C1q/tumor necrosis factor-related protein 12 (CTRP12) plays a protective role in coronary artery disease (CAD) by reducing vascular inflammation. Whether CTRP12 could predict the occurrence of CAD and in-stent restenosis (ISR) occurrence after percutaneous coronary intervention (PCI) treatment remains unknown.
Methods
This retrospective cohort study included patients with CAD who underwent PCI and had serum samples collected at baseline, 24 h, and 72 h post-PCI. The Gensini score was used to assess the severity of coronary artery stenosis. Serum CTRP12 levels were measured using an ELISA kit. Follow-up evaluation of ISR was performed using coronary angiography.
Results
Serum CTRP12 levels were significantly lower in CAD patients than healthy controls (p < 0.001). A negative correlation was found between CTRP12 levels and both the Gensini score (r = −0.37, p < 0.001) and hs-CRP levels (r = −0.43, p < 0.001). Dynamic analysis revealed a significant reduction in CTRP12 levels 24 h post-PCI, with partial recovery observed at 72 h, although levels remained lower than baseline. Patients with ISR consistently demonstrated lower CTRP12 levels than those without ISR (NISR) at all time points. Receiver operating characteristic curve analysis indicated that CTRP12 levels at 24 h post-PCI exhibited the highest predictive accuracy for ISR occurrence.
Conclusion
Serum CTRP12 level may serve as a potential biomarker for diagnosing CAD and predicting ISR occurrence, with significant correlations to disease severity and dynamic changes after PCI.
{"title":"Changes of Serum CTRP12 in Patients With Coronary Artery Disease After the Treatment of Percutaneous Coronary Intervention and Its Relationship With In-Stent Restenosis","authors":"Botao Zhao, Yuchao Shen","doi":"10.1002/clc.70233","DOIUrl":"10.1002/clc.70233","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>C1q/tumor necrosis factor-related protein 12 (CTRP12) plays a protective role in coronary artery disease (CAD) by reducing vascular inflammation. Whether CTRP12 could predict the occurrence of CAD and in-stent restenosis (ISR) occurrence after percutaneous coronary intervention (PCI) treatment remains unknown.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This retrospective cohort study included patients with CAD who underwent PCI and had serum samples collected at baseline, 24 h, and 72 h post-PCI. The Gensini score was used to assess the severity of coronary artery stenosis. Serum CTRP12 levels were measured using an ELISA kit. Follow-up evaluation of ISR was performed using coronary angiography.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Serum CTRP12 levels were significantly lower in CAD patients than healthy controls (<i>p</i> < 0.001). A negative correlation was found between CTRP12 levels and both the Gensini score (r = −0.37, <i>p</i> < 0.001) and hs-CRP levels (r = −0.43, <i>p</i> < 0.001). Dynamic analysis revealed a significant reduction in CTRP12 levels 24 h post-PCI, with partial recovery observed at 72 h, although levels remained lower than baseline. Patients with ISR consistently demonstrated lower CTRP12 levels than those without ISR (NISR) at all time points. Receiver operating characteristic curve analysis indicated that CTRP12 levels at 24 h post-PCI exhibited the highest predictive accuracy for ISR occurrence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Serum CTRP12 level may serve as a potential biomarker for diagnosing CAD and predicting ISR occurrence, with significant correlations to disease severity and dynamic changes after PCI.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.70233","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951009","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>Zhang et al. report a statistically robust association between the CYP3A5 rs776746 polymorphism and ticagrelor-related dyspnea in patients with acute coronary syndrome, proposing this variant as a candidate biomarker for individualized antiplatelet therapy [<span>1</span>]. While the genetic signal itself is convincing, the broader clinical interpretation of this finding warrants a more cautious and contextualized discussion.</p><p>A central issue is the implicit assumption that ticagrelor-related dyspnea represents an adverse effect that necessarily undermines treatment success. Accumulating evidence suggests that ticagrelor-induced dyspnea is frequently mild, transient, and poorly correlated with objective respiratory dysfunction, while ticagrelor continuation is often associated with superior ischemic protection [<span>2</span>]. Framing dyspnea primarily as a safety liability may therefore overemphasize tolerability at the expense of long-term cardiovascular benefit.</p><p>Relatedly, the manuscript risks conflating biological association with clinical actionability. Identification of a genotype linked to dyspnea does not automatically justify preemptive drug switching, particularly in the absence of evidence that genotype-guided de-escalation preserves ischemic efficacy. Prior pharmacogenetic experiences in antiplatelet therapy have shown that altering treatment based solely on surrogate markers may inadvertently increase thrombotic risk [<span>3</span>].</p><p>Another underexplored dimension is the competing mechanistic interpretation of dyspnea as a pharmacodynamic signature rather than a toxic effect. Ticagrelor-induced increases in adenosine signaling have been associated not only with dyspnea but also with cardioprotective and anti-inflammatory effects. From this perspective, dyspnea may identify patients with heightened biological responsiveness rather than impaired drug tolerance [<span>4</span>]. Genetic stratification that selectively removes such patients from ticagrelor therapy could paradoxically exclude those deriving the greatest benefit.</p><p>Finally, the proposal of routine CYP3A5 genotyping raises broader questions about feasibility and proportionality. Current guidelines emphasize simplicity, timeliness, and net clinical benefit in acute coronary syndrome management. Introducing genetic testing for a largely non-life-threatening symptom risks increasing complexity without clear outcome-level gains [<span>5</span>]. Precision medicine should refine decision-making, not fragment it.</p><p>In this context, the findings by Zhang et al. are best viewed as hypothesis-generating, highlighting the biological heterogeneity of ticagrelor response rather than defining an immediate clinical algorithm. Future studies should focus on whether dyspnea- or genotype-guided strategies meaningfully improve patient-centered outcomes while preserving ischemic protection.</p><p>The authors declare no conflicts of interest.</p><p>Data sharing i
{"title":"Is Ticagrelor-Related Dyspnea a Liability or a Biomarker of Response?","authors":"Abdülmelik Birgün, Abdullah Sarıhan, Macit Kalçık","doi":"10.1002/clc.70258","DOIUrl":"10.1002/clc.70258","url":null,"abstract":"<p>Zhang et al. report a statistically robust association between the CYP3A5 rs776746 polymorphism and ticagrelor-related dyspnea in patients with acute coronary syndrome, proposing this variant as a candidate biomarker for individualized antiplatelet therapy [<span>1</span>]. While the genetic signal itself is convincing, the broader clinical interpretation of this finding warrants a more cautious and contextualized discussion.</p><p>A central issue is the implicit assumption that ticagrelor-related dyspnea represents an adverse effect that necessarily undermines treatment success. Accumulating evidence suggests that ticagrelor-induced dyspnea is frequently mild, transient, and poorly correlated with objective respiratory dysfunction, while ticagrelor continuation is often associated with superior ischemic protection [<span>2</span>]. Framing dyspnea primarily as a safety liability may therefore overemphasize tolerability at the expense of long-term cardiovascular benefit.</p><p>Relatedly, the manuscript risks conflating biological association with clinical actionability. Identification of a genotype linked to dyspnea does not automatically justify preemptive drug switching, particularly in the absence of evidence that genotype-guided de-escalation preserves ischemic efficacy. Prior pharmacogenetic experiences in antiplatelet therapy have shown that altering treatment based solely on surrogate markers may inadvertently increase thrombotic risk [<span>3</span>].</p><p>Another underexplored dimension is the competing mechanistic interpretation of dyspnea as a pharmacodynamic signature rather than a toxic effect. Ticagrelor-induced increases in adenosine signaling have been associated not only with dyspnea but also with cardioprotective and anti-inflammatory effects. From this perspective, dyspnea may identify patients with heightened biological responsiveness rather than impaired drug tolerance [<span>4</span>]. Genetic stratification that selectively removes such patients from ticagrelor therapy could paradoxically exclude those deriving the greatest benefit.</p><p>Finally, the proposal of routine CYP3A5 genotyping raises broader questions about feasibility and proportionality. Current guidelines emphasize simplicity, timeliness, and net clinical benefit in acute coronary syndrome management. Introducing genetic testing for a largely non-life-threatening symptom risks increasing complexity without clear outcome-level gains [<span>5</span>]. Precision medicine should refine decision-making, not fragment it.</p><p>In this context, the findings by Zhang et al. are best viewed as hypothesis-generating, highlighting the biological heterogeneity of ticagrelor response rather than defining an immediate clinical algorithm. Future studies should focus on whether dyspnea- or genotype-guided strategies meaningfully improve patient-centered outcomes while preserving ischemic protection.</p><p>The authors declare no conflicts of interest.</p><p>Data sharing i","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.70258","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145950956","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}
Patients with acute coronary syndrome (ACS) face a significantly increased risk of cardiovascular events due to vulnerable plaques. However, no clear evidence supports performing preventive percutaneous coronary intervention (PCI) for non-flow-limiting vulnerable plaques. To address this gap, the PASSIVATE-CAP study was designed to investigate the therapeutic potential of drug-coated balloon (DCB) for treating non-flow-limiting vulnerable plaques.
Methods
The PASSIVATE-CAP study is an investigator-initiated, prospective, randomized, multicenter, open-label superiority trial focusing on acute coronary syndrome (ACS) patients with non-flow-limiting vulnerable plaques in non-culprit vessels. In this study, eligible patients will be randomized at a 1:1 ratio into two groups: patients who received guideline-directed medical therapy (GDMT) and patients who received GDMT combined with a drug-coated balloon (DCB). The primary endpoint was the minimal lumen area of the target lesion 1 year after randomization. The secondary endpoints encompass a range of factors, including the proportion of patients with vulnerable plaques in the target vessel, fibrous cap thickness, lipid core arc of the target lesion, minimal lumen area of the target vessel, among others. The study has been registered on Clinicaltrials.gov (Identifier: NCT06416813).
Results: The PASSIVATE-CAP study enrolled its first patient on July 14, 2025, with projected enrollment completion by January 31, 2027. As of December 28, 2025, 6 patients have been enrolled. The anticipated study end date, marking the completion of the follow-up period, is January 31, 2028.
Conclusions
The PASSIVATE-CAP study represents the first prospective, randomized, multicenter, open-label trial designed to explore the therapeutic value of DCB for the treatment of vulnerable plaques within the ACS patient population.
{"title":"Rationale and Design of the PASSIVATE-CAP Trial: The Preventive Intervention Value of Drug-Coated Balloons in Vulnerable Coronary Atherosclerotic Plaques","authors":"Zhongxiu Chen, Junyan Zhang, Minggang Zhou, Shichu Liang, Yong Chen, Chen Li, Hua Wang, Jiafu Wei, Baotao Huang, Mian Wang, Yong He, for the PASSIVATE-CAP trial investigator","doi":"10.1002/clc.70243","DOIUrl":"10.1002/clc.70243","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients with acute coronary syndrome (ACS) face a significantly increased risk of cardiovascular events due to vulnerable plaques. However, no clear evidence supports performing preventive percutaneous coronary intervention (PCI) for non-flow-limiting vulnerable plaques. To address this gap, the PASSIVATE-CAP study was designed to investigate the therapeutic potential of drug-coated balloon (DCB) for treating non-flow-limiting vulnerable plaques.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The PASSIVATE-CAP study is an investigator-initiated, prospective, randomized, multicenter, open-label superiority trial focusing on acute coronary syndrome (ACS) patients with non-flow-limiting vulnerable plaques in non-culprit vessels. In this study, eligible patients will be randomized at a 1:1 ratio into two groups: patients who received guideline-directed medical therapy (GDMT) and patients who received GDMT combined with a drug-coated balloon (DCB). The primary endpoint was the minimal lumen area of the target lesion 1 year after randomization. The secondary endpoints encompass a range of factors, including the proportion of patients with vulnerable plaques in the target vessel, fibrous cap thickness, lipid core arc of the target lesion, minimal lumen area of the target vessel, among others. The study has been registered on Clinicaltrials.gov (Identifier: NCT06416813).</p>\u0000 \u0000 <p><b>Results:</b> The PASSIVATE-CAP study enrolled its first patient on July 14, 2025, with projected enrollment completion by January 31, 2027. As of December 28, 2025, 6 patients have been enrolled. The anticipated study end date, marking the completion of the follow-up period, is January 31, 2028.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>The PASSIVATE-CAP study represents the first prospective, randomized, multicenter, open-label trial designed to explore the therapeutic value of DCB for the treatment of vulnerable plaques within the ACS patient population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/clc.70243","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145950935","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 article by Çöteli et al. [<span>1</span>] reporting long-term outcomes of catheter ablation in patients with ventricular tachycardia-related electrical storm (VT-ES). The study confirms that catheter ablation is beneficial for managing ES, especially during the acute phase. Also, this high-risk group faces substantial long-term morbidity and mortality following the procedure. These data are valuable for guiding ES management, but several methodological limitations may undermine the reliability and generalizability of the findings and warrant further discussion.</p><p>First, the retrospective, single-center design and small sample size of 65 patients limit the generalizability of the findings. Notably, the wide, unstratified age range (18–85 years) introduces bias because age is a well-known risk factor for cardiovascular disease (CVD). Hence, most of the CVD studies use age stratification or restricted ranges to minimize this bias [<span>2, 3</span>], a safeguard that was absent here which constitutes a significant limitation.</p><p>Second, the authors identify left ventricular ejection fraction (LVEF) as the strongest predictor of post-ablation mortality. However, the mean LVEF in this cohort was 35.3 ± 13%. It characterizes a heterogeneous group with advanced systolic dysfunction and a correspondingly high sudden-death risk. This observation mainly mirrors the population's preexisting high-risk profile rather than an independent ablation effect. Because reduced LVEF itself is a well-established determinant of mortality [<span>1</span>], as a result, long-term outcomes may be confounded by ongoing disease progression, thereby limiting the clinical utility of the findings. Moreover, current guidelines use 40% LVEF as a critical prognostic threshold for heart failure [<span>4</span>]. In a recent report, patients with ischemic heart disease, VT, and LVEF > 30% derive more long-term benefit from early ablation than those with LVEF < 30% [<span>5</span>]. The impact of catheter ablation on long-term outcome could not be properly interpreted due to not performing any subgroup analysis for either of these LVEF thresholds, nor serial postoperative LVEF measurements.</p><p>In addition, competitive risks hinder subgroup analysis between ischemic and non-ischemic groups. Given an all-cause mortality rate of 40%, a number of patients died from end-stage heart failure before any recurrence of VT occurred, rendering the traditional Kaplan−Meier method inappropriate. Because it ignores competing risks and consequently misrepresents clinical reality, we recommend that Cumulative incidence functions and Gray's test are better suited to quantify the risks of recurrence and death, thereby enabling an accurate evaluation of ablation's antiarrhythmic efficacy.</p><p>To sum things up, methodological limitations warrant caution when interpreting the findings. Nevertheless, the study provides insightful evidence on the long-ter
{"title":"Long-Term Outcomes and Follow-Up Management in Patients With Ventricular Tachycardia Electrical Storm After Catheter Ablation","authors":"Zhijie Song, Haizhen Guo","doi":"10.1002/clc.70259","DOIUrl":"10.1002/clc.70259","url":null,"abstract":"<p>We read with great interest the article by Çöteli et al. [<span>1</span>] reporting long-term outcomes of catheter ablation in patients with ventricular tachycardia-related electrical storm (VT-ES). The study confirms that catheter ablation is beneficial for managing ES, especially during the acute phase. Also, this high-risk group faces substantial long-term morbidity and mortality following the procedure. These data are valuable for guiding ES management, but several methodological limitations may undermine the reliability and generalizability of the findings and warrant further discussion.</p><p>First, the retrospective, single-center design and small sample size of 65 patients limit the generalizability of the findings. Notably, the wide, unstratified age range (18–85 years) introduces bias because age is a well-known risk factor for cardiovascular disease (CVD). Hence, most of the CVD studies use age stratification or restricted ranges to minimize this bias [<span>2, 3</span>], a safeguard that was absent here which constitutes a significant limitation.</p><p>Second, the authors identify left ventricular ejection fraction (LVEF) as the strongest predictor of post-ablation mortality. However, the mean LVEF in this cohort was 35.3 ± 13%. It characterizes a heterogeneous group with advanced systolic dysfunction and a correspondingly high sudden-death risk. This observation mainly mirrors the population's preexisting high-risk profile rather than an independent ablation effect. Because reduced LVEF itself is a well-established determinant of mortality [<span>1</span>], as a result, long-term outcomes may be confounded by ongoing disease progression, thereby limiting the clinical utility of the findings. Moreover, current guidelines use 40% LVEF as a critical prognostic threshold for heart failure [<span>4</span>]. In a recent report, patients with ischemic heart disease, VT, and LVEF > 30% derive more long-term benefit from early ablation than those with LVEF < 30% [<span>5</span>]. The impact of catheter ablation on long-term outcome could not be properly interpreted due to not performing any subgroup analysis for either of these LVEF thresholds, nor serial postoperative LVEF measurements.</p><p>In addition, competitive risks hinder subgroup analysis between ischemic and non-ischemic groups. Given an all-cause mortality rate of 40%, a number of patients died from end-stage heart failure before any recurrence of VT occurred, rendering the traditional Kaplan−Meier method inappropriate. Because it ignores competing risks and consequently misrepresents clinical reality, we recommend that Cumulative incidence functions and Gray's test are better suited to quantify the risks of recurrence and death, thereby enabling an accurate evaluation of ablation's antiarrhythmic efficacy.</p><p>To sum things up, methodological limitations warrant caution when interpreting the findings. Nevertheless, the study provides insightful evidence on the long-ter","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12784165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932329","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}
Muhammad Umer Sohail, Ruqiat Masooma Batool, Muhammad Saad, Saad Ahmed Waqas, Asad Ali Ahmed Cheema, Abdul Mannan Khan Minhas
Background: Despite declines since the 1960s, cardiovascular diseases (CVDs) remain the leading cause of mortality in the United States. However, recent data indicate stabilization or increases in certain regions, highlighting persistent disparities. This study analyzes trends in states with the highest and lowest CVD-related age-adjusted mortality rates (AAMRs) from 1999 to 2019.
Methods: Using CDC WONDER, we conducted a retrospective analysis of CVD-related mortality in adults aged ≥ 25 years. AAMRs were calculated using ICD-10 codes I00-I99, and trends were assessed using Joinpoint regression for annual percent change (APC) and average annual percent change (AAPC).
Results: Between 1999 and 2019, national AAMR declined from 798.47 to 595.56 per 100 000 (AAPC: -1.5%, 95% CI: -1.8% to -1.2%). Mississippi had the highest AAMR (902.23) with the slowest decline, whereas Arizona had the lowest (530.40) with a steeper reduction. Males (702.15), non-Hispanic Black individuals (850.32), and nonmetropolitan populations (645.21) had persistently higher mortality. Urban-rural disparities widened over time.
Conclusion: State-level variations in CVD mortality reflect persistent socioeconomic, behavioral, and healthcare disparities. These findings highlight widening regional gaps and emphasize the need for stronger, state-specific public health strategies, improved access to preventive care, and targeted interventions for disproportionately affected groups. Strengthening surveillance systems, expanding evidence-based cardiovascular prevention programs, and addressing structural determinants of health will be essential to reduce the observed disparities and sustain long-term progress in CVD mortality reduction across the United States.
{"title":"States With Highest and Lowest Cardiovascular Disease-Related Mortality in the United States (1999-2019): Top and Bottom 3.","authors":"Muhammad Umer Sohail, Ruqiat Masooma Batool, Muhammad Saad, Saad Ahmed Waqas, Asad Ali Ahmed Cheema, Abdul Mannan Khan Minhas","doi":"10.1002/clc.70256","DOIUrl":"https://doi.org/10.1002/clc.70256","url":null,"abstract":"<p><strong>Background: </strong>Despite declines since the 1960s, cardiovascular diseases (CVDs) remain the leading cause of mortality in the United States. However, recent data indicate stabilization or increases in certain regions, highlighting persistent disparities. This study analyzes trends in states with the highest and lowest CVD-related age-adjusted mortality rates (AAMRs) from 1999 to 2019.</p><p><strong>Methods: </strong>Using CDC WONDER, we conducted a retrospective analysis of CVD-related mortality in adults aged ≥ 25 years. AAMRs were calculated using ICD-10 codes I00-I99, and trends were assessed using Joinpoint regression for annual percent change (APC) and average annual percent change (AAPC).</p><p><strong>Results: </strong>Between 1999 and 2019, national AAMR declined from 798.47 to 595.56 per 100 000 (AAPC: -1.5%, 95% CI: -1.8% to -1.2%). Mississippi had the highest AAMR (902.23) with the slowest decline, whereas Arizona had the lowest (530.40) with a steeper reduction. Males (702.15), non-Hispanic Black individuals (850.32), and nonmetropolitan populations (645.21) had persistently higher mortality. Urban-rural disparities widened over time.</p><p><strong>Conclusion: </strong>State-level variations in CVD mortality reflect persistent socioeconomic, behavioral, and healthcare disparities. These findings highlight widening regional gaps and emphasize the need for stronger, state-specific public health strategies, improved access to preventive care, and targeted interventions for disproportionately affected groups. Strengthening surveillance systems, expanding evidence-based cardiovascular prevention programs, and addressing structural determinants of health will be essential to reduce the observed disparities and sustain long-term progress in CVD mortality reduction across the United States.</p>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":"e70256"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988220","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}
Background: This study aimed to investigate regional myocardial strain and fibrosis distribution to analyze the apical sparing pattern and the relation with hypertrophy in hypertension.
Methods: This study included clinical and experimental animal investigations. Seventy-three hypertensive patients were divided into two groups: hypertension without left ventricular hypertrophy (HT-NLVH) and hypertension with LVH (HT-LVH). Six 16-week-old male spontaneously hypertensive rats (SHR) and six age-matched male Wistar-Kyoto (WKY) rats were included in this experiment. Echocardiographic measurements were obtained. Myocardial strain indexes, including global longitudinal strain (GLS), the basal, middle, and apical segmental LS (LS-bas, LS-mid, LS-ap), and the proportion of LS-ap/(LS-bas + LS-mid + LS-ap) (P-ap) were measured. The histological collagen volume fraction (CVF) and perivascular collagen area (PVCA) of basal and apical segments (CVF-bas, CVF-ap, PVCA-bas, PVCA-ap) were observed in all rats.
Results: Despite preserved systolic function (FS, LVEF), the HT-NLVH and HT-LVH groups exhibited diastolic impairment (elevated LAVI, E/e') (all p < 0.05). LS-ap declined only in HT-LVH, while LS-mid and LS-bas worsened from HT-NLVH to HT-LVH, and the HT-LVH group exhibited a significantly elevated P-ap (all p < 0.05). P-ap was associated with LV remodeling indexes and E/e' (all p < 0.05). Compared with WKY, LS-bas decreased in SHR (p < 0.05). The SHR group demonstrated significantly elevated PVCA-bas, PVCA-ap, and CVF-bas (p < 0.05), while the CVF-ap had no significant difference.
Conclusion: Myocardial dysfunction and fibrosis exhibited regional heterogeneity with predominant basal damage and apical sparing in hypertensive cardiac hypertrophy. This apical-sparing pattern correlated significantly with both diastolic dysfunction and hypertrophic progression, suggesting its potential as a clinically observable hallmark.
{"title":"Apical Sparing of Longitudinal Strain and Myocardial Fibrosis in Hypertensive Patients and Spontaneously Hypertensive Rats: Based on Speckle Tracking and Histological Analysis.","authors":"Chunyan Huang, Yongxin Wu, Meiyan Lin, Yupeng Chen, Shengnan Lin, Liyun Fu, Huimei Huang","doi":"10.1002/clc.70255","DOIUrl":"10.1002/clc.70255","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to investigate regional myocardial strain and fibrosis distribution to analyze the apical sparing pattern and the relation with hypertrophy in hypertension.</p><p><strong>Methods: </strong>This study included clinical and experimental animal investigations. Seventy-three hypertensive patients were divided into two groups: hypertension without left ventricular hypertrophy (HT-NLVH) and hypertension with LVH (HT-LVH). Six 16-week-old male spontaneously hypertensive rats (SHR) and six age-matched male Wistar-Kyoto (WKY) rats were included in this experiment. Echocardiographic measurements were obtained. Myocardial strain indexes, including global longitudinal strain (GLS), the basal, middle, and apical segmental LS (LS-bas, LS-mid, LS-ap), and the proportion of LS-ap/(LS-bas + LS-mid + LS-ap) (P-ap) were measured. The histological collagen volume fraction (CVF) and perivascular collagen area (PVCA) of basal and apical segments (CVF-bas, CVF-ap, PVCA-bas, PVCA-ap) were observed in all rats.</p><p><strong>Results: </strong>Despite preserved systolic function (FS, LVEF), the HT-NLVH and HT-LVH groups exhibited diastolic impairment (elevated LAVI, E/e') (all p < 0.05). LS-ap declined only in HT-LVH, while LS-mid and LS-bas worsened from HT-NLVH to HT-LVH, and the HT-LVH group exhibited a significantly elevated P-ap (all p < 0.05). P-ap was associated with LV remodeling indexes and E/e' (all p < 0.05). Compared with WKY, LS-bas decreased in SHR (p < 0.05). The SHR group demonstrated significantly elevated PVCA-bas, PVCA-ap, and CVF-bas (p < 0.05), while the CVF-ap had no significant difference.</p><p><strong>Conclusion: </strong>Myocardial dysfunction and fibrosis exhibited regional heterogeneity with predominant basal damage and apical sparing in hypertensive cardiac hypertrophy. This apical-sparing pattern correlated significantly with both diastolic dysfunction and hypertrophic progression, suggesting its potential as a clinically observable hallmark.</p>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":"e70255"},"PeriodicalIF":2.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12805527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984544","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>Evelo et al.'s recent work examines the differences between genders in how often combination evidence-based medicines (cEBMs) are prescribed after ST-elevation myocardial infarction (STEMI). The authors indicate that when controlling for other variables that may account for this trend, the gap between men and women lessens. However, it seems to merit further examination since the reduced unadjusted disparity (66% vs. 72.8%) continues to be a clinical gap similar to that reported in the treatment of women who have experienced an acute coronary syndrome [<span>1-3</span>].</p><p>A number of factors that are unique to women (e.g., age, comorbidities) may cloud true disparities, since eliminating those factors will allow you to understand the true difference between men and women when addressing providers' failure to deliver proper care to either gender based on factors such as biological predisposition.</p><p>In addition, the single-center design of this study reduces the extent to which the findings can be applied to the population as a whole, since it has been demonstrated multiple times through larger multi-center studies that women are less likely than men to receive guideline-recommended treatments and invasive interventions at a variety of healthcare facilities [<span>1, 3, 4</span>].</p><p>The increased prescribing rates observed in this study may be attributed to the practices of the institution rather than a trend in the overall population. Additionally, the day after discharge (DAD) measure of cEBM did not capture any changes in medications, de-prescribing, or patient-directed discontinuation that occurred prior to discharge. Real-world adherence after an MI will have a significant impact on post-MI outcomes and limited interpretation of long-term implications. Further investigation is necessary. Women received percutaneous coronary interventions (PCI) and CABG less often compared to men, even though cardiology guidelines state that both processes are equally beneficial and that secondary preventive therapies for both genders are beneficial [<span>5</span>].</p><p>In Evelo et al., PCI was an independent predictor of an increased likelihood of receiving cEBM, suggesting that procedural differences may indirectly perpetuate differences in drug therapies, as well. The findings of this study, indicating a greater 6-month rate of both stroke and death for females, are consistent with the male-to-female ratio of outcomes reported in prior studies [<span>1, 6, 7</span>]. Although it is not possible to draw causal conclusions from this data, there is a need to investigate whether any of the clinically modifiable parameters, including intensity of treatment, clinician bias, or avoidance of prescribing due to perceived risk, contribute to the downstream sex disparity in outcomes.</p><p>Evelo et al. make an important first step in this area; however, there are many ways to build upon this foundation through continued research. Future studies shoul
{"title":"“Sex-Based Inequities in Post-STEMI Secondary Prevention: A Critical Appraisal and Path Forward”","authors":"Ibadullah Tahir, Hunain Shahbaz","doi":"10.1002/clc.70252","DOIUrl":"10.1002/clc.70252","url":null,"abstract":"<p>Evelo et al.'s recent work examines the differences between genders in how often combination evidence-based medicines (cEBMs) are prescribed after ST-elevation myocardial infarction (STEMI). The authors indicate that when controlling for other variables that may account for this trend, the gap between men and women lessens. However, it seems to merit further examination since the reduced unadjusted disparity (66% vs. 72.8%) continues to be a clinical gap similar to that reported in the treatment of women who have experienced an acute coronary syndrome [<span>1-3</span>].</p><p>A number of factors that are unique to women (e.g., age, comorbidities) may cloud true disparities, since eliminating those factors will allow you to understand the true difference between men and women when addressing providers' failure to deliver proper care to either gender based on factors such as biological predisposition.</p><p>In addition, the single-center design of this study reduces the extent to which the findings can be applied to the population as a whole, since it has been demonstrated multiple times through larger multi-center studies that women are less likely than men to receive guideline-recommended treatments and invasive interventions at a variety of healthcare facilities [<span>1, 3, 4</span>].</p><p>The increased prescribing rates observed in this study may be attributed to the practices of the institution rather than a trend in the overall population. Additionally, the day after discharge (DAD) measure of cEBM did not capture any changes in medications, de-prescribing, or patient-directed discontinuation that occurred prior to discharge. Real-world adherence after an MI will have a significant impact on post-MI outcomes and limited interpretation of long-term implications. Further investigation is necessary. Women received percutaneous coronary interventions (PCI) and CABG less often compared to men, even though cardiology guidelines state that both processes are equally beneficial and that secondary preventive therapies for both genders are beneficial [<span>5</span>].</p><p>In Evelo et al., PCI was an independent predictor of an increased likelihood of receiving cEBM, suggesting that procedural differences may indirectly perpetuate differences in drug therapies, as well. The findings of this study, indicating a greater 6-month rate of both stroke and death for females, are consistent with the male-to-female ratio of outcomes reported in prior studies [<span>1, 6, 7</span>]. Although it is not possible to draw causal conclusions from this data, there is a need to investigate whether any of the clinically modifiable parameters, including intensity of treatment, clinician bias, or avoidance of prescribing due to perceived risk, contribute to the downstream sex disparity in outcomes.</p><p>Evelo et al. make an important first step in this area; however, there are many ways to build upon this foundation through continued research. Future studies shoul","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145849014","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>While we found the article by Zhang and collaborators to be very interesting, numerous methodological limitations impair the reliability and clinical usefulness of the results and conclusions. Of particular concern is the limitation of the genetic scope to two SNPs, CYP3A4 rs2242480 and CYP3A5 rs776746. This restricts the research to only acting on two SNPs that were indicated as being involved in the pharmacokinetics and/or pharmacodynamics of ticagrelor and other agents that produce adverse effects.</p><p>Prior studies have firmly established the roles of SLCO1B1, ABCB1, UGT2B7, and P2Y12 allele variations in influencing ticagrelor bioavailability and dyspnea risk [<span>1-3</span>]. If the current study does not account for these genes, it may result in a large-scale shortage of genetic information to assess and incorrectly attribute the effects of other genes and environmental variables to just one SNP. It is also very disconcerting that key clinical outcomes are clearly underpowered. Low rates of ticagrelor-associated bleeding/revascularization events were recorded; a prior pharmacogenomic study indicated that to detect the genetic modality of rare events, one must conduct studies with large, multi-institutional cohorts [<span>4</span>].</p><p>The evidence of significantly low statistical power regarding major clinical outcomes evaluated is equally alarming. The frequency of ticagrelor-related occurrence of bleeding and revascularization is low, and previous pharmacogenomic studies identified that large, multicenter studies have the necessary statistical power to detect the effects of genetic variations on these rare clinical outcomes [<span>4</span>]. The small number of occurrences reported by Zhang et al. (e.g., 13 bleeding events) severely limited statistical power, resulting in an increased possibility of producing false negative results, thus making their conclusion of “no association” highly questionable.</p><p>The results of this study show a higher training accuracy but a significantly lower testing accuracy than what was found in other studies, indicating an unstable model. The authors, however, interpret this result as having biological meaning; a more cautious approach would take into account the risk of overfitting that GMDR has when using a large number of training sets [<span>5</span>]. In addition to the lack of confounding variables for the evaluation of dyspnea, there are multiple reasons why patients taking ticagrelor may experience dyspnea due to conditions other than the drug itself, for example, baseline pulmonary condition, vagal sensitivity, renal function, and other prescriptive medications, including β-blockers and ACE inhibitors [<span>3-6</span>].</p><p>Studies have shown that renal dysfunction and platelet reactivity are independent predictors of the severity of dyspnea [<span>3-7</span>]. The paper by Zhang et al. excluded several cardiopulmonary disorders; however, they did not rectify for the residual varia
{"title":"“Reconsidering CYP3A4/5 Genotyping for Ticagrelor Safety: Critical Appraisal of a Narrow Genetic Framework”","authors":"Ibadullah Tahir, Hunain Shahbaz","doi":"10.1002/clc.70251","DOIUrl":"10.1002/clc.70251","url":null,"abstract":"<p>While we found the article by Zhang and collaborators to be very interesting, numerous methodological limitations impair the reliability and clinical usefulness of the results and conclusions. Of particular concern is the limitation of the genetic scope to two SNPs, CYP3A4 rs2242480 and CYP3A5 rs776746. This restricts the research to only acting on two SNPs that were indicated as being involved in the pharmacokinetics and/or pharmacodynamics of ticagrelor and other agents that produce adverse effects.</p><p>Prior studies have firmly established the roles of SLCO1B1, ABCB1, UGT2B7, and P2Y12 allele variations in influencing ticagrelor bioavailability and dyspnea risk [<span>1-3</span>]. If the current study does not account for these genes, it may result in a large-scale shortage of genetic information to assess and incorrectly attribute the effects of other genes and environmental variables to just one SNP. It is also very disconcerting that key clinical outcomes are clearly underpowered. Low rates of ticagrelor-associated bleeding/revascularization events were recorded; a prior pharmacogenomic study indicated that to detect the genetic modality of rare events, one must conduct studies with large, multi-institutional cohorts [<span>4</span>].</p><p>The evidence of significantly low statistical power regarding major clinical outcomes evaluated is equally alarming. The frequency of ticagrelor-related occurrence of bleeding and revascularization is low, and previous pharmacogenomic studies identified that large, multicenter studies have the necessary statistical power to detect the effects of genetic variations on these rare clinical outcomes [<span>4</span>]. The small number of occurrences reported by Zhang et al. (e.g., 13 bleeding events) severely limited statistical power, resulting in an increased possibility of producing false negative results, thus making their conclusion of “no association” highly questionable.</p><p>The results of this study show a higher training accuracy but a significantly lower testing accuracy than what was found in other studies, indicating an unstable model. The authors, however, interpret this result as having biological meaning; a more cautious approach would take into account the risk of overfitting that GMDR has when using a large number of training sets [<span>5</span>]. In addition to the lack of confounding variables for the evaluation of dyspnea, there are multiple reasons why patients taking ticagrelor may experience dyspnea due to conditions other than the drug itself, for example, baseline pulmonary condition, vagal sensitivity, renal function, and other prescriptive medications, including β-blockers and ACE inhibitors [<span>3-6</span>].</p><p>Studies have shown that renal dysfunction and platelet reactivity are independent predictors of the severity of dyspnea [<span>3-7</span>]. The paper by Zhang et al. excluded several cardiopulmonary disorders; however, they did not rectify for the residual varia","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848991","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}
Yasin Özen, Mustafa Bilal Ozbay, Zahin Shahriar, Hüseyin Tezcan, Tugay Dedebali, Abdullah Tunçez, Muhammed Ulvi Yalçin, Kadri Murat Gürses, Bülent Özbay
Background
Naples Prognostic Score (NPS), a composite index incorporating inflammatory and nutritional markers, has emerged as a potential prognostic tool in various cardiovascular conditions; however, no meta-analysis has yet pooled the available evidence to comprehensively assess its prognostic utility.
Objectives
To evaluate the association of NPS with clinical outcomes, including all-cause mortality, in-hospital mortality, no-reflow (NR) phenomenon, and left ventricular ejection fraction (LVEF), in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI).
Methods
MEDLINE, Cochrane, and EMBASE databases were searched for studies comparing high and low NPS groups in ACS patients undergoing PCI. Random-effects models were used to pool risk ratios (RR) for binary outcomes and mean differences (MD) for continuous outcomes. Heterogeneity was assessed with I² statistics. Statistical analyses were performed using Review Manager 5.4, and R, version 4.2.2.
Results
We included seven studies comprising 13 268 patients, with 5628 (42.4%) patients in the low NPS group. Low NPS was significantly associated with decreased all-cause mortality (RR: 0.42; 95% CI: 0.32–0.55; I² = 48%) and decreased incidence of NR (RR: 0.60; 95% CI: 0.40–0.88; I² = 83%). Patients with low NPS also had higher LVEF (MD: −2.69%; 95% CI: −3.41 to −1.97; I² = 99%). No significant difference was observed in in-hospital mortality (RR: 0.54; 95% CI: 0.28–1.05; I² = 94%).
Conclusion
In ACS patients undergoing PCI, elevated NPS was associated with worse clinical outcomes. These findings support the use of NPS as a practical, biomarker-based tool for risk stratification in this population.
{"title":"Naples Prognostic Score and Clinical Outcomes After PCI for Acute Coronary Syndrome: A Systematic Review and Meta-Analysis","authors":"Yasin Özen, Mustafa Bilal Ozbay, Zahin Shahriar, Hüseyin Tezcan, Tugay Dedebali, Abdullah Tunçez, Muhammed Ulvi Yalçin, Kadri Murat Gürses, Bülent Özbay","doi":"10.1002/clc.70247","DOIUrl":"10.1002/clc.70247","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Naples Prognostic Score (NPS), a composite index incorporating inflammatory and nutritional markers, has emerged as a potential prognostic tool in various cardiovascular conditions; however, no meta-analysis has yet pooled the available evidence to comprehensively assess its prognostic utility.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objectives</h3>\u0000 \u0000 <p>To evaluate the association of NPS with clinical outcomes, including all-cause mortality, in-hospital mortality, no-reflow (NR) phenomenon, and left ventricular ejection fraction (LVEF), in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>MEDLINE, Cochrane, and EMBASE databases were searched for studies comparing high and low NPS groups in ACS patients undergoing PCI. Random-effects models were used to pool risk ratios (RR) for binary outcomes and mean differences (MD) for continuous outcomes. Heterogeneity was assessed with I² statistics. Statistical analyses were performed using Review Manager 5.4, and R, version 4.2.2.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We included seven studies comprising 13 268 patients, with 5628 (42.4%) patients in the low NPS group. Low NPS was significantly associated with decreased all-cause mortality (RR: 0.42; 95% CI: 0.32–0.55; I² = 48%) and decreased incidence of NR (RR: 0.60; 95% CI: 0.40–0.88; I² = 83%). Patients with low NPS also had higher LVEF (MD: −2.69%; 95% CI: −3.41 to −1.97; I² = 99%). No significant difference was observed in in-hospital mortality (RR: 0.54; 95% CI: 0.28–1.05; I² = 94%).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In ACS patients undergoing PCI, elevated NPS was associated with worse clinical outcomes. These findings support the use of NPS as a practical, biomarker-based tool for risk stratification in this population.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848924","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}
To evaluate the incremental value of non-gated chest CT coronary artery calcium score in enhancing GRACE score prediction of major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).
Methods
A retrospective cohort study was conducted on 324 ACS patients undergoing PCI and non-gated chest CT. Patients were divided into MACE (n = 100) and non-MACE (n = 224) groups with a median follow-up of 18.7 months. The predictive performance of the GRACE score, Agatston score, and combined clinical composite model was evaluated using receiver operating characteristic (ROC) curves and survival analysis based on optimal cutoff values.
Results
Model 3 (GRACE + CACS) demonstrated AUC values of 0.798 and 0.827 in the training and testing cohorts, respectively, significantly outperforming Model 1 (GRACE) (training AUC = 0.702; testing AUC = 0.758). Model 4, incorporating clinical features, demonstrated optimal predictive performance (training set AUC = 0.806; testing set AUC = 0.857). The AUC differences were statistically significant (p < 0.05). Survival curves revealed the highest MACE incidence (94.4%, p < 0.01) in the high-risk combined Ga1 group (GRACE ≥ 140 and Agatston ≥ 400).
Conclusion
The non-gated chest CT coronary calcification score significantly enhances the predictive value of the GRACE score for major adverse coronary events (MACE) after coronary intervention. When combined with clinical indicators, the predictive power is further improved. Sensitivity analysis confirms the robustness of this finding, providing a reliable tool for clinical risk stratification.
{"title":"Incremental Value of Non-Gated Chest CT Coronary Artery Calcium Score in Predicting Major Adverse Cardiovascular Events by GRACE Score After Percutaneous Coronary Intervention in Patients With Acute Coronary Syndrome","authors":"Zhaoyuan Xing, Haoyan Pan, Huan Ding, Jianing Chen, ZiGuang Huang, Jing Wen, Zhe Zhang, Baoying Zhao, Xu Dai","doi":"10.1002/clc.70242","DOIUrl":"10.1002/clc.70242","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>To evaluate the incremental value of non-gated chest CT coronary artery calcium score in enhancing GRACE score prediction of major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>A retrospective cohort study was conducted on 324 ACS patients undergoing PCI and non-gated chest CT. Patients were divided into MACE (<i>n</i> = 100) and non-MACE (<i>n</i> = 224) groups with a median follow-up of 18.7 months. The predictive performance of the GRACE score, Agatston score, and combined clinical composite model was evaluated using receiver operating characteristic (ROC) curves and survival analysis based on optimal cutoff values.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Model 3 (GRACE + CACS) demonstrated AUC values of 0.798 and 0.827 in the training and testing cohorts, respectively, significantly outperforming Model 1 (GRACE) (training AUC = 0.702; testing AUC = 0.758). Model 4, incorporating clinical features, demonstrated optimal predictive performance (training set AUC = 0.806; testing set AUC = 0.857). The AUC differences were statistically significant (<i>p</i> < 0.05). Survival curves revealed the highest MACE incidence (94.4%, <i>p</i> < 0.01) in the high-risk combined Ga1 group (GRACE ≥ 140 and Agatston ≥ 400).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The non-gated chest CT coronary calcification score significantly enhances the predictive value of the GRACE score for major adverse coronary events (MACE) after coronary intervention. When combined with clinical indicators, the predictive power is further improved. Sensitivity analysis confirms the robustness of this finding, providing a reliable tool for clinical risk stratification.</p>\u0000 </section>\u0000 </div>","PeriodicalId":10201,"journal":{"name":"Clinical Cardiology","volume":"49 1","pages":""},"PeriodicalIF":2.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12746471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145848960","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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