Current Cardiology Reviews最新文献

{"title":"Disparities in Peripheral Artery Disease-related Mortality in Chronic Inflammatory Disease in the United States from 1999 to 2020.","authors":"April Olson, Hoang Nhat Pham, Ramzi Ibrahim, Mohammed Salih, Amitoj Singh, Mamas A Mamas","doi":"10.2174/011573403X353038241125050631","DOIUrl":"https://doi.org/10.2174/011573403X353038241125050631","url":null,"abstract":"<p><strong>Introduction: </strong>Peripheral arterial disease (PAD) is a marker of significant atherosclerotic cardiovascular disease and is associated with greater healthcare burden and worse prognosis in individuals with chronic inflammatory disease (CID). We aimed to investigate temporal trends and disparities of PAD-related mortality in populations with CID from 1999-2020 across six common CIDs (i.e., chronic viral hepatitis, human immunodeficiency virus, inflammatory bowel disease, psoriasis, rheumatoid arthritis, and systemic lupus erythematosus).</p><p><strong>Methods: </strong>United States (US) PAD and CID-related mortality and demographic data from 1999- 2020 were extracted from the CDC database through the multiple-cause-of-death files. Ageadjusted mortality rates (AAMR) per 1,000,000 and 95% confidence intervals were standardized to the 2000 US population. The mortality trends were analyzed using Joinpoint Regression.</p><p><strong>Results: </strong>A total of 22,175 PAD-related deaths were recorded in the population with CID between 1999 and 2020. Mortality remained stable during the 22-year period (AAPC -0.04%, p=0.95) with a cumulative AAMR of 4.64. Mortality was highest in rural counties (AAMR 5.27), and among non-Hispanic Black populations (AAMR 7.06). Among the CID subtypes, PAD mortality was highest in populations with RA (AAMR 2.48) and lowest in populations with psoriasis (AAMR 0.11).</p><p><strong>Conclusion: </strong>Our findings highlight the disparities of PAD mortality in patients with CID, with the Black population and rural communities disproportionately affected. Further investigation with individual- level data is warranted to identify the contributing factors for the observed disparities.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Atrial Fibrillation Ablation in Heart Failure and Preserved Ejection Fraction: An Observational Study of Risk Factors for Heart Failure Hospitalization.","authors":"Rundi Qi, Hailei Liu, Yue Zhu, Nan Wu, Kexin Wang, Xiangwei Ding, Zhoushan Gu, Mingfang Li, Hongwu Chen, Weizhu Ju, Xin Li, Minglong Chen","doi":"10.2174/011573403X348844241129111639","DOIUrl":"https://doi.org/10.2174/011573403X348844241129111639","url":null,"abstract":"<p><strong>Introduction: </strong>Long-term heart failure hospitalization (HFH) after radiofrequency catheter ablation (RFCA) in atrial fibrillation (AF) patients with heart failure and preserved ejection fraction (HFpEF) and its risk factors remain to be investigated.</p><p><strong>Methods: </strong>AF patients with HFpEF who underwent RFCA from January, 2014 to December, 2018 from three centers were retrospectively included. Patients were assigned to the training and testing cohorts, respectively. In the training cohort, logistic regression analyses were performed to discriminate those with and without HFH. A scoring system was developed accordingly and validated.</p><p><strong>Results: </strong>A total of 417 AF patients with HFpEF receiving RFCA were enrolled. About 35 patients (8.4%) had HFH for 6 years. In the training cohort, the use of diuretics, atrial tachycardia (AT)/AF recurrence, prior HFH, and female sex were independent predictors of HFH in the multivariable analysis. A DAPF score (ranging from 0 to 9.0) was developed. The area under the receiver operating characteristic curve (AUC) of the DAPF score was 0.880 (95% CI, 0.830- 0.929). A DAPF score ≥3.5 could predict HFH with a sensitivity of 81.8% and a specificity of 74.6%. The performance in the testing cohort remained robust (AUC, 0.858; 95% CI, 0.749- 0.967).</p><p><strong>Conclusion: </strong>HFH in patients with AF and HFpEF after RFCA is not rare. The DAPF score could predict the risk of HFH in AF patients with HFpEF after RFCA and guide our treatment strategy.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142806384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Perspectives: Unraveling Cardiovascular Dynamics in High-Altitude Realms.","authors":"Kanishk Aggarwal, Mayur Srinivas Pathan, Mayank Dhalani, Inder P Kaur, Fnu Anamika, Vasu Gupta, Dilip Kumar Jayaraman, Rohit Jain","doi":"10.2174/011573403X308818241030051249","DOIUrl":"10.2174/011573403X308818241030051249","url":null,"abstract":"<p><p>High-altitude regions pose distinctive challenges for cardiovascular health because of decreased oxygen levels, reduced barometric pressure, and colder temperatures. Approximately 82 million people live above 2400 meters, while over 100 million people visit these heights annually. Individuals ascending rapidly or those with pre-existing cardiovascular conditions are particularly vulnerable to altitude-related illnesses, including Acute Mountain Sickness (AMS) and Chronic Mountain Sickness (CMS). The cardiovascular system struggles to adapt to hypoxic stress, which can lead to arrhythmias, systemic hypertension, and right ventricular failure. Pathophysiologically, high-altitude exposure triggers immediate increases in cardiac output and heart rate, often due to enhanced sympathetic activity. Over time, acclimatisation involves complex changes, such as reduced stroke volume and increased blood volume. The pulmonary vasculature also undergoes significant alterations, including hypoxic pulmonary vasoconstriction and vascular remodelling, contributing to conditions, like pulmonary hypertension and high-altitude pulmonary edema. Genetic adaptations in populations living at high altitudes, such as gene variations linked to hypoxia response, further influence these physiological processes. Regarding cardiovascular disease risk, stable coronary artery disease patients generally do not face significant adverse outcomes at altitudes up to 3500 meters. However, those with unstable angina or recent cardiac interventions should avoid high-altitude exposure to prevent exacerbation. Remarkably, high-altitude living correlates with reduced cardiovascular mortality rates, possibly due to improved air quality and hypoxia-induced adaptations. Additionally, there is a higher incidence of congenital heart disease among children born at high altitudes, highlighting the profound impact of hypoxia on heart development. Understanding these dynamics is crucial for managing risks and improving health outcomes in high-altitude environments.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetic Cardiomyopathy: An Update on Emerging Pathological Mechanisms.","authors":"Chirag Kakkar, Veerta Sharma, Ashi Mannan, Gaurav Gupta, Sachin Singh, Puneet Kumar, Kamal Dua, Amarjot Kaur, Shareen Singh, Sonia Dhiman, Thakur Gurjeet Singh","doi":"10.2174/011573403X331870241025094307","DOIUrl":"https://doi.org/10.2174/011573403X331870241025094307","url":null,"abstract":"<p><p>Diabetic Cardiomyopathy (DCM) is a notable consequence of diabetes mellitus, distinguished by cardiac dysfunction that occurs separately from coronary artery disease or hypertension. A recent study has revealed an intricate interaction of pathogenic processes that contribute to DCM. Important aspects involve the dysregulation of glucose metabolism, resulting in heightened oxidative stress and impaired mitochondrial function. In addition, persistent high blood sugar levels stimulate inflammatory pathways, which contribute to the development of heart fibrosis and remodelling. Additionally, changes in the way calcium is managed and the presence of insulin resistance are crucial factors in the formation and advancement of DCM. This may be due to the involvement of many molecular mechanistic pathways such as NLRP3, NF- κB, PKC, and MAPK with their downstream associated signaling pathways. Gaining a comprehensive understanding of these newly identified pathogenic pathways is crucial in order to design precise therapy approaches that can enhance the results for individuals suffering from diabetes. In addition, this review offers an in-depth review of not just pathogenic pathways and molecular mechanistic pathways but also diagnostic methods, treatment options, and clinical trials.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582221","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heart Rate Variability and Heart Failure with Reduced Ejection Fraction: A Systematic Review of Literature.","authors":"Michiaki Nagai, Hallum Ewbank, Yukiko Nakano, Benjamin J Scherlag, Sunny S Po, Tarun W Dasari","doi":"10.2174/011573403X327105241021180916","DOIUrl":"https://doi.org/10.2174/011573403X327105241021180916","url":null,"abstract":"<p><strong>Introduction: </strong>Autonomic impairment is a hallmark of heart failure with reduced ejection fraction (HFrEF). While there have been studies on general values for each index of heart rate variability (HRV) analysis in HFrEF, a systematic review comprehensively examining representative values in HFrEF is lacking.</p><p><strong>Methods: </strong>We searched PubMed, Embase, and Cochrane databases to extract studies reporting representative values of HRV metrics in HFrEF.</p><p><strong>Results: </strong>A total of 470 HFrEF patients from 6 studies were included in the review. In general, time and frequency domains were abnormally lower in HFrEF, portending a worse prognosis. In HFrEF, the mean or median value of the standard deviation of NN interval, root mean square successive difference, pNN50, and low-frequency power/high-frequency power were 40 to 121 msec, 19 to 62 msec, 1.3 to 14%, and 1.00 to 1.73, respectively.</p><p><strong>Conclusion: </strong>In this systematic review, most HRV metrics were found to be calculated from 24- hour Holter recordings and were lower in HFrEF patients with poor prognosis.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Review of Coronary Artery Anatomy Relevant to Cardiac Surgery.","authors":"Emeka B Kesieme, Benjamin Omoregbee, Dumbor L Ngaage, Mark H D Danton","doi":"10.2174/011573403X321942241023112517","DOIUrl":"https://doi.org/10.2174/011573403X321942241023112517","url":null,"abstract":"<p><p>In order to perform safe cardiac surgery, a knowledge of applied coronary artery anatomy and its variants is essential for cardiac surgeons. In normal individuals, the right and the left coronary arteries arise from the corresponding sinuses of Valsalva within the aortic root. From the cardiac surgical perspective, the coronary artery is divided into the left main coronary artery, its branches (the left anterior descending artery and the circumflex artery), and the right coronary artery. With high-risk cardiac surgeries, including redo procedures, becoming increasingly performed, abnormal courses and variations of the coronary arteries, if not recognized, can predispose the patient to avoidable coronary injuries, resulting in adverse outcomes of cardiac surgical procedures. We aim to describe normal and applied coronary anatomy, common coronary artery variants previously reported, and their clinical relevance to both adult and paediatric cardiac surgery.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557352","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling the Complexities: Exploring Mechanisms of Anthracycline-Induced Cardiotoxicity.","authors":"Rohit Tayal, Ashi Mannan, Shareen Singh, Sonia Dhiman, Thakur Gurjeet Singh","doi":"10.2174/011573403X322928241021100631","DOIUrl":"https://doi.org/10.2174/011573403X322928241021100631","url":null,"abstract":"<p><p>The coexistence of cancer and heart disease, both prominent causes of illness and death, is further exacerbated by the detrimental impact of chemotherapy. Anthracycline-induced cardiotoxicity is an unfortunate side effect of highly effective therapy in treating different types of cancer; it presents a significant challenge for both clinicians and patients due to the considerable risk of cardiotoxicity. Despite significant progress in understanding these mechanisms, challenges persist in identifying effective preventive and therapeutic strategies, rendering it a subject of continued research even after three decades of intensive global investigation. The molecular targets and signaling pathways explored provide insights for developing targeted therapies, emphasizing the need for continued research to bridge the gap between preclinical understanding and clinical applications. This review provides a comprehensive exploration of the intricate mechanisms underlying anthracycline-induced cardiotoxicity, elucidating the interplay of various signaling pathways leading to adverse cellular events, including cardiotoxicity and death. It highlights the extensive involvement of pathways associated with oxidative stress, inflammation, apoptosis, and cellular stress responses, offering insights into potential and unexplored targets for therapeutic intervention in mitigating anthracycline-induced cardiac complications. A comprehensive understanding of the interplay between anthracyclines and these complexes signaling pathways is crucial for developing strategies to prevent or mitigate the associated cardiotoxicity. Further research is needed to outline the specific contributions of these pathways and identify potential therapeutic targets to improve the safety and efficacy of anthracycline-based cancer treatment. Ultimately, advancements in understanding anthracycline-induced cardiotoxicity mechanisms will facilitate the development of more efficacious preventive and treatment approaches, thereby improving outcomes for cancer patients undergoing anthracycline-based chemotherapy.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Wnt Pathways with Small Molecules as New Approach in Cardiovascular Disease.","authors":"Seyed Mehdi Mousavi, Fatemeh Jalali-Zefrei, Mohammad Shourmij, Shiva Tabaghi, Amirhesam Davari, Saeed Bahador Khalili, Soghra Farzipour, Arsalan Salari","doi":"10.2174/011573403X333038241023153349","DOIUrl":"https://doi.org/10.2174/011573403X333038241023153349","url":null,"abstract":"<p><p>The increasing incidences of morbidity and mortality associated with cardiovascular diseases represent significant difficulties for clinical treatment and have a major impact on patient health. Wnt signaling pathways are highly conserved and are well known for their regulatory roles in embryonic development, tissue regeneration, and adult tissue homeostasis. Wnt signaling is classified into two distinct pathways: canonical Wnt/β-catenin signaling and noncanonical pathways, including planar cell polarity and Wnt/Ca2+ pathways. A growing body of experimental evidence suggests the involvement of both canonical and non-canonical Wnt signaling pathways in the development of cardiovascular diseases, including myocardial hypertrophy, arrhythmias, diabetic cardiomyopathy, arrhythmogenic cardiomyopathy, and myocardial infarction. Thus, to enhance patient quality of life, diagnosing and treating cardiac illnesses may require a thorough understanding of the molecular functions played by the Wnt pathway in these disorders. Many small-molecule inhibitors specifically target various components within the Wnt signaling pathways, such as Frizzled, Disheveled, Porcupine, and Tankyrase. This study aims to present an overview of the latest findings regarding the functions of Wnt signaling in human cardiac disorders and possible inhibitors of Wnt, which could lead to novel approaches for treating cardiac ailments.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142557353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin Resistance, Hyperinsulinemia and Atherosclerosis: Insights into Pathophysiological Aspects and Future Therapeutic Prospects.","authors":"Georgios S Papaetis, Anastasia Sacharidou, Ioannis C Michaelides, Konstantinos C Mikellidis, Stylianos A Karvounaris","doi":"10.2174/011573403X314035241006185109","DOIUrl":"https://doi.org/10.2174/011573403X314035241006185109","url":null,"abstract":"<p><p>Insulin resistance describes the lack of activity of a known quantity of insulin (exogenous or endogenous) to promote the uptake of glucose and its utilization in an individual, as much as it does in metabolically normal individuals. On the cellular level, it suggests insufficient power of the insulin pathway (from the insulin receptor downstream to its final substrates) that is essential for multiple mitogenic and metabolic aspects of cellular homeostasis. Atherosclerosis is a slow, complex, and multifactorial pathobiological process in medium to large arteries and involves several tissues and cell types (immune, vascular, and metabolic cells). Inflammatory responses and immunoregulation are key players in its development and progression. This paper examines the possible pathophysiological mechanisms that govern the connection of insulin resistance, hyperinsulinemia, and the closely associated cardiometabolic syndrome with atherosclerosis, after exploring thoroughly both in vitro and in vivo (preclinical and clinical) evidence. It also discusses the importance of visualizing and developing novel therapeutic strategies and targets for treatment, to face this metabolic state through its genesis.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Non-rodent Models of Atherosclerosis: Repurposing of Existing Drugs and Search for Novel Treatment Strategies.","authors":"Siarhei A Dabravolski, Victoria A Khotina, Mikhail A Popov, Victor Y Glanz, Vasily N Sukhorukov, Alexander N Orekhov","doi":"10.2174/011573403X316529240919103119","DOIUrl":"https://doi.org/10.2174/011573403X316529240919103119","url":null,"abstract":"<p><p>Atherosclerosis and associated cardiovascular diseases are the leading causes of illness and mortality worldwide. The development of atherosclerosis is a complex process involving oxidative stress, surplus lipid deposition and retention, endothelial dysfunction, and chronic inflammation. Developing novel anti-atherogenic and repurposing existing drugs requires the use of suitable animal models to characterise the fundamental mechanisms underlying atherosclerosis initiation and progression and to evaluate potential therapeutic effects. Commonly used rodent models, however, are not always appropriate, and other models may be required to translate these discoveries into valuable preventive and treatment agents for human applications. Recent advances in gene-editing tools for large animals have allowed the creation of animals that develop atherosclerosis faster and more similarly to humans in terms of lesion localisation and histopathology. In this review, we discuss the major advantages and drawbacks of the main non-rodent animal models of atherosclerosis, particularly rabbits, pigs, zebrafish, and non-human primates. Moreover, we review the application of recently invented novel therapeutic methods and agents, and repurposed existing drugs (such as antidiabetic and anticancer) for atherosclerosis treatment, the efficacy of which is verified on non-rodent animal models of atherosclerosis. In total, the proper selection of a suitable animal model of atherosclerosis facilitates reproducible and rigorous translational research in repurposing of existing drugs, discovering new therapeutic strategies, and validating novel anti-atherosclerotic drugs.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":" ","pages":""},"PeriodicalIF":2.4,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142371203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}