists in patients with heart failure with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF [<span>1</span>]). The authors should be acknowledged for their timely and rigorous synthesis of contemporary randomized data, contributing meaningfully to an important therapeutic gap in HFpEF. Despite these strengths, several limitations inherent to the available evidence deserve emphasis to appropriately contextualize the findings.</p><p>First, although all included studies were randomized, many HFpEF outcomes were obtained from post-hoc or secondary analyses of trials mainly designed for obesity, diabetes, or broad cardiovascular risk reduction (e.g., SELECT, FLOW, and EXSCEL). Such analyses are informative but are not well powered for HFpEF-specific endpoints and may be impacted by variations in heart-failure diagnosis and adjudication, thereby limiting causal inference despite randomization [<span>2</span>].</p><p>Second, care should be taken when interpreting the lack of a statistically significant effect on cardiovascular or all-cause mortality. The pooled analysis appears underpowered to identify mortality differences, given relatively short follow-up periods and low absolute numbers of deaths in several contributing trials, including SUMMIT. In HFpEF, mortality benefits often require longer follow-up and larger event numbers to become apparent [<span>3, 4</span>].</p><p>Third, the generalizability of these findings is limited by the obesity dominant nature of the study populations, with mean body-mass indices consistently above 34 kg/m². Since HFpEF is a heterogeneous syndrome, the observed benefits likely apply mainly to obesity-related or metabolically driven HFpEF. However, extrapolation to lean or non-metabolic HFpEF phenotypes should be undertaken cautiously [<span>5, 6</span>].</p><p>In summary, this meta-analysis provides valuable evidence that incretin-based therapies may be a promising adjunctive strategy for selected patients with HFpEF, especially those with obesity and metabolic dysfunction. However, the above limitations highlight the need for prospective, HFpEF-specific randomized trials with broader follow-up and diverse phenotypic representation to clarify the role of these agents across the HFpEF spectrum.</p><p>The author received no specific funding for this work.</p><p>The author has nothing to report.</p><p>The author declares no conflicts of interest.</p><p>No new data was created or generated in this work.</p>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12741511/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>Ivabradine demonstrates notable efficacy in ameliorating clinical outcomes among patients with chronic systolic heart failure, yet its therapeutic implications in the context of acute heart failure remain a subject of contention. In a comparative analysis conducted by Tsai et al. the investigators evaluated clinical ramifications following the initiation of ivabradine in individuals experiencing acute decompensated heart failure, juxtaposed with a cohort of contemporaneously matched counterparts devoid of ivabradine exposure [<span>1</span>]. The study discerned a consistent and positive therapeutic impact of ivabradine, with no discernible divergences of statistical significance observed between the groups treated with ivabradine and those without, particularly concerning incidences of heart failure-related hospitalization and cardiovascular mortality.</p><p>Ivabradine finds clinical indication in individuals exhibiting intolerance to beta-blockers, an established cornerstone therapy pivotal for effecting reverse remodeling and fostering enhanced clinical outcomes in patients with systolic heart failure [<span>2</span>]. The authors' investigation revealed a substantial proportion of participants characterized by relatively preserved blood pressure and an absence of significant bradycardia, with approximately 30% of them concurrently administered calcium blockers [<span>1</span>]. It is imperative for the authors to elucidate the reasons underpinning beta-blocker intolerance within their study cohort. Of note, acute heart failure does not categorically mandate the complete cessation of beta-blocker therapy [<span>3</span>].</p><p>The therapeutic potential of ivabradine extends beyond mere symptom alleviation, encompassing the facilitation of optimal hemodynamics conducive to the judicious titration of beta-blockers [<span>4</span>]. The study lacks clarification regarding whether the authors undertook a robust up-titration of heart failure medications subsequent to the initiation of ivabradine [<span>1</span>]. This aggressive approach could potentially yield indirect improvements in clinical outcomes by virtue of ivabradine's stabilizing influence on hemodynamics.</p><p>The determination of an optimal heart rate in individuals grappling with acute heart failure remains an unresolved quandary. A suboptimal reduction in heart rate may inadvertently diminish cardiac output and exacerbate hemodynamic instability. To address this concern, our team advocates a novel methodology for heart rate optimization. Specifically, we propose the minimization of overlap between the E-wave and A-wave in Doppler echocardiographic trans-mitral flow during ivabradine therapy as a strategy to maximize cardiac output [<span>4</span>]. The authors should explicate their rationale for selecting the target heart rate in their study, shedding light on the considerations that informed this crucial parameter.</p><p>The authors have nothing to report.</p><p>The authors de
{"title":"Optimal Heart Rate Modulation Therapy Using Ivabradine in Individuals With Acute Heart Failure","authors":"Naoya Kataoka, Teruhiko Imamura","doi":"10.1002/clc.70248","DOIUrl":"10.1002/clc.70248","url":null,"abstract":"<p>Ivabradine demonstrates notable efficacy in ameliorating clinical outcomes among patients with chronic systolic heart failure, yet its therapeutic implications in the context of acute heart failure remain a subject of contention. In a comparative analysis conducted by Tsai et al. the investigators evaluated clinical ramifications following the initiation of ivabradine in individuals experiencing acute decompensated heart failure, juxtaposed with a cohort of contemporaneously matched counterparts devoid of ivabradine exposure [<span>1</span>]. The study discerned a consistent and positive therapeutic impact of ivabradine, with no discernible divergences of statistical significance observed between the groups treated with ivabradine and those without, particularly concerning incidences of heart failure-related hospitalization and cardiovascular mortality.</p><p>Ivabradine finds clinical indication in individuals exhibiting intolerance to beta-blockers, an established cornerstone therapy pivotal for effecting reverse remodeling and fostering enhanced clinical outcomes in patients with systolic heart failure [<span>2</span>]. The authors' investigation revealed a substantial proportion of participants characterized by relatively preserved blood pressure and an absence of significant bradycardia, with approximately 30% of them concurrently administered calcium blockers [<span>1</span>]. It is imperative for the authors to elucidate the reasons underpinning beta-blocker intolerance within their study cohort. Of note, acute heart failure does not categorically mandate the complete cessation of beta-blocker therapy [<span>3</span>].</p><p>The therapeutic potential of ivabradine extends beyond mere symptom alleviation, encompassing the facilitation of optimal hemodynamics conducive to the judicious titration of beta-blockers [<span>4</span>]. The study lacks clarification regarding whether the authors undertook a robust up-titration of heart failure medications subsequent to the initiation of ivabradine [<span>1</span>]. This aggressive approach could potentially yield indirect improvements in clinical outcomes by virtue of ivabradine's stabilizing influence on hemodynamics.</p><p>The determination of an optimal heart rate in individuals grappling with acute heart failure remains an unresolved quandary. A suboptimal reduction in heart rate may inadvertently diminish cardiac output and exacerbate hemodynamic instability. To address this concern, our team advocates a novel methodology for heart rate optimization. Specifically, we propose the minimization of overlap between the E-wave and A-wave in Doppler echocardiographic trans-mitral flow during ivabradine therapy as a strategy to maximize cardiac output [<span>4</span>]. The authors should explicate their rationale for selecting the target heart rate in their study, shedding light on the considerations that informed this crucial parameter.</p><p>The authors have nothing to report.</p><p>The authors de","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12741481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sheng Xu, Yaodong Guo, Hao Xin, Shanshan Zhuo, Yang Zhao, Yanna Jiang, Yuanqi Huang, Chunyan Huang, Tao Chen, Qi Chen, Qianru Zhao, Dan Wang, Xiao Liu, Zhiwei Yan
Background and Objective
Exercise mediates cardiac adaptation in a dose-dependent manner, and each sport has unique demands on the cardiovascular system. Given the long-term effects of key confounding variables such as age, sex, and exercise dose, knowledge gained from one sport cannot be generalized to all sports. Therefore, it is necessary to explore the potential dose-response relationships between different sports and cardiovascular adaptations on a broader time scale, and to explore the regulatory role of key factors such as age and sex.
Methods
The China-ACE study will be a prospective longitudinal cohort study involving approximately 500 elite athletes of different sexes, ages, and sports (rowing, canoeing, cycling, triathlon, weightlifting, wrestling, judo, swimming, basketball, badminton, boxing, and beach volleyball) from three provincial sports centers. All athletes will undergo two screenings within 1 year, during which their exercise load and dose will be recorded via quantitative and semi-quantitative methods. The screening will include measuring cardiovascular function, body composition, electrocardiogram, heart rate variability, echocardiography, cardiopulmonary function, circulating biochemical markers, sex hormones, lower limb muscle function, and physical performance.
Conclusion
The China-ACE study will elucidate the potential dose-response relationship between exercise load and cardiovascular adaptation, cardiopulmonary function, skeletal muscle function, and physical performance by continuously tracking the exercise load and exercise dose of athletes in different sports and exploring the potential role of age and sex in these adaptations. This may inform individualized training and cardiovascular prevention for athletes and extend the current understanding of sports cardiology.
{"title":"China Elite Athletes Cardiovascular hEath (China-ACE) Study: A Protocol for a Multicenter Prospective Cohort","authors":"Sheng Xu, Yaodong Guo, Hao Xin, Shanshan Zhuo, Yang Zhao, Yanna Jiang, Yuanqi Huang, Chunyan Huang, Tao Chen, Qi Chen, Qianru Zhao, Dan Wang, Xiao Liu, Zhiwei Yan","doi":"10.1002/clc.70241","DOIUrl":"10.1002/clc.70241","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Objective</h3>\u0000 \u0000 <p>Exercise mediates cardiac adaptation in a dose-dependent manner, and each sport has unique demands on the cardiovascular system. Given the long-term effects of key confounding variables such as age, sex, and exercise dose, knowledge gained from one sport cannot be generalized to all sports. Therefore, it is necessary to explore the potential dose-response relationships between different sports and cardiovascular adaptations on a broader time scale, and to explore the regulatory role of key factors such as age and sex.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The China-ACE study will be a prospective longitudinal cohort study involving approximately 500 elite athletes of different sexes, ages, and sports (rowing, canoeing, cycling, triathlon, weightlifting, wrestling, judo, swimming, basketball, badminton, boxing, and beach volleyball) from three provincial sports centers. All athletes will undergo two screenings within 1 year, during which their exercise load and dose will be recorded via quantitative and semi-quantitative methods. The screening will include measuring cardiovascular function, body composition, electrocardiogram, heart rate variability, echocardiography, cardiopulmonary function, circulating biochemical markers, sex hormones, lower limb muscle function, and physical performance.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The China-ACE study will elucidate the potential dose-response relationship between exercise load and cardiovascular adaptation, cardiopulmonary function, skeletal muscle function, and physical performance by continuously tracking the exercise load and exercise dose of athletes in different sports and exploring the potential role of age and sex in these adaptations. This may inform individualized training and cardiovascular prevention for athletes and extend the current understanding of sports cardiology.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12723624/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145809719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medicaid Expansion (ME) under the Affordable Care Act sought to improve health access though not all states expanded Medicaid. Our goal is to examine whether ME impacts 30-day post-discharge mortality rates for heart failure (HF) hospitalizations.
Methods
We constructed a data set incorporating 30-day HF mortality and hospital service area (HSA) characteristics using five sources: (1) Centers for Medicare and Medicaid Services, (2) Medicaid Budget and Expenditure System, (3) US Census Bureau, (4) Dartmouth Atlas of Healthcare, (5) Kaiser Family Foundation. We categorized states as expanding Medicaid by 2014 or not expanding until 2020, excluding five states that expanded between 2014 and 2020. A difference-in-difference (DID) model, adjusted for hospital and HSA factors, was used for analysis.
Results
Among 3839 hospitals, 52% were in ME states. Before 2014, 30-day mortality rates were higher in non-ME state hospitals than in ME state hospitals (11.6% vs. 11.4%; p < 0.001). After 2014, rates increased in non-ME state hospitals (change = 0.11%, 95% CI: 0.04% to 0.18%) but remained unchanged in ME state hospitals (change = 0.01%, 95% CI: –0.07% to 0.08%). The adjusted DID analysis showed a significant disparity in trends between ME and non-ME states (adjusted DID: −0.11%, 95% CI: –0.21% to –0.02%; p = 0.02). A dose-response relationship revealed that each increase of 10,000 new Medicaid enrollees was associated with 0.002% (95% CI: –0.003 to –0.001; p < 0.001) reduced 30-day HF mortality.
Conclusions
Hospitals in ME states maintained stable mortality rates, contrasting with increases in non-ME states, suggesting that improved healthcare access through ME contributed to better outcomes.
{"title":"Medicaid Expansion and 30-Day Mortality After Heart Failure Hospitalization: A Nationwide Study","authors":"Julianne Ghiorzi, Julie D. Sill, Rehan Qayyum","doi":"10.1002/clc.70240","DOIUrl":"10.1002/clc.70240","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Medicaid Expansion (ME) under the Affordable Care Act sought to improve health access though not all states expanded Medicaid. Our goal is to examine whether ME impacts 30-day post-discharge mortality rates for heart failure (HF) hospitalizations.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We constructed a data set incorporating 30-day HF mortality and hospital service area (HSA) characteristics using five sources: (1) Centers for Medicare and Medicaid Services, (2) Medicaid Budget and Expenditure System, (3) US Census Bureau, (4) Dartmouth Atlas of Healthcare, (5) Kaiser Family Foundation. We categorized states as expanding Medicaid by 2014 or not expanding until 2020, excluding five states that expanded between 2014 and 2020. A difference-in-difference (DID) model, adjusted for hospital and HSA factors, was used for analysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Among 3839 hospitals, 52% were in ME states. Before 2014, 30-day mortality rates were higher in non-ME state hospitals than in ME state hospitals (11.6% vs. 11.4%; <i>p</i> < 0.001). After 2014, rates increased in non-ME state hospitals (change = 0.11%, 95% CI: 0.04% to 0.18%) but remained unchanged in ME state hospitals (change = 0.01%, 95% CI: –0.07% to 0.08%). The adjusted DID analysis showed a significant disparity in trends between ME and non-ME states (adjusted DID: −0.11%, 95% CI: –0.21% to –0.02%; <i>p</i> = 0.02). A dose-response relationship revealed that each increase of 10,000 new Medicaid enrollees was associated with 0.002% (95% CI: –0.003 to –0.001; <i>p</i> < 0.001) reduced 30-day HF mortality.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Hospitals in ME states maintained stable mortality rates, contrasting with increases in non-ME states, suggesting that improved healthcare access through ME contributed to better outcomes.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12717469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145793084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I read with great interest the article by Meunier et al. reporting the 3-year outcomes of a stent-less strategy (SLS) that used scoring balloon lesion preparation followed by paclitaxel-coated balloon angioplasty (DCB), with a bailout drug-eluting stent (DES) only when required [1]. The prospective, all-comers design and the long follow-up provide valuable real-world data on this evolving “leave-nothing-behind” approach, extending earlier 1-year evidence from the same group [2].
The authors are to be commended for proposing a practical algorithm in routine care and for introducing the “metal index” as a simple way to capture stent burden. The high proportion of patients eligible for SLS (≈85%) and the very low 3-year target lesion revascularization (TLR) rate in the DCB-only group (2.6%) are encouraging findings.
Some points, however, deserve clarification. First, patients in the bailout-DES group had longer lesions and more complex anatomy (multivessel disease, chronic total occlusion, bifurcation lesions). These are well-known predictors of adverse outcomes, and residual confounding may explain their higher TLR rates. Second, the main analysis relied on unadjusted Kaplan–Meier curves; a multivariable Cox model adjusting for lesion length, clinical presentation, left ventricular function, and lesion type would help clarify whether the metal index or SLS independently predicts TLR. Third, antiplatelet therapy was heterogeneous and incompletely described; given that prolonged dual therapy was common even in DCB patients, reporting both ischemic and bleeding outcomes is essential. Finally, ~8% of patients were lost to follow-up; sensitivity analyses would increase confidence in the results.
Comparable long-term results with “less DES” strategies have been described in chronic total occlusion cohorts, supporting the concept of minimizing stent burden when feasible [3].
In summary, the SLS algorithm is promising, safe, and associated with low 3-year TLR rates. Larger multicenter randomized trials with standardized lesion preparation and prespecified bleeding endpoints are needed to confirm these findings.
{"title":"Letter to the Editor: Long-Term Effectiveness of a Stent-Less Strategy With Drug-Coated Balloon in Coronary Artery Disease: 3-Year Follow-Up","authors":"Hamza Rashid","doi":"10.1002/clc.70236","DOIUrl":"10.1002/clc.70236","url":null,"abstract":"<p>I read with great interest the article by Meunier et al. reporting the 3-year outcomes of a stent-less strategy (SLS) that used scoring balloon lesion preparation followed by paclitaxel-coated balloon angioplasty (DCB), with a bailout drug-eluting stent (DES) only when required [<span>1</span>]. The prospective, all-comers design and the long follow-up provide valuable real-world data on this evolving “leave-nothing-behind” approach, extending earlier 1-year evidence from the same group [<span>2</span>].</p><p>The authors are to be commended for proposing a practical algorithm in routine care and for introducing the “metal index” as a simple way to capture stent burden. The high proportion of patients eligible for SLS (≈85%) and the very low 3-year target lesion revascularization (TLR) rate in the DCB-only group (2.6%) are encouraging findings.</p><p>Some points, however, deserve clarification. First, patients in the bailout-DES group had longer lesions and more complex anatomy (multivessel disease, chronic total occlusion, bifurcation lesions). These are well-known predictors of adverse outcomes, and residual confounding may explain their higher TLR rates. Second, the main analysis relied on unadjusted Kaplan–Meier curves; a multivariable Cox model adjusting for lesion length, clinical presentation, left ventricular function, and lesion type would help clarify whether the metal index or SLS independently predicts TLR. Third, antiplatelet therapy was heterogeneous and incompletely described; given that prolonged dual therapy was common even in DCB patients, reporting both ischemic and bleeding outcomes is essential. Finally, ~8% of patients were lost to follow-up; sensitivity analyses would increase confidence in the results.</p><p>Comparable long-term results with “less DES” strategies have been described in chronic total occlusion cohorts, supporting the concept of minimizing stent burden when feasible [<span>3</span>].</p><p>In summary, the SLS algorithm is promising, safe, and associated with low 3-year TLR rates. Larger multicenter randomized trials with standardized lesion preparation and prespecified bleeding endpoints are needed to confirm these findings.</p><p>Sincerely,</p><p>The author has nothing to report.</p>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12715587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>We read with great interest the observational study by Meunier et al. evaluating a stent-less strategy using drug-coated balloons (DCB) in coronary artery disease (CAD) [<span>1</span>]. The present single-center observational study evaluating the long-term effectiveness of a stent-less strategy with DCB angioplasty in CAD undoubtedly adds to the literature regarding contemporary percutaneous coronary intervention (PCI) [<span>1</span>]. Nevertheless, methodological limitations remain that could impact the reliability and generalizability of the findings, which were not fully addressed in the manuscript. Most critically, the absence of randomization and reliance on operator discretion for allocating stent-less versus bailout drug-eluting stent (DES) strategies raises concerns regarding selection bias and confounding. Randomized controlled trials (RCTs) such as BASKET-SMALL 2 and PICCOLETO II have demonstrated the importance of random allocation in minimizing selection bias and ensuring comparability across intervention arms, thereby providing more robust estimates of relative effectiveness between DCB and DES strategies [<span>2, 3</span>]. Employing a multicenter randomized design, as recommended in recent consensus statements, would also enhance external validity and facilitate application to broader clinical practice [<span>4, 5</span>]. Another key limitation relates to the lack of core laboratory adjudication and systematic use of intravascular imaging for lesion assessment and procedural outcome validation. RCTs and multicenter DCB registries increasingly mandate independent angiographic review and intravascular imaging such as OCT or IVUS to rigorously evaluate lesion morphology, residual stenosis, and dissection severity [<span>4</span>]. Studies have shown that core lab adjudication substantially reduces inter-observer variability and measurement bias, thereby improving endpoint ascertainment and clinical trial integrity [<span>5, 6</span>]. Furthermore, the manuscript provides insufficient detail regarding standardization and stratification of concomitant antiplatelet therapy, which may have influenced outcome measurements such as major adverse cardiac events and bleeding rates. The heterogeneity in antiplatelet regimens was noted but not adjusted for in the primary analyses. Recent RCTs including TWILIGHT and TICO have demonstrated that clearly defined, protocolized antiplatelet regimens and stratified reporting are essential for interpreting ischemic and bleeding risk profiles in PCI populations [<span>7, 8</span>]. To address these limitations, future studies should prioritize multicenter RCT designs with independent core laboratory angiographic adjudication and routine use of contemporary intravascular imaging. Endpoints must be standardized according to consensus definitions, with adjustment for confounders including antiplatelet therapy regimens, in line with recommendations from leading international PCI trials and expert stat
{"title":"Advancing the Design of Observational Studies in Drug-Coated Balloon Angioplasty: Bridging Practice With Evidence-Based Standards","authors":"Kunal Mahajan, Jaibharat Sharma, Surender Himral, Vivek Rana, Shekhar Vohra","doi":"10.1002/clc.70238","DOIUrl":"10.1002/clc.70238","url":null,"abstract":"<p>We read with great interest the observational study by Meunier et al. evaluating a stent-less strategy using drug-coated balloons (DCB) in coronary artery disease (CAD) [<span>1</span>]. The present single-center observational study evaluating the long-term effectiveness of a stent-less strategy with DCB angioplasty in CAD undoubtedly adds to the literature regarding contemporary percutaneous coronary intervention (PCI) [<span>1</span>]. Nevertheless, methodological limitations remain that could impact the reliability and generalizability of the findings, which were not fully addressed in the manuscript. Most critically, the absence of randomization and reliance on operator discretion for allocating stent-less versus bailout drug-eluting stent (DES) strategies raises concerns regarding selection bias and confounding. Randomized controlled trials (RCTs) such as BASKET-SMALL 2 and PICCOLETO II have demonstrated the importance of random allocation in minimizing selection bias and ensuring comparability across intervention arms, thereby providing more robust estimates of relative effectiveness between DCB and DES strategies [<span>2, 3</span>]. Employing a multicenter randomized design, as recommended in recent consensus statements, would also enhance external validity and facilitate application to broader clinical practice [<span>4, 5</span>]. Another key limitation relates to the lack of core laboratory adjudication and systematic use of intravascular imaging for lesion assessment and procedural outcome validation. RCTs and multicenter DCB registries increasingly mandate independent angiographic review and intravascular imaging such as OCT or IVUS to rigorously evaluate lesion morphology, residual stenosis, and dissection severity [<span>4</span>]. Studies have shown that core lab adjudication substantially reduces inter-observer variability and measurement bias, thereby improving endpoint ascertainment and clinical trial integrity [<span>5, 6</span>]. Furthermore, the manuscript provides insufficient detail regarding standardization and stratification of concomitant antiplatelet therapy, which may have influenced outcome measurements such as major adverse cardiac events and bleeding rates. The heterogeneity in antiplatelet regimens was noted but not adjusted for in the primary analyses. Recent RCTs including TWILIGHT and TICO have demonstrated that clearly defined, protocolized antiplatelet regimens and stratified reporting are essential for interpreting ischemic and bleeding risk profiles in PCI populations [<span>7, 8</span>]. To address these limitations, future studies should prioritize multicenter RCT designs with independent core laboratory angiographic adjudication and routine use of contemporary intravascular imaging. Endpoints must be standardized according to consensus definitions, with adjustment for confounders including antiplatelet therapy regimens, in line with recommendations from leading international PCI trials and expert stat","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12703820/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p>Sudden cardiac death (SCD) remains an unresolved issue even in the contemporary era of implantable cardioverter-defibrillator therapy (ICD), largely because of the difficulty in accurate risk prediction. The present study sought to identify clinical features of SCD victims with non-ischemic myocardial fibrosis [<span>1</span>]. The authors found that fragmented QRS complexes or a history of transient loss of consciousness (TLOC) were major characteristics of such patients. While this is an important contribution, several concerns arise.</p><p>Our group previously reported that the presence of a J-wave, reflecting repolarization abnormalities—similar to QT prolongation and T-wave inversion—was associated with ventricular fibrillation as the terminal electrocardiographic event [<span>2</span>]. Conversely, a fragmented QRS represents an abnormality of depolarization rather than repolarization. In the present study, were the terminal electrocardiograms (ECGs) of SCD victims with fragmented QRS more commonly asystole or pulseless electrical activity rather than ventricular fibrillation? How do the authors interpret the relationship between different types of polarization abnormalities and the final rhythm observed? Clarifying this relationship would be crucial for risk stratification and further pathophysiological understanding.</p><p>Another concern lies in the limited availability of clinical data. Only 28% of victims had ECGs available, and merely 11% had both ECG and medical history [<span>1</span>]. Such a restricted dataset raises the possibility of selection bias and questions the generalizability of the findings. Moreover, TLOC, although frequent, is not necessarily of cardiac origin. Without detailed adjudication, including differentiation from neurological or reflex-mediated causes, the specificity of this marker as an indicator of impending SCD remains uncertain.</p><p>The pathophysiological link between fragmented QRS and myocardial fibrosis was also insufficiently addressed [<span>1</span>]. Prior studies have demonstrated that fragmented QRS may reflect impaired conduction due to localized scar or interstitial fibrosis, and that it correlates with abnormal global longitudinal strain [<span>3</span>]. Moreover, fragmented QRS is also associated with arrhythmic events in other entities such as Brugada syndrome. However, whether fragmented QRS in the setting of primary myocardial fibrosis is merely a surrogate of structural remodeling or a direct arrhythmogenic substrate remains unanswered.</p><p>It should also be emphasized that the features highlighted in this study—fragmented QRS and TLOC—are neither novel nor specific to primary myocardial fibrosis. Given that ICD implantation cannot be justified in all individuals with these findings alone, we believe these markers should be integrated into a broader, multi-modal risk stratification strategy. Cardiac magnetic resonance imaging to detect diffuse or patchy fibrosis, genetic testing f
{"title":"Detailed Association Between Electrocardiogram Abnormality and Primary Myocardial Fibrosis","authors":"Yu Nomoto, Naoya Kataoka, Teruhiko Imamura","doi":"10.1002/clc.70237","DOIUrl":"10.1002/clc.70237","url":null,"abstract":"<p>Sudden cardiac death (SCD) remains an unresolved issue even in the contemporary era of implantable cardioverter-defibrillator therapy (ICD), largely because of the difficulty in accurate risk prediction. The present study sought to identify clinical features of SCD victims with non-ischemic myocardial fibrosis [<span>1</span>]. The authors found that fragmented QRS complexes or a history of transient loss of consciousness (TLOC) were major characteristics of such patients. While this is an important contribution, several concerns arise.</p><p>Our group previously reported that the presence of a J-wave, reflecting repolarization abnormalities—similar to QT prolongation and T-wave inversion—was associated with ventricular fibrillation as the terminal electrocardiographic event [<span>2</span>]. Conversely, a fragmented QRS represents an abnormality of depolarization rather than repolarization. In the present study, were the terminal electrocardiograms (ECGs) of SCD victims with fragmented QRS more commonly asystole or pulseless electrical activity rather than ventricular fibrillation? How do the authors interpret the relationship between different types of polarization abnormalities and the final rhythm observed? Clarifying this relationship would be crucial for risk stratification and further pathophysiological understanding.</p><p>Another concern lies in the limited availability of clinical data. Only 28% of victims had ECGs available, and merely 11% had both ECG and medical history [<span>1</span>]. Such a restricted dataset raises the possibility of selection bias and questions the generalizability of the findings. Moreover, TLOC, although frequent, is not necessarily of cardiac origin. Without detailed adjudication, including differentiation from neurological or reflex-mediated causes, the specificity of this marker as an indicator of impending SCD remains uncertain.</p><p>The pathophysiological link between fragmented QRS and myocardial fibrosis was also insufficiently addressed [<span>1</span>]. Prior studies have demonstrated that fragmented QRS may reflect impaired conduction due to localized scar or interstitial fibrosis, and that it correlates with abnormal global longitudinal strain [<span>3</span>]. Moreover, fragmented QRS is also associated with arrhythmic events in other entities such as Brugada syndrome. However, whether fragmented QRS in the setting of primary myocardial fibrosis is merely a surrogate of structural remodeling or a direct arrhythmogenic substrate remains unanswered.</p><p>It should also be emphasized that the features highlighted in this study—fragmented QRS and TLOC—are neither novel nor specific to primary myocardial fibrosis. Given that ICD implantation cannot be justified in all individuals with these findings alone, we believe these markers should be integrated into a broader, multi-modal risk stratification strategy. Cardiac magnetic resonance imaging to detect diffuse or patchy fibrosis, genetic testing f","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12703648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mushood Ahmed, Muhammad Burhan, Aimen Shafiq, Tallal Mushtaq Hashmi, Raheel Ahmed, Marat Fudim, Robert J. Mentz, Gregg C. Fonarow
This comprehensive meta-analysis reveals that GLP-1 and dual GLP-1/GIP receptor agonists are associated with reduced risk of composite cardiovascular endpoints and worsening heart failure events. However, no statistically significant differences were observed regarding all-cause or cardiovascular mortality.
{"title":"GLP-1 and Dual GLP-1/GIP Receptor Agonists in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Systematic Review and Meta-Analysis","authors":"Mushood Ahmed, Muhammad Burhan, Aimen Shafiq, Tallal Mushtaq Hashmi, Raheel Ahmed, Marat Fudim, Robert J. Mentz, Gregg C. Fonarow","doi":"10.1002/clc.70234","DOIUrl":"https://doi.org/10.1002/clc.70234","url":null,"abstract":"<p>This comprehensive meta-analysis reveals that GLP-1 and dual GLP-1/GIP receptor agonists are associated with reduced risk of composite cardiovascular endpoints and worsening heart failure events. However, no statistically significant differences were observed regarding all-cause or cardiovascular mortality.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"48 12","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.70234","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145739827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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