American journal of cardiovascular disease最新文献

{"title":"Efficacy of exercise and electromagnetic field therapy on cardiovascular disease risk in patients with type 2 diabetes mellitus. Randomized controlled trial.","authors":"Ashraf Abdelaal Mohamed Abdelaal, Alaa Abdulhafiz Khushhal, Anwar Abdelgayed Ebid, Abeer Ramadan Ibrahim","doi":"10.62347/DTRJ2656","DOIUrl":"10.62347/DTRJ2656","url":null,"abstract":"<p><p>Type 2 diabetes mellitus predisposes patients to abnormally increased atherosclerotic cardiovascular disease risk and deteriorated lower extremity functional status. Objective: To evaluate the effect of combined application of moderate to high intensity interval training and low frequency pulsed electromagnetic therapy on atherosclerotic cardiovascular disease risk and lower extremity function in older adults with type 2 diabetes mellitus. Fifty-four patients (age 45-60 years) with type 2 diabetes mellitus were randomly allocated into four groups: group A underwent moderate to high intensity interval training plus low frequency pulsed electromagnetic therapy for 8 weeks (n=13), group B received low frequency pulsed electromagnetic therapy (n=14), group C underwent moderate to high intensity interval training (n=13), and group D were the controls (n=14). The 10-year atherosclerotic cardiovascular disease risk was evaluated using the Atherosclerotic Cardiovascular Disease Risk Estimator Plus tool, while lower extremity function was assessed using the Short Physical Performance Battery. Statistical comparisons were conducted within and between groups using SPSS 20. A <i>P</i>-value <0.05 was considered statistically significant. After 8 weeks, the atherosclerotic cardiovascular disease risk significantly decreased by -10.91% (P<0.001) and -6.66% (P<0.001) in groups A and C, respectively, non-significantly decreased by -0.16% (P=0.43) in group B, and non-significantly increased by 1.35% (P=0.24) in group D. The lower extremity function significantly increased by 64.62% (P<0.001), 27.48% (P=0.001), and 48.49% (P<0.001) in groups A, B, and C, respectively. There was a non-significant increase of 0.5% (P=0.73) in group D. In conclusion, the combined application of moderate-to-high-intensity interval training and low-frequency pulsed electromagnetic therapy programmes was effective in improving atherosclerotic cardiovascular disease risk and lower extremity function in older adults with type 2 diabetes mellitus. Furthermore, the moderate-to-high-intensity interval training programme is more effective than low-frequency pulsed electromagnetic therapy in improving atherosclerotic cardiovascular disease risk and lower extremity function in patients with type 2 diabetes mellitus.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"509-521"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A normal and particularly small left atrial size measured during echocardiography MAY NOT suggest low likelihood of moderate or severe left ventricular systolic dysfunction.","authors":"Gregory Mints, Jina Bai, Arthur Evans","doi":"10.62347/XBIY9426","DOIUrl":"10.62347/XBIY9426","url":null,"abstract":"<p><p>This is letter to the editor: we point to a statistical error in a recent article published in the journal by Movahed MR, Soltani Moghadam A. <i>A normal and particularly small (<35 mm) left atrial size measured during echocardiography suggests low likelihood of moderate or severe left ventricular systolic dysfunction</i>, which may have resulted in a biased conclusion.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"522-523"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pyroptosis in cardiovascular diseases: molecular mechanisms, pathological roles, and therapeutic implications.","authors":"Xue-Song Liu, Zhao-Yu Li, Shi-Tong Wang, Qian Qiao, Xue-Rui Ye, Lu Cheng, Yong Hu, Lei Zhu, Jian-Lin Yang, Hao-Ling Zhang, Jing-Jing Zhang","doi":"10.62347/MTTP3167","DOIUrl":"10.62347/MTTP3167","url":null,"abstract":"<p><p>Each year, cardiovascular diseases (CVDs) claim millions of lives worldwide, making them one of the biggest causes of deaths globally. More often than not, the inflammatory response is the principal disease mechanism behind the onset and development of CVDs. The study seeks to elucidate the mechanistic role of pyroptosis in CVDs and to summarize the current progress of potential therapeutic strategies targeting pyroptotic pathways. Pyroptosis is a form of PCD, which is inflammatory and mediated through an inflammasome and gasdermin complex. In the past few years, it has emerged as a crucial mechanism possibly explaining protracted inflammation and tissue damage. There is evidence suggesting that pyroptosis contributes to multiple CVDs. Indeed, it may induce disruption of endothelial barrier and plaque instability in atherosclerosis (AS). Also, it may aggravate ischemia-reperfusion injury (IRI) and reduce repair processes in case of myocardial infarction (MI). Finally, it may drive ventricular remodeling and functional impairment in heart failure (HF). Cell death and immune activation are further aggravated by a vicious cycle between pyroptosis and inflammation. Recent studies indicate that therapeutic interventions focused on key molecules, including the NLRP3 inflammasome, caspase-1, and gasdermin D (GSDMD), along with combination therapies consisting of antioxidants and inflammation inhibitors, exhibit significant cardioprotective effects. Additionally, one's diet, exercise and other lifestyle choices impact pyroptotic pathways and influence the risk of CVD. We should include pyroptosis as a form of cell death in future research only. Further, it would be necessary to identify reliable biomarkers for all of these forms of cell death for their therapeutic mechanisms.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"477-508"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816780/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of prior pacemaker implantation on length of stay in acute diastolic heart failure: a propensity score-matched analysis.","authors":"Ashot Batikyan, Vahagn Tamazyan, Hakob Harutyunyan, Aleksan Khachatryan, Donclair Brown, Michail Spanos, Tamara Simpson, Steve Kong, Miroslav Radulovic","doi":"10.62347/NQRJ9167","DOIUrl":"10.62347/NQRJ9167","url":null,"abstract":"<p><strong>Objectives: </strong>Permanent pacemakers are widely used to manage symptomatic bradyarrhythmias and conduction disorders; however, their impact on hospitalization outcomes, such as length of stay, in patients with acute decompensated diastolic heart failure remains unclear. This study aimed to assess whether prior pacemaker implantation independently affects hospital length of stay using data from the 2018-2019 National Inpatient Sample database.</p><p><strong>Methods: </strong>A total of 14,523 adult patients hospitalized with acute diastolic heart failure were identified, including 855 with a history of pacemaker implantation. Propensity score matching was conducted to adjust for baseline differences, and competing risks regression was performed to account for the competing risk of in-hospital mortality.</p><p><strong>Results: </strong>Before matching, pacemaker recipients were older and had a higher burden of comorbidities; unadjusted analysis showed a modest but statistically significant association with shorter length of stay (sHR = 1.075; 95% CI: 1.010-1.144; P = 0.023). After matching, this association was attenuated and no longer significant (sHR = 1.081; 95% CI: 0.992-1.178; P = 0.077). Comorbid conditions, particularly chronic kidney disease, liver disease, and pulmonary hypertension, were stronger predictors of prolonged hospitalization.</p><p><strong>Conclusions: </strong>These findings suggest that pacemaker status alone does not independently affect the length of stay in patients hospitalized with acute diastolic heart failure, highlighting the importance of managing comorbidities to potentially reduce hospital length of stay in this vulnerable population, although further studies are warranted to confirm these observations.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"387-394"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis in ischemia-reperfusion injury: molecular mechanisms and therapeutic strategies.","authors":"Ya-Li Wei, Lu Cheng, Xiao-Yu Chen, Qian Qiao, Xue-Rui Ye, Di Wang, Hao-Ling Zhang, Zhi-Jing Song, Wei Wang, Jing-Jing Zhang","doi":"10.62347/OLGV6926","DOIUrl":"10.62347/OLGV6926","url":null,"abstract":"<p><p>Ferroptosis is a novel form of programmed cell death characterized by iron-dependent lipid peroxidation (LPO). It has been widely demonstrated in the last years to play a crucial pathogenic role in ischemia-reperfusion injury (IRI). The pathological basis for ferroptosis is established through disturbances in energy metabolism, iron homeostasis and mitochondrial injury during ischemic phase. During the following period of reperfusion, the surge in reactive oxygen species (ROS), along with the liberation of inflammatory mediators, and the aggravation of LPO, will further stimulate peroxidase 4 (GPX4) inactivation and augment iron load in the cells, which will greatly intensify bodily tissue injury. Ferroptosis, which operates through intricate cross-regulation with oxidative stress, immune-inflammatory responses, and autophagy, forms a multi-tiered positive feedback loop that actively contributes to injury-repair imbalance IRI pathogenesis across various organs, including the heart, brain, liver and kidney. Studies show that tissue damage and recovery can be improved by targeting system Xc^-, GPX4, ACSL4, TfR1, and NCOA4 in the body. This review summarizes the mechanisms, organ-specific manifestations, and current therapeutic strategies of ferroptosis in IRI. It is helpful for the theoretical foundation and potential direction of clinical targeted therapy.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"405-441"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816776/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel gain-of-function mutation <i>SCN5A</i>-N470K associated with African American familial atrial fibrillation.","authors":"Xinyu Cao, Faisal A Darbar, Xin Wu, Lu Zhang, Dawood Darbar, Liang Hong","doi":"10.62347/YGWN5773","DOIUrl":"10.62347/YGWN5773","url":null,"abstract":"<p><strong>Objectives: </strong>The cardiac sodium channel Nav1.5, encoded by the <i>SCN5A</i> gene, is crucial for the generation and propagation of cardiac action potential. While SCN5A mutations have been linked to familial atrial fibrillation (AF), the functional impact of certain mutations remains unclear. This study aims to identify new <i>SCN5A</i> mutation associated with AF and investigate the mechanism of the mutation dysregulation of SCN5A channel function underlying AF.</p><p><strong>Methods: </strong>We identified a three-generation African American family with a history of familial AF. Functional characterization of an SCN5A mutation was performed using whole-cell patch-clamp recordings in HEK cells expressing the recombinant mutant channels.</p><p><strong>Results: </strong>The proband, along with his mother and maternal grandmother, all presented with early-onset symptomatic paroxysmal AF, which co-segregated with the <i>SCN5A</i>-N470K mutation. The N470K mutation exhibited different electrophysiological properties when compared to the wild-type channel. Functional evaluation of the <i>SCN5A</i>-N470K variant revealed an increased peak sodium current, a hyperpolarizing shift in the voltage-dependence of steady-state activation, and a depolarizing shift in voltage-dependent inactivation. Additionally, N470K mutation did not produce significantly larger persistent current.</p><p><strong>Conclusion: </strong>The <i>SCN5A</i>-N470K mutation represents a gain-of-function alteration characterized by increased peak sodium current, and enhanced window current defined by the overlap of voltage-dependent inactivation and activation curves. These changes may alter myocardial excitability or conduction, providing a plausible mechanism by which the <i>SCN5A</i>-N470K mutation increases susceptibility to AF in this African American family.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"357-365"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miRNA regulatory networks as precision diagnostic and therapeutic targets in pulmonary arterial hypertension: from molecular cascades to clinical translation.","authors":"Zhaoyu Li, Hongyang Ding, Xuehai Liu, Di Wang, Haolong Zhang, Rui Zhao, Haoling Zhang, Zhijing Song, Wei Wang, Jingjing Zhang","doi":"10.62347/RGTY8619","DOIUrl":"10.62347/RGTY8619","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is a fatal disease with extremely poor prognosis, primarily driven by persistent pulmonary vascular remodeling. The disease often presents insidiously and progresses rapidly. Although current targeted therapies may slow disease progression, they fall far short of reversing pathological changes, underscoring the urgent need for novel therapeutic breakthroughs and precise diagnostic approaches. Within this context, microRNA (miRNA) regulatory networks - key nodes of epigenetic regulation - have emerged as a potential bridge between basic science and clinical translation. Increasing evidence has shown that specific miRNAs, by targeting signaling pathways such as PI3K/AKT and TGF-β/Smad, orchestrate complex multi-target molecular cascades that critically regulate pathological processes, including endothelial dysfunction, abnormal proliferation and phenotypic switching of smooth muscle cells, inflammatory activation, and metabolic remodeling. These mechanisms ultimately drive irreversible vascular remodeling. Aberrant expression patterns of miRNAs are not only closely associated with disease severity but also hold great promise as non-invasive biomarkers, facilitating early detection, subtype classification, and prognostic assessment of PAH. Importantly, miRNA-targeted nucleic acid therapeutics have demonstrated therapeutic potential in preclinical models, including reversal of vascular remodeling and improvement of hemodynamics, highlighting their potential in future precision medicine strategies. However, clinical translation faces multiple barriers, such as poor targeting efficiency of delivery systems, unpredictable off-target effects, significant inter-individual variability, and lack of standardized efficacy evaluation frameworks. Therefore, systematic breakthroughs are urgently needed. This review aims to comprehensively summarize the role of miRNA regulatory networks in the pathogenesis, diagnosis, and treatment of PAH, with a particular emphasis on their central position in shaping early-stage precision intervention strategies.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 6","pages":"335-356"},"PeriodicalIF":1.3,"publicationDate":"2025-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12816772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146017098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in cardiovascular gene therapy: a systematic review of nanoparticle-based delivery strategies for atherosclerosis.","authors":"Mahan Khani, Kianoush Shahryari, Samira Masoumi, Maryam Alipour, Zahra Mirzaye, Maryam Fathollahzadeh, Fatemeh Atefat, Behnaz Bastami, Mahsa Rostami Ghezeljeh, Hanie Khalili, Nikoo Navidighaziani, Hossein Zare, Vajihe Kooshamoghadam, Sepehr Ramezanipour, Ghazaleh Elahabadi, Samaneh Dodge, Faizeh Parvandi, Tina Fattahi, Amirhosein Ghafouri-Asbagh, Farbod Khosravi, Mahsa Asadi Anar","doi":"10.62347/WAHG9031","DOIUrl":"10.62347/WAHG9031","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS), the primary cause of cardiovascular morbidity and mortality, involves chronic vascular inflammation and plaque formation. While conventional therapies target systemic risk factors, their limited plaque-specific effects and adverse profiles have driven the exploration of targeted delivery systems. Nanoparticle-mediated delivery of nucleic acid therapies offers a promising strategy to modulate inflammation and promote plaque regression at the molecular level. This study aimed to systematically evaluate recent preclinical evidence on the effectiveness of functionalized nanoparticles for delivering nucleic acid-based therapies to atherosclerotic plaques.</p><p><strong>Methods: </strong>This systematic review, conducted in accordance with the PRISMA 2020 guidelines, evaluated preclinical studies published between 2018 and 2024 that utilized nanoparticles to deliver siRNA, miRNA inhibitors, or antisense oligonucleotides (ASOs) to atherosclerotic plaques. Data extraction included nanoparticle type, targeting ligands, size, loading efficiency, administration route, and therapeutic outcomes. Comparative figures were generated, including a bar chart of plaque reduction efficacy by nanoparticle type and a qualitative heatmap mapping functionalization strategies to molecular targets.</p><p><strong>Results: </strong>Fifteen animal studies met the inclusion criteria. Nanoparticles varied in size (5-190 nm), composition (cyclodextrin, gold, polymeric, lipid-based), and targeting mechanisms (e.g., VCAM1, CD36, integrin ligands). High efficacy was reported for functionalized carriers targeting macrophages or inflammatory pathways, with plaque reductions up to 65.8%. Visual analyses highlighted cyclodextrin-integrin and rHDL-based systems as top-performing strategies, while a heatmap revealed preferred pairings of delivery ligands with nucleic acid targets.</p><p><strong>Conclusion: </strong>Functionalized nanoparticles demonstrate robust preclinical efficacy for delivering nucleic acids to atherosclerotic plaques. These findings support their potential for targeted, multimodal therapy in cardiovascular disease, warranting further clinical investigation into scalable, biocompatible delivery platforms.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 5","pages":"247-266"},"PeriodicalIF":1.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12629888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of sivelestat on postoperative outcomes in patients with acute type A aortic dissection and hypoxemia: a retrospective analysis.","authors":"Yong Lei, Guiying Zhu, Peidong Li, Ziao Lu, Kanglin Xu, Junning Liu","doi":"10.62347/GXHN5984","DOIUrl":"10.62347/GXHN5984","url":null,"abstract":"<p><strong>Objectives: </strong>Preoperative hypoxemia in patients with acute type A aortic dissection (ATAAD) increases the risk of Postoperative pulmonary complications (PPCs). Sivelestat, which is used for acute lung injury has not been extensively studied in ATAAD patients who develop preoperative hypoxemia. This study first aims to evaluate the impact of sivelestat on the duration of postoperative mechanical ventilation and the length of stay in the Intensive Care Unit (ICU) for patients with ATAAD complicated by hypoxemia. Secondly, we investigate the effects of sodium sivelestat on the oxygenation index (OI, PaO₂/FiO₂) and serum inflammatory factors of patients.</p><p><strong>Methods: </strong>In this retrospective study, 143 patients diagnosed with ATAAD undergoing total aortic arch replacement with stent grafting (Sun's) at our hospital (2021-2024) were grouped into sivelestat and non-sivelestat groups. We obtained and compared patient data including demographics, hospitalization, ventilation, and perioperative biomarkers.</p><p><strong>Results: </strong>In total, 79 patients (55.2%) experienced preoperative hypoxemia based on the inclusion criteria. Eventually, 65 patients were enrolled in the study after excluding 14 patients. The postoperative PaO₂/FiO₂ decreased in both groups. The postoperative PaO₂/FiO₂ was significantly higher in the sivelestat group than in the non-sivelestat group at 3d (T2), 5d (T3), and 7d (T4). White blood cell count (WBCc) and neutrophil count (NEUTc) at T3 and T4, as well as a neutrophil percentage (NEUT%) at T4 in the sivelesta group were lower than that in the non-sivelestat group. Additionally, the C-reactive protein (CRP) and Interleukin-6(IL-6) levels in the sivelesta group at T3 and T4 were reduced. The mechanical ventilation duration, ICU, and hospital length of stay in the sivelesta group were shortened. Other clinical indices displayed no significant differences.</p><p><strong>Conclusion: </strong>In summary, patients with ATAAD and preoperative hypoxemia have lower postoperative PaO₂/FiO₂. Besides, sivelestat improves postoperative PaO₂/FiO₂, reduces inflammation, and shortens ventilation as well as ICU/hospital stay in ATAAD patients with preoperative hypoxemia.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 5","pages":"267-277"},"PeriodicalIF":1.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12629884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multidimensional approach to assess cardiovascular disease risk combining biochemical, hematological, lipid ratios, atherosclerotic cardiovascular disease, and WHO/ISH 10-year risk estimators: a cross-sectional study.","authors":"Wakwella Kt Nuwanthika, Dinithi Ik Welivitigoda, Nimesha N Senadeera, Darshana U Kottahachchi, Chathuranga B Ranaweera, Namal K Wijesinghe","doi":"10.62347/LKAH6981","DOIUrl":"10.62347/LKAH6981","url":null,"abstract":"<p><p>Cardiovascular disease (CVD), a leading global health concern and the primary cause of death worldwide, is often associated with atherosclerosis and cardiac events.</p><p><strong>Objective: </strong>This study evaluated biochemical and hematological parameters as predictors of CVD risk using atherosclerotic CVD and World Health Organization/International Society of Hypertension risk scores (WHO/ISH).</p><p><strong>Methodology: </strong>102 volunteer participants representing 69 males (67.6%) and 33 females (32.4%) from the Health and Administrative Staff of University Hospital-General Sir John Kotelawala Defence University, Sri Lanka, were selected. Patient demographics, biometrics, clinical parameters, and behavioral risk factors were collected. Laboratory parameters: complete blood count, lipid profile, aspartate and alanine aminotransferases were performed. The 10-year CVD risk was estimated using the \"ASCVD-Risk Estimator-Plus\" and WHO/ISH risk score charts; South Asia and Southeast Asia. The data were analyzed using IBM-SPSS-version26.</p><p><strong>Results: </strong>The study population showed strong to moderate-strong correlations within the hematological, biochemical, and risk estimators, but not between these parameters. Platelets-to-Lymphocytes Ratio (PLR) had a strong, significant positive correlation with the Neutrophils-to-Lymphocyte Ratio (NLR) and a moderately strong, significant positive correlation with Platelets and NLR (r=0.446; P<0.001), indicating the inflammatory response, atherosclerosis with increased CVD risk. In the regression analysis, the HDL-LDL ratio was found to independently predict the TC-HDL ratio and successfully combined the WHO/ISH risk estimators with the collected biochemical, hematological, clinical, biometric, and behavioral risk factors by introducing highly predictive, well-fit equations. The ROC analysis indicated that once the HDL-LDL-ratio reduces below 0.39, ASCVD-10-year-risk (ASCVD_10) and ASCVD-lifetime-risk (ASCVD_LT) increase to 4.95 and 37.5, respectively.</p><p><strong>Conclusion: </strong>A strong positive correlation was found between NLR, PLR, and CVD risk, with a moderate correlation between PLT and NLR. ASCVD_10 showed a reliable link with ASCVD_OP and ASCVD_LT, marking the first comparison of all three risk types. Predictive equations were developed by integrating WHO/ISH scores and other parameters. The TC-HDL ratio significantly correlated with the HDL-LDL ratio, enabling a cut-off value to predict ASCVD_10 risk and associated hematological and biochemical markers.</p>","PeriodicalId":7427,"journal":{"name":"American journal of cardiovascular disease","volume":"15 5","pages":"278-295"},"PeriodicalIF":1.3,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12629885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}