World Journal of Cardiology最新文献

{"title":"Coronary heart disease with pulmonary embolism: A case report.","authors":"Jun-Qing Xu, Meng-Xin Jiang, Feng Wang, Kai-Qiang Yang, Ying-Jiang Xu, Yu-Jiu Wang, Sheng-Jun Dong","doi":"10.4330/wjc.v17.i2.101588","DOIUrl":"10.4330/wjc.v17.i2.101588","url":null,"abstract":"<p><strong>Background: </strong>Coronary heart disease (CHD) and pulmonary embolism (PE) are thrombotic diseases. Patients with CHD and PE are common in clinical practice. However, the clinical diagnosis of PE is challenging due to overlapping primary symptoms, such as chest tightness and dyspnea. This confluence frequently leads to the misdiagnosis of PE, thus precipitating treatment delays and compromising patient outcomes. Herein, we report the case of a patient with both diseases who underwent surgery and medication therapy.</p><p><strong>Case summary: </strong>A 51-year-old man with a history of hypertension for 2 years visited a local hospital because of paroxysmal chest tightness for 1 d and was diagnosed with CHD. However, he refused hospitalization. He visited our hospital for the treatment of recurring symptoms. A comprehensive examination after admission revealed elevated D-dimer levels, and computed tomography pulmonary angiography was performed to confirm the diagnosis of PE. The patient successfully underwent coronary artery bypass grafting with anticoagulant and antiplatelet drugs and had a prognosis.</p><p><strong>Conclusion: </strong>D-dimer is useful in screening for PE, whereas computed tomography pulmonary angiography is important for diagnosis. For patients with CHD and PE, coronary artery bypass grafting combined with anticoagulant and antiplatelet therapy is feasible.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 2","pages":"101588"},"PeriodicalIF":1.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11886396/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586995","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":"Red blood cell distribution width to albumin ratio is correlated with prognosis of patients in coronary care unit.","authors":"Jiao-Ni Wang, Ze-Song Hu, Yong-Wei Yu, Xiao-Hui Peng","doi":"10.4330/wjc.v17.i2.103273","DOIUrl":"10.4330/wjc.v17.i2.103273","url":null,"abstract":"<p><strong>Background: </strong>As red blood cell distribution width (RDW) and albumin have been shown to be independent predictors of mortality from various diseases, this study aimed to investigate the effect of the RDW to albumin ratio (RA) as an independent predictor of the prognosis of patients admitted to the coronary care unit (CCU).</p><p><strong>Aim: </strong>To use the RDW and albumin level to predict the prognosis of patients in the CCU.</p><p><strong>Methods: </strong>Data were obtained from the Medical Information Mart Intensive Care III database. The primary outcome was 365-day all-cause mortality, whereas the secondary outcomes were 30- and 90-day all-cause mortality, hospital length of stay (LOS), and CCU LOS. Cox proportional hazards regression model, propensity score matching, and receiver operating characteristic curve analyses were used.</p><p><strong>Results: </strong>The hazard ratio (95% confidence interval) of the upper tertile (RA > 4.66) was 1.62 (1.29 to 2.03) when compared with the reference (RA < 3.84) in 365-day all-cause mortality. This trend persisted after adjusting for demographic and clinical variables in the propensity score-matching analysis. Similar trends were observed for the secondary outcomes of hospital and CCU LOS. Receiver operating characteristic curve analysis was performed by combining the RA and sequential organ failure assessment (SOFA) scores, and the C-statistic was higher than that of the SOFA scores (0.733 <i>vs</i> 0.702, <i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>RA is an independent prognostic factor in patients admitted to the CCU. RA combined with the SOFA score can improve the predictive ability of the SOFA score. However, our results should be verified in future prospective studies.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 2","pages":"103273"},"PeriodicalIF":1.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11886393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143587359","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":"Combinatorial approach to treat iron overload cardiomyopathy in pediatric patients with thalassemia-major: A systematic review and meta-analysis.","authors":"Moaz Safwan, Mariam Safwan Bourgleh, Aseel Alsudays, Khawaja Husnain Haider","doi":"10.4330/wjc.v17.i2.103733","DOIUrl":"10.4330/wjc.v17.i2.103733","url":null,"abstract":"<p><strong>Background: </strong>Iron overload cardiomyopathy is a significant cause of morbidity and mortality in transfusion-dependent thalassemia patients. Standard iron chelation therapy is less efficient in alleviating iron accumulation in many organs, especially when iron enters the cells <i>via</i> specific calcium channels.</p><p><strong>Aim: </strong>To validate our hypothesis that adding amlodipine to the iron chelation regimen is more efficient in alleviating myocardial iron overload.</p><p><strong>Methods: </strong>Five databases, including PubMed, Cochrane Library, Embase, ScienceDirect, and ClinicalTrials.gov, were systematically searched, and three randomized controlled trials involving 144 pediatric patients with transfusion-dependent thalassemia were included in our meta-analysis based on the predefined eligibility criteria. The quality of the included studies was assessed based on the Cochrane collaboration tool for bias assessment. The primary outcome assessed was myocardial-T2 and myocardial iron concentration, while the secondary results showed serum ferritin level, liver iron concentration, and treatment adverse outcomes. Weighted mean difference and odds ratio were calculated to measure the changes in the estimated treatment effects.</p><p><strong>Results: </strong>During the follow-up period, Amlodipine treatment significantly improved cardiac T2 by 2.79 ms compared to the control group [95% confidence interval (CI): 0.34-5.24, <i>P</i> = 0.03, <i>I</i> ² = 0%]. Additionally, a significant reduction of 0.31 in myocardial iron concentration was observed with amlodipine treatment compared to the control group [95%CI: -0.38-(-0.25), <i>P</i> < 0.00001, <i>I</i> ² = 0%]. Liver iron concentration was slightly lower in the amlodipine group by -0.04 mg/g, but this difference was not statistically significant (95%CI: -0.33-0.24, <i>P</i> = 0.77, <i>I</i> ² = 0%). Amlodipine also showed a non-significant trend toward a reduction in serum ferritin levels (-328.86 ng/mL, 95%CI: -1212.34-554.62, <i>P</i> = 0.47, <i>I</i> ² = 90%). Regarding safety, there were no significant differences between the groups in the incidence of gastrointestinal upset, hypotension, or lower limb edema.</p><p><strong>Conclusion: </strong>Amlodipine with iron chelation therapy significantly improved cardiac parameters, including cardiac-T2 and myocardial iron, in patients with transfusion-dependent thalassemia without causing significant adverse events but enhancing the efficacy of iron chelation therapy.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 2","pages":"103733"},"PeriodicalIF":1.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11886390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586884","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":"Comprehensive understanding of a rare disease: Cardiac metastatic tumor, a double-center 10-year case review.","authors":"Ling-Yun Luo, Tian-Shu Yang, Zhen He, Li Lin, Xue-Lian Luo","doi":"10.4330/wjc.v17.i2.101851","DOIUrl":"10.4330/wjc.v17.i2.101851","url":null,"abstract":"<p><strong>Background: </strong>Cardiac metastatic tumors (CMTs) are rare yet pose significant medical concerns. Clinical studies on CMT are limited, particularly those involving multicenter data analysis.</p><p><strong>Aim: </strong>To systematically analyze the etiology, sources, classification, treatment, and prognosis of CMT.</p><p><strong>Methods: </strong>A total of 226 CMT patients from two centers (2013 to 2023) were reviewed, and 153 tumor patients from China Health and Retirement Longitudinal Study were used as controls. The survival rates of 96 CMT patients were tracked through medical records and telephone follow-ups. Logistic regression and survival analyses were conducted to characterize CMT.</p><p><strong>Results: </strong>CMTs were predominantly male (67.26% <i>vs</i> 39.47%, <i>P</i> < 0.001). Intracardiac metastasis patients had worse heart and coagulation function than pericardial metastasis patients (prothrombin time: 13.90 <i>vs</i> 13.30, <i>P</i> = 0.002), D-dimer levels (2.16 <i>vs</i> 0.85, <i>P</i> = 0.001), B-type natriuretic peptide (BNP) levels (324.00 <i>vs</i> 136.50, <i>P</i> = 0.004), and troponin levels (5.35 <i>vs</i> 0.03, <i>P</i> < 0.001)). Lung and liver cancers were the predominant primary tumor types in CMT. Patients with lung cancer (76.40% <i>vs</i> 30.77%) and thymoma (7.45% <i>vs</i> 1.54%) exhibited a higher prevalence of pericardial metastasis, while those with liver cancer (35.38% <i>vs</i> 0.62%) showed a higher prevalence of intracardiac metastasis. Overall survival was better for pericardial metastasis than for intracardiac metastasis patients (median survival: 419 days <i>vs</i> 129 days, log-rank test <i>P</i> = 0.0029). Cox proportional hazards model revealed that advanced age [hazard ratio (HR) = 1.034, 95% confidence interval (95%CI): 1.011-1.057] and higher BNP and troponin levels (HR = 1.011, 95%CI: 1.004-1.018) were associated with worse survival. Surgery significantly improved the survival rate of patients. The median survival time was 275 days for patients who did not undergo surgery and 708 days for those who had surgery (log-rank test <i>P</i> = 0.0128).</p><p><strong>Conclusion: </strong>Clinicians should consider CMT in the male lung or liver cancer patients with cardiac symptoms. Abnormal coagulation, impaired heart function, tumor location, and age are key prognostic factors for CMT. Surgical intervention is the preferred treatment option, as it significantly prolongs median survival.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 2","pages":"101851"},"PeriodicalIF":1.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11886389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143586994","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":"Metabolic dysfunction-associated steatotic liver disease and type 2 diabetes: A dual threat to cardiac dysfunction progression.","authors":"Wei Wang, Charlie Cooper","doi":"10.4330/wjc.v17.i1.102467","DOIUrl":"10.4330/wjc.v17.i1.102467","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), particularly in patients with type 2 diabetes mellitus (T2DM), is increasingly recognized as a multi-system disease that affects both hepatic and cardiovascular health. This study explores the association between MASLD-related liver fibrosis and cardiac dysfunction, focusing on how liver fibrosis contributes to cardiac remodeling and dysfunction. Cernea <i>et al</i>'s research highlights the strong correlation between liver fibrosis and changes in left ventricular mass, left atrial dimensions, and systolic and diastolic function in diabetic patients. Notably, the study suggests a protective role of sex-hormone binding protein against cardiac remodeling. These findings underline the importance of early detection of liver fibrosis using non-invasive markers like fibrosis-4 index and nonalcoholic fatty liver disease fibrosis scores, which may offer dual protection for both liver and heart health in T2DM patients. Moreover, this study calls for further research into the shared pathogenic mechanisms, including inflammation and fibrosis pathways, between the liver and heart. It advocates for the integration of liver fibrosis screening into cardiovascular risk management, urging clinicians to adopt a more holistic approach in treating patients with MASLD and T2DM. The research has broad implications for preventing cardiovascular complications and improving outcomes in this high-risk population.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"102467"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755129/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047880","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":"Demographic trends in mortality with older population due to atrial fibrillation and flutter from 1999-2020.","authors":"Mahnoor Sukaina, Marium Waheed, Shafi Rehman, Md Al Hasibuzzaman, Rabab Meghani","doi":"10.4330/wjc.v17.i1.99933","DOIUrl":"10.4330/wjc.v17.i1.99933","url":null,"abstract":"<p><p>Atrial fibrillation (AF)/atrial flutter (AFL) is the most common sustained cardiac arrhythmia. The known risk factors for developing AF/AFL include age, structural heart disease, hypertension, diabetes mellitus, or hyperthyroidism. This study aims to attribute the trends in AF/AFL-related mortalities over the past two decades 1999-2020 concerning race and sex and disparity among them. To the best of our knowledge, this is the first study that estimates the trends and mortality due to AF/AFL from 1999-2020 in older adults in the United States. In this 21-year analysis of mortality data, we found a constant increase in mortality rates due to AF/AFL in older adults. From 1999 to 2020, the overall mortality in older adults aged 65 and above, regardless of sex and race, is found to be almost doubled <i>i.e.</i> about a 50.2% increase in the number of deaths due to AF/AFL. Furthermore, other confounding risk factors such has obesity, prior myocardial infarction, inflammation, hypertension, birth weight, diabetes mellitus, hyperthyroidism, hormone replacement therapy in menopausal women increases the risk in the occurrence or recurrent occurrence of AF.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"99933"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047859","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 sodium-glucose cotransporter-2 inhibitors on pulmonary vascular cell function and arterial remodeling.","authors":"Jing-Jing Zhang, Xue-Rui Ye, Xue-Song Liu, Hao-Ling Zhang, Qian Qiao","doi":"10.4330/wjc.v17.i1.101491","DOIUrl":"10.4330/wjc.v17.i1.101491","url":null,"abstract":"<p><p>Sodium-glucose cotransporter-2 (SGLT-2) inhibitors represent a cutting-edge class of oral antidiabetic therapeutics that operate through selective inhibition of glucose reabsorption in proximal renal tubules, consequently augmenting urinary glucose excretion and attenuating blood glucose levels. Extensive clinical investigations have demonstrated their profound cardiovascular efficacy. Parallel basic science research has elucidated the mechanistic pathways through which diverse SGLT-2 inhibitors beneficially modulate pulmonary vascular cells and arterial remodeling. Specifically, these inhibitors exhibit promising potential in enhancing pulmonary vascular endothelial cell function, suppressing pulmonary smooth muscle cell proliferation and migration, reversing pulmonary arterial remodeling, and maintaining hemodynamic equilibrium. This comprehensive review synthesizes current literature to delineate the mechanisms by which SGLT-2 inhibitors enhance pulmonary vascular cell function and reverse pulmonary remodeling, thereby offering novel therapeutic perspectives for pulmonary vascular diseases.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"101491"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047874","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":"Umbilical cord-derived mesenchymal stromal cells: Promising therapy for heart failure.","authors":"Ya-Lun Li, En-Guo Chen, Bing-Bing Ren","doi":"10.4330/wjc.v17.i1.101153","DOIUrl":"10.4330/wjc.v17.i1.101153","url":null,"abstract":"<p><p>Heart failure (HF) is a complex syndrome characterized by the reduced capacity of the heart to adequately fill or eject blood. Currently, HF remains a leading cause of morbidity and mortality worldwide, imposing a substantial burden on global healthcare systems. Recent advancements have highlighted the therapeutic potential of mesenchymal stromal cells (MSCs) in managing HF. Notably, umbilical cord-derived MSCs (UC-MSCs) have demonstrated superior clinical potential compared to traditional bone marrow-derived MSCs; this is evident in their non-invasive collection process, higher proliferation efficacy, and lower immunogenicity and tumorigenicity, as substantiated by preclinical studies. Although the feasibility and safety of UC-MSCs have been tested in animal models, the application of UC-MSCs in HF treatment remains challenged by issues such as inaccurate targeted migration and low survival rates of UC-MSCs. Therefore, further research and clinical trials are imperative to advance the clinical application of UC-MSCs.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"101153"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143048022","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":"Global hotspots and trends on environmental exposure and cardiovascular disease from 1999 to 2022.","authors":"Xin-Jie Zhang, Qing Tan, Zheng-Yu Xu, Song Wen, Shu-Bo Chen","doi":"10.4330/wjc.v17.i1.102409","DOIUrl":"10.4330/wjc.v17.i1.102409","url":null,"abstract":"<p><strong>Background: </strong>The increasing risk of cardiovascular disease (CVD) associated with worsening environmental exposure is a critical health concern garnering global research attention.</p><p><strong>Aim: </strong>To systematically assess the scope and characteristics of research on the relationship between environmental exposure and CVD.</p><p><strong>Methods: </strong>A thorough examination of publications on the relationship between environmental exposure and CVD from 1999 to 2022 was carried out by extensively screening the literature using the Web of Science Core Collection. The language of the selected publications was standardized to English. Afterward, different academic tools such as CiteSpace, VOSviewer, HistCite, Python, Matplotlib, and Bibliometrix were utilized to examine the research trends in this field.</p><p><strong>Results: </strong>The study's findings indicated a steady increase in scientific publications among the 1640 analyzed documents, peaking in 2022 with 197 publications. The United States emerged as the leading nation regarding high-quality publications and international collaboration. Harvard University was identified as the most prolific institution. \"Environmental research\" was the most frequently contributing journal, and Muenzel T was recognized as the top contributor. Current research hotspots are primarily concentrated on themes such as \"cardiovascular disease\", \"exposure\", \"risk\", \"mortality\", and \"air pollution\".</p><p><strong>Conclusion: </strong>This study highlights increasing research on the link between environmental exposure and CVD, identifying key exposures and diseases while emphasizing the need for further investigation into underlying mechanisms.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"102409"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047871","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":"Pathogenic genes and clinical prognosis in hypertrophic cardiomyopathy.","authors":"Ying Hong, Hu-Tao Xi, Xin-Yi Yang, Wilber W Su, Xiao-Ping Li","doi":"10.4330/wjc.v17.i1.99595","DOIUrl":"10.4330/wjc.v17.i1.99595","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is an autosomal dominant inherited cardiomyopathy characterized by left ventricular hypertrophy. It is one of the chief causes of sudden cardiac death in younger people and athletes. Molecular-genetic studies have confirmed that the vast majority of HCM is caused by mutations in genes encoding sarcomere proteins. HCM has a relatively wide phenotypic heterogeneity, varying from asymptomatic to sudden cardiac death, because of the many different mutations and pathogenic genes underlying it. Many studies have explored the clinical symptoms and prognosis of HCM, emphasizing the importance of genotype in evaluating patient prognosis and guiding the clinical management of HCM. To elaborate the main pathogenic genes and phenotypic prognosis in HCM to promote a better understanding of this genetic disease. Retrospective analysis of literature to evaluate the association between underlying gene mutations and clinical phenotypes in HCM patients. As sequencing technology advances, the pathogenic gene mutation spectrum and phenotypic characteristics of HCM are gradually becoming clearer. HCM is a widespread inherited disease with a highly variable clinical phenotype. The precise mechanisms linking known pathogenic gene mutations and the clinical course of this heterogeneous condition remain elusive.</p>","PeriodicalId":23800,"journal":{"name":"World Journal of Cardiology","volume":"17 1","pages":"99595"},"PeriodicalIF":1.9,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11755131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047896","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}