Ahmed El-Medany, Vanessa Kandoole, Nicholas Lonsdale, Gemina Doolub, Ioannis Felekos
{"title":"In-stent Thrombosis and COVID-19 Infection: Current Insights on the Mechanistic Relationship.","authors":"Ahmed El-Medany, Vanessa Kandoole, Nicholas Lonsdale, Gemina Doolub, Ioannis Felekos","doi":"10.2174/1573403X18666220512142019","DOIUrl":"10.2174/1573403X18666220512142019","url":null,"abstract":"<p><p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been demonstrated as a major risk factor in inducing coronary stent thrombosis due to its propensity to create a pro-thrombotic state. This review explores the mechanisms that may contribute to the increased thrombosis risk seen in COVID-19. Furthermore, we discuss the patient and haematological factors that predispose to an increased risk of stent thrombosis, as well as the role of certain antiplatelet and anticoagulation therapies, including ticagrelor and enoxaparin, that may reduce the likelihood and severity of in-stent thrombosis, in SARS-CoV-2 infection. To counter the proinflammatory and pro-thrombotic state shown in COVID-19, anti-thrombotic therapy in the future may be optimised using point-of-care platelet inhibition testing and inflammation-modifying therapies. Large-scale randomised trials with long-term follow-up are increasingly necessary to assess the intersection of COVID-19 and stent optimisation as well as the reduction of stent thrombosis after drug-eluting stent (DES) implantation.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10201881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9217801","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":"Coronary Bifurcation Stenting: Review of Current Techniques and Evidence.","authors":"Surya Kiran Aedma, Anant Naik, Arun Kanmanthareddy","doi":"10.2174/1573403X18666220406113517","DOIUrl":"10.2174/1573403X18666220406113517","url":null,"abstract":"<p><strong>Background: </strong>Coronary bifurcation stenting constitutes 20% of all PCI performed. Given the extensive prevalence of bifurcation lesions, various techniques have sought to optimally stent the bifurcation to improve revascularization while also decreasing rates of stent thrombosis and lesion recurrence. Advanced techniques, such as planned two-stent approaches, have been shown to have improved outcomes but also require fluoroscopy and procedure time, posing an economic argument as well as a patient-outcome one.</p><p><strong>Objective: </strong>Because of the many strategies posited in the literature, it becomes essential to objectively evaluate evidence from randomized controlled trials and meta-analyses to help determine the optimal stenting strategy.</p><p><strong>Methods: </strong>We reviewed the clinical evidence on the efficacy of coronary bifurcation stenting.</p><p><strong>Results: </strong>In this paper, we review the most recent randomized controlled trials and meta-analyses on the efficacy of various stenting techniques and advances in stenting technologies published to gauge the current state of understanding and chart where the field is heading.</p><p><strong>Conclusion: </strong>Bifurcation stenting is a maturing problem in the field of interventional cardiology that is adapting to the needs of the patients and advances in technology.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10201883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10665385","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":"Modern Concepts of the Role of Fine Particles (PM 2.5) in the Genesis of Atherosclerosis and Myocardial Damage: Clinical and Epidemiological Data, the Main Pathophysiological Mechanisms.","authors":"Aleksey Michailovich Chaulin, Artem Konstantinovich Sergeev","doi":"10.2174/1573403X18666220817103105","DOIUrl":"10.2174/1573403X18666220817103105","url":null,"abstract":"<p><p>Due to the fact that atherosclerotic cardiovascular diseases (CVDs) dominate in the structure of morbidity, disability and mortality of the population, the study of the risk factors for the development of atherosclerotic CVDs, as well as the study of the underlying pathogenetic mechanisms thereof, is the most important area of scientific research in modern medicine. Understanding these aspects will allow improving the set of treatment and preventive measures and activities. One of the important risk factors for the development of atherosclerosis, which has been actively studied recently, is air pollution with fine particulate matter (PM 2.5). According to clinical and epidemiological data, the level of air pollution with PM 2.5 exceeds the normative indicators in most regions of the world and is associated with subclinical markers of atherosclerosis and mortality from atherosclerotic CVDs. The aim of this article is to systematize and discuss in detail the role of PM 2.5 in the development of atherosclerosis and myocardial damage with the consideration of epidemiological and pathogenetic aspects. Materials and Methods: This narrative review is based on the analysis of publications in the Medline, PubMed, and Embase databases. The terms \"fine particles\" and \"PM 2.5\" in combination with \"pathophysiological mechanisms,\" \"cardiovascular diseases\", \"atherosclerosis\", \"cardiac troponins\", \"myocardial damage\" and \"myocardial injury\" were used to search publications. Conclusion: According to the conducted narrative review, PM 2.5 should be regarded as the significant risk factor for the development of atherosclerotic CVDs. The pro-atherogenic effect of fine particulate matter is based on several fundamental and closely interrelated pathophysiological mechanisms: endothelial dysfunction, impaired lipid metabolism, increased oxidative stress and inflammatory reactions, impaired functioning of the vegetative nervous system and increased activity of the hemostatic system. In addition, PM 2.5 causes subclinical damage to cardiac muscle cells by several mechanisms: apoptosis, oxidative stress, decreased oxygen delivery due to coronary atherosclerosis and ischemic damage of cardiomyocytes. Highly sensitive cardiac troponins are promising markers for detecting subclinical myocardial damage in people living in polluted regions.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10201893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10133353","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}
Luai Madanat, Ruby Gupta, Paul Weber, Navneet Kumar, Rohit Chandra, Hycienth Ahaneku, Yatharth Bansal, Joseph Anderson, Abhay Bilolikar, Ishmael Jaiyesimi
{"title":"Cardiotoxicity of Biological Therapies in Cancer Patients: An In-depth Review.","authors":"Luai Madanat, Ruby Gupta, Paul Weber, Navneet Kumar, Rohit Chandra, Hycienth Ahaneku, Yatharth Bansal, Joseph Anderson, Abhay Bilolikar, Ishmael Jaiyesimi","doi":"10.2174/1573403X18666220531094800","DOIUrl":"10.2174/1573403X18666220531094800","url":null,"abstract":"<p><p>Cardiotoxicity from chemotherapy regimens has been long reported. However, the understanding of cardiac side effects of biological therapies is rapidly evolving. With cancer patients achieving higher life expectancy due to the use of personalized medicine and novel targeted anticancer agents, the occurrence of cardiotoxicity is becoming more significant. Novel biological therapies include anti-HER2 antibodies, tyrosine kinase inhibitors, bruton kinase inhibitors, antivascular endothelial growth factors, proteasome inhibitors, immunomodulator drugs, and immune checkpoint inhibitors. Potential cardiovascular toxicities linked to these anticancer agents include hypertension, arrhythmias, QT prolongation, myocardial ischemia and infarction, left ventricular dysfunction, congestive heart failure, and thromboembolism. Cardiac biomarkers, electrocardiography, echocardiography and magnetic resonance imaging are common diagnostic modalities used for early detection of these complications and timely intervention. This review discusses the various types of cardiotoxicities caused by novel anticancer biologic agents, their molecular and pathophysiological mechanisms, risk factors, and diagnostic and management strategies that can be used to prevent, minimize, and treat them.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10280990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10151296","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":"Stem Cells and Congenital Heart Disease: The Future Potential Clinical Therapy Beyond Current Treatment.","authors":"Katherine Julian, Nikita Garg, Narutoshi Hibino, Rohit Jain","doi":"10.2174/1573403X18666220531093326","DOIUrl":"10.2174/1573403X18666220531093326","url":null,"abstract":"<p><p>Congenital heart disease (CHD) is the most common congenital anomaly in newborns. Current treatment for cyanotic CHD largely relies on the surgical intervention; however, significant morbidity and mortality for patients with CHD remain. Recent research to explore new avenues of treating CHD includes the utility of stem cells within the field. Stem cells have since been used to both model and potentially treat CHD. Most clinical applications to date have focused on hypoplastic left heart syndrome. Here, we examine the current role of stem cells in CHD and discuss future applications within the field.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10201894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9774360","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}
Pupalan Iyngkaran, Charlotte Hespe, Fahad Hanna, John D Horowitz, Malcolm Battersby, Craig Nelson, Sharon Andrew, Maximilian P de Courten
{"title":"The Wider Considerations in Closing Chronic Disease Gaps - Focus on Heart Failure and Implementation.","authors":"Pupalan Iyngkaran, Charlotte Hespe, Fahad Hanna, John D Horowitz, Malcolm Battersby, Craig Nelson, Sharon Andrew, Maximilian P de Courten","doi":"10.2174/1573403X18666220512160737","DOIUrl":"10.2174/1573403X18666220512160737","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) is predominately a chronic disease. There are overlaps in HF and chronic disease research and care. Chronic disease and HF research are conducted with multiple goals. The overarching goal is \"optimized patient outcomes at maximum costeffectiveness\". However, observations on patients can come with many variables; thus, we see differences in clinical translation. This document discusses an argument for three important gaps common to HF and chronic disease, i.e., screening, self-management, and patient-reported outcomes (PRO), and provides a glance of how it could fit into the evidence tree. Pertinent arguments for a framework for health services and models of care are provided as a prelude to future consensus.</p><p><strong>Methodology: </strong>1) A preliminary literature review to identify a taxonomy for cardiovascular research, and 2) a review of the published literature describing the translation of research studies into clinical practice for cardiovascular disorders. A spectrum from observational to large randomized controlled trials to post-marketing studies were identified.</p><p><strong>Discussion: </strong>A brief discussion on traditional research and differences focusing on screening, mixed methods research concepts, and chronic diseases models of care. Six steps to facilitate this: 1) Research design; 2) Research application (translation) i. routine ii. challenges; 3. Transforming research to translational level; 4. Funding and infrastructure; 5. Clinical Centres of Research Excellence (CCRE) and collaboration; 6. Governance and cost-effectiveness.</p><p><strong>Conclusion: </strong>Implementation research that aims to link research findings to improved patient outcomes in an efficient and effective way is a neglected area. Skills required to perform implementation research are complex. Ways to maximize translational impacts for chronic disease research to clinical practice are described in a HF context.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10201899/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9775690","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}
Riccardo Proietti, Andrea S Giordani, Calò A Lorenzo
{"title":"ROCK (RhoA/Rho Kinase) Activation in Atrial Fibrillation: Molecular Pathways and Clinical Implications.","authors":"Riccardo Proietti, Andrea S Giordani, Calò A Lorenzo","doi":"10.2174/1573403X19666221117092951","DOIUrl":"10.2174/1573403X19666221117092951","url":null,"abstract":"<p><p>Among the complex mechanisms of AF pathogenesis, intracellular calcium overload and oxidative stress play a major role, both triggered by inflammatory processes. The additional basic event taking place in AF is atrial fibrotic remodeling, again triggered by oxidative stress, which is determined by connexins rearrangement and differentiation of fibroblasts into active collagensecreting myofibroblasts. RhoA/ROCK system is the final pathway of a wide spectrum of molecular effectors such as Angiotensin II, platelet-derived growth factor, connective tissue growth factor and transforming growth factor β, that overall determine calcium dysregulation and pro-fibrotic remodeling. Both in experimental and clinical studies, RhoA/ROCK activation has been linked to superoxide ion production, fibrotic remodeling and connexins rearrangement, with important consequences for AF pathogenesis. ROCK pathway inhibition may therefore be a therapeutic or preventive target for special AF subgroups of patients.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":1.9,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10280999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9777873","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":"Countermeasures for Maintaining Cardiovascular Health in Space Missions.","authors":"Jhilam Pramanik, Akash Kumar, Lakshay Panchal, Bhupendra Prajapati","doi":"10.2174/1573403X19666230330083225","DOIUrl":"10.2174/1573403X19666230330083225","url":null,"abstract":"<p><p>During space exploration, the human body is subjected to altered atmospheric environments and gravity, exposure to radiation, sleep disturbance, and mental pressures; all these factors are responsible for cardiovascular diseases. Under microgravity, the physiological changes related to cardiovascular diseases are the cephalic fluid shift, dramatic reduction in central venous pressure, changes in blood rheology and endothelial function, cerebrovascular abnormalities, headaches, optic disc edema, intracranial hypertension, congestion of the jugular vein, facial swelling, and loss of taste. Generally, five countermeasures are used to maintain cardiovascular health (during and after space missions), including shielding, nutritional, medicinal, exercise, and artificial gravity. This article concludes with how to reduce space missions' impact on cardiovascular health with the help of various countermeasures.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518885/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9882993","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}
Michael Dangl, Michael Albosta, Hoda Butros, Matthias Loebe
{"title":"Temporary Mechanical Circulatory Support: Left, Right, and Biventricular Devices.","authors":"Michael Dangl, Michael Albosta, Hoda Butros, Matthias Loebe","doi":"10.2174/1573403X19666230314115853","DOIUrl":"10.2174/1573403X19666230314115853","url":null,"abstract":"<p><p>Temporary mechanical circulatory support (MCS) encompasses a wide array of invasive devices, which provide short-term hemodynamic support for multiple clinical indications. Although initially developed for the management of cardiogenic shock, indications for MCS have expanded to include prophylactic insertion prior to high-risk percutaneous coronary intervention, treatment of acute circulatory failure following cardiac surgery, and bridging of end-stage heart failure patients to more definitive therapies, such as left ventricular assist devices and cardiac transplantation. A wide variety of devices are available to provide left ventricular, right ventricular, or biventricular support. The choice of a temporary MCS device requires consideration of the clinical scenario, patient characteristics, institution protocols, and provider familiarity and training. In this review, the most common forms of left, right, and biventricular temporary MCS are discussed, along with their indications, contraindications, complications, cannulations, hemodynamic effects, and available clinical data.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10518886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9934374","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":"Appraisal of Cardiovascular Risk Factors, Biomarkers, and Ocular Imaging in Cardiovascular Risk Prediction.","authors":"Julie S Moore, M Andrew Nesbit, Tara Moore","doi":"10.2174/1573403X19666230727101926","DOIUrl":"10.2174/1573403X19666230727101926","url":null,"abstract":"<p><p>Cardiovascular disease remains a leading cause of death worldwide despite the use of available cardiovascular disease risk prediction tools. Identification of high-risk individuals via risk stratification and screening at sub-clinical stages, which may be offered by ocular screening, is important to prevent major adverse cardiac events. Retinal microvasculature has been widely researched for potential application in both diabetes and cardiovascular disease risk prediction. However, the conjunctival microvasculature as a tool for cardiovascular disease risk prediction remains largely unexplored. The purpose of this review is to evaluate the current cardiovascular risk assessment methods, identifying gaps in the literature that imaging of the ocular microcirculation may have the potential to fill. This review also explores the themes of machine learning, risk scores, biomarkers, medical imaging, and clinical risk factors. Cardiovascular risk classification varies based on the population assessed, the risk factors included, and the assessment methods. A more tailored, standardised and feasible approach to cardiovascular risk prediction that utilises technological and medical imaging advances, which may be offered by ocular imaging, is required to support cardiovascular disease prevention strategies and clinical guidelines.</p>","PeriodicalId":10832,"journal":{"name":"Current Cardiology Reviews","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10636798/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9873761","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}