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Responses Triggered by the Immune System in Hypertensive Conditions and Repercussions on Target Organ Damage: A Review. 免疫系统在高血压条件下触发的反应和对靶器官损伤的反应:综述。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220920090632
Carlos Henrique Nascimento Domingues da Silva, Idrys Henrique Leite Guedes, Jefferson Carlos Santos de Lima, João Marcelo Duarte Ribeiro Sobrinho, Angela Amancio Dos Santos

Background: Hypertension is a chronic, multifactorial clinical condition characterized by sustained high blood pressure levels. It is often associated with functional-structural alterations of target organs, which include heart, brain, kidneys, and vasculature.

Objective: This study highlights the recent correlation between the immune system and hypertension and its repercussions on target-organ damage.

Methods: The descriptors used for the search of the study were "hypertension", "immunity", and "target organs". The methodology of the study followed the main recommendations of the PRISMA statement.

Results: The damage to the vasculature arises mainly from the migration of T cells and monocytes that become pro-inflammatory in the adventitia, releasing TNF-α, IFN-γ, and IL-17, which induce endothelial damage and hinder vascular relaxation. In the renal context, the inflammatory process associated with hypertension culminates in renal invasion by leukocytes, which contribute to the injury of this organ by mechanisms of intense sympathetic stimulation, activation of the reninangiotensin system, sodium retention, and aggravation of oxidative stress. In the cardiac context, hypertension increases the expression of pro-inflammatory elements, such as B, T, and NK cells, in addition to the secretion of IFN-γ, IL-17, IL-23, and TNF-α from angiotensin II, reactive oxygen species, and aldosterone. This pro-inflammatory action is also involved in brain damage through SphK1. In view of the above, the participation of the immune system in hypertension-induced injuries seems to be unequivocal.

Conclusion: Therefore, understanding the multifactorial mechanisms related to hypertension will certainly allow for more efficient interventions in this condition, preventing target organ damage.

背景:高血压是一种慢性、多因素的临床疾病,其特征是持续的高血压水平。它通常与靶器官的功能结构改变有关,靶器官包括心脏、大脑、肾脏和血管系统。目的:本研究强调了免疫系统与高血压及其对靶器官损伤的影响之间的最新相关性。方法:用于检索研究的描述符为“高血压”、“免疫”和“靶器官”。研究方法遵循了PRISMA声明的主要建议。结果:血管系统的损伤主要源于T细胞和单核细胞的迁移,它们在外膜中成为促炎细胞,释放TNF-α、IFN-γ和IL-17,诱导内皮损伤并阻碍血管舒张。在肾脏方面,与高血压相关的炎症过程最终导致白细胞侵袭肾脏,白细胞通过强烈的交感神经刺激、肾素-血管紧张素系统的激活、钠滞留和氧化应激的加重等机制导致该器官的损伤。在心脏方面,除了血管紧张素II、活性氧和醛固酮分泌IFN-γ、IL-17、IL-23和TNF-α外,高血压还会增加促炎元素如B、T和NK细胞的表达。这种促炎作用也通过SphK1参与脑损伤。鉴于上述情况,免疫系统参与高血压诱导的损伤似乎是明确的。结论:因此,了解与高血压相关的多因素机制必将有助于对这种情况进行更有效的干预,预防靶器官损伤。
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引用次数: 0
Endless Journey of Adenosine Signaling in Cardioprotective Mechanism of Conditioning Techniques: Clinical Evidence. 腺苷信号在条件调节技术心脏保护机制中的无尽旅程:临床证据。
IF 2.4 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2023-01-01 DOI: 10.2174/1573403X19666230612112259
Kuldeep Kumar, Nirmal Singh, Harlokesh Narayan Yadav, Leonid Maslov, Amteshwar Singh Jaggi

Myocardial ischemic injury is a primary cause of death among various cardiovascular disorders. The condition occurs due to an interrupted supply of blood and vital nutrients (necessary for normal cellular activities and viability) to the myocardium, eventually leading to damage. Restoration of blood supply to ischemic tissue is noted to cause even more lethal reperfusion injury. Various strategies, including some conditioning techniques, like preconditioning and postconditioning, have been developed to check the detrimental effects of reperfusion injury. Many endogenous substances have been proposed to act as initiators, mediators, and end effectors of these conditioning techniques. Substances, like adenosine, bradykinin, acetylcholine, angiotensin, norepinephrine, opioids, etc., have been reported to mediate cardioprotective activity. Among these agents, adenosine has been widely studied and suggested to have the most pronounced cardioprotective effects. The current review article highlights the role of adenosine signaling in the cardioprotective mechanism of conditioning techniques. The article also provides an insight into various clinical studies that substantiate the applicability of adenosine as a cardioprotective agent in myocardial reperfusion injury.

心肌缺血性损伤是各种心血管疾病死亡的主要原因。这种情况的发生是由于心肌的血液和重要营养物质(正常细胞活动和生存能力所必需的)供应中断,最终导致损伤。缺血组织血液供应的恢复会导致更致命的再灌注损伤。已经开发了各种策略,包括一些预处理和后处理技术,以检查再灌注损伤的有害影响。许多内源性物质被认为是这些条件调节技术的起始物、介质和末端效应物。腺苷、缓激肽、乙酰胆碱、血管紧张素、去甲肾上腺素、阿片类药物等物质已被报道可介导心脏保护活性。在这些药物中,腺苷已被广泛研究,并被认为具有最显著的心脏保护作用。目前的综述文章强调腺苷信号在条件反射技术的心脏保护机制中的作用。这篇文章还深入了解了各种临床研究,这些研究证实了腺苷作为心脏保护剂在心肌再灌注损伤中的适用性。
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引用次数: 0
In-stent Thrombosis and COVID-19 Infection: Current Insights on the Mechanistic Relationship. 血栓形成与新冠肺炎感染:机制关系的最新见解。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220512142019
Ahmed El-Medany, Vanessa Kandoole, Nicholas Lonsdale, Gemina Doolub, Ioannis Felekos

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.

严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)感染已被证明是诱发冠状动脉支架血栓形成的主要风险因素,因为它容易产生促血栓状态。这篇综述探讨了可能导致新冠肺炎血栓形成风险增加的机制。此外,我们还讨论了易导致支架内血栓形成风险增加的患者和血液学因素,以及某些抗血小板和抗凝疗法的作用,包括替卡格雷和依诺肝素,这些疗法可能会降低严重急性呼吸系统综合征冠状病毒2型感染中支架内血栓的可能性和严重程度。为了对抗新冠肺炎中显示的促炎和促血栓状态,未来的抗血栓治疗可能会使用血小板抑制测试和炎症调节疗法进行优化。具有长期随访的大规模随机试验对于评估新冠肺炎与支架优化的交叉点以及药物洗脱支架(DES)植入后支架血栓形成的减少越来越有必要。
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引用次数: 0
Coronary Bifurcation Stenting: Review of Current Techniques and Evidence. 冠状动脉分叉支架:当前技术和证据综述。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220406113517
Surya Kiran Aedma, Anant Naik, Arun Kanmanthareddy

Background: 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.

Objective: 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.

Methods: We reviewed the clinical evidence on the efficacy of coronary bifurcation stenting.

Results: 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.

Conclusion: 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.

背景:冠状动脉分叉支架置入术占所有经皮冠状动脉介入治疗的20%。鉴于分叉病变的广泛流行,各种技术都在寻求最佳的分叉支架,以改善血运重建,同时降低支架血栓形成和病变复发率。先进的技术,如计划的双支架入路,已被证明具有改善的结果,但也需要荧光镜检查和手术时间,这既是一个经济论点,也是一个患者结果论点。目的:由于文献中提出了许多策略,因此客观评估随机对照试验和荟萃分析的证据以帮助确定最佳支架植入策略变得至关重要。方法:回顾分析冠状动脉分叉支架置入术疗效的临床证据。结果:在这篇论文中,我们回顾了最近发表的关于各种支架技术疗效和支架技术进展的随机对照试验和荟萃分析,以衡量当前的理解状态,并绘制该领域的发展方向。结论:分叉支架术是介入心脏病学领域中一个成熟的问题,它适应了患者的需求和技术的进步。
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引用次数: 0
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. 细颗粒物(PM2.5)在动脉粥样硬化和心肌损伤发生中作用的现代概念:临床和流行病学数据,主要病理生理机制。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220817103105
Aleksey Michailovich Chaulin, Artem Konstantinovich Sergeev

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.

由于动脉粥样硬化性心血管疾病(CVD)在人群的发病率、致残率和死亡率结构中占主导地位,研究动脉粥样硬化性心血管病发展的危险因素及其潜在的发病机制是现代医学最重要的科学研究领域。了解这些方面将有助于改进一套治疗和预防措施及活动。细颗粒物(PM2.5)的空气污染是动脉粥样硬化发展的重要危险因素之一,近年来一直在积极研究。根据临床和流行病学数据,PM2.5的空气污染水平超过了世界大多数地区的标准指标,并与动脉粥样硬化的亚临床标志物和动脉粥样硬化性心血管疾病的死亡率有关。本文的目的是从流行病学和发病机制的角度,系统地详细讨论PM2.5在动脉粥样硬化和心肌损伤发展中的作用。材料和方法:这篇叙述性综述基于对Medline、PubMed和Embase数据库中出版物的分析。术语“细颗粒物”和“PM2.5”与“病理生理机制”、“心血管疾病”、“动脉粥样硬化”、“心肌肌钙蛋白”、“心脏损伤”和“心肌损伤”一起用于搜索出版物。结论:根据所进行的叙述性综述,PM2.5应被视为动脉粥样硬化性心血管疾病发展的重要危险因素。细颗粒物的促动脉粥样硬化作用基于几个基本且密切相关的病理生理机制:内皮功能障碍、脂质代谢受损、氧化应激和炎症反应增加、植物神经系统功能受损和止血系统活性增加。此外,PM2.5通过几种机制对心肌细胞造成亚临床损伤:细胞凋亡、氧化应激、冠状动脉粥样硬化导致的氧气输送减少和心肌细胞的缺血性损伤。高灵敏度的心肌肌钙蛋白是检测污染地区人群亚临床心肌损伤的有前途的标志物。
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引用次数: 0
Cardiotoxicity of Biological Therapies in Cancer Patients: An In-depth Review. 癌症患者生物治疗的心脏毒性:一个深入的回顾。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220531094800
Luai Madanat, Ruby Gupta, Paul Weber, Navneet Kumar, Rohit Chandra, Hycienth Ahaneku, Yatharth Bansal, Joseph Anderson, Abhay Bilolikar, Ishmael Jaiyesimi

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.

化疗方案的心脏毒性早已有报道。然而,对生物疗法心脏副作用的理解正在迅速发展。随着癌症患者因使用个性化药物和新型靶向抗癌药物而获得更高的预期寿命,心脏毒性的发生变得更加显著。新型生物疗法包括抗HER2抗体、酪氨酸激酶抑制剂、布鲁顿激酶抑制剂、抗血管内皮生长因子、蛋白酶体抑制剂、免疫调节剂和免疫检查点抑制剂。与这些抗癌药物相关的潜在心血管毒性包括高血压、心律失常、QT延长、心肌缺血和梗死、左心室功能障碍、充血性心力衰竭和血栓栓塞。心脏生物标志物、心电图、超声心动图和磁共振成像是用于早期发现这些并发症和及时干预的常见诊断模式。这篇综述讨论了新型抗癌生物制剂引起的各种类型的心脏毒性,它们的分子和病理生理机制,危险因素,以及可用于预防、减少和治疗它们的诊断和管理策略。
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引用次数: 0
Stem Cells and Congenital Heart Disease: The Future Potential Clinical Therapy Beyond Current Treatment. 干细胞与先天性心脏病:当前治疗之外的未来潜在临床治疗。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220531093326
Katherine Julian, Nikita Garg, Narutoshi Hibino, Rohit Jain

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.

先天性心脏病(CHD)是新生儿最常见的先天性畸形。目前紫绀型冠心病的治疗在很大程度上依赖于手术干预;然而,CHD患者的发病率和死亡率仍然很高。最近探索治疗冠心病新途径的研究包括干细胞在该领域的应用。干细胞已经被用于建模和潜在的治疗CHD。迄今为止,大多数临床应用都集中在左心发育不全综合征上。在这里,我们研究了干细胞在冠心病中的当前作用,并讨论了该领域的未来应用。
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引用次数: 0
The Wider Considerations in Closing Chronic Disease Gaps - Focus on Heart Failure and Implementation. 缩小慢性病差距的更广泛考虑-关注心力衰竭和实施。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X18666220512160737
Pupalan Iyngkaran, Charlotte Hespe, Fahad Hanna, John D Horowitz, Malcolm Battersby, Craig Nelson, Sharon Andrew, Maximilian P de Courten

Background: 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.

Methodology: 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.

Discussion: 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.

Conclusion: 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.

背景:心力衰竭(HF)主要是一种慢性疾病。HF和慢性病的研究和护理存在重叠。慢性病和HF的研究有多个目标。总体目标是“以最大的成本效益优化患者结果”。然而,对患者的观察可能有许多变量;因此,我们看到了临床翻译中的差异。本文件讨论了HF和慢性病常见的三个重要差距的论点,即筛查、自我管理和患者报告结果(PRO),并简要介绍了如何将其纳入证据树。提供了关于卫生服务框架和护理模式的相关论点,作为未来共识的前奏。方法:1)初步文献综述,以确定心血管研究的分类;2)已发表文献综述,描述将心血管疾病的研究转化为临床实践。确定了从观察性试验到大型随机对照试验再到上市后研究的范围。讨论:简要讨论传统研究和差异,重点是筛查、混合方法研究概念和慢性病护理模式。促进这一点的六个步骤:1)研究设计;2) 研究应用(翻译)一、常规二。挑战;3.将研究转化为翻译水平;4.资金和基础设施;5.卓越临床研究中心(CCRE)及其合作;6.治理和成本效益。结论:旨在以高效和有效的方式将研究结果与改善患者结果联系起来的实施研究是一个被忽视的领域。执行实施研究所需的技能是复杂的。在HF背景下描述了最大限度地将慢性病研究转化为临床实践的方法。
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引用次数: 0
ROCK (RhoA/Rho Kinase) Activation in Atrial Fibrillation: Molecular Pathways and Clinical Implications. 心房颤动中的ROCK(RhoA/Rho激酶)激活:分子途径和临床意义。
IF 1.9 Q2 Medicine Pub Date : 2023-01-01 DOI: 10.2174/1573403X19666221117092951
Riccardo Proietti, Andrea S Giordani, Calò A Lorenzo

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.

在房颤发病机制的复杂机制中,细胞内钙超载和氧化应激起着重要作用,两者都是由炎症过程引发的。房颤中发生的另一个基本事件是心房纤维化重塑,再次由氧化应激触发,氧化应激由连接蛋白重排和成纤维细胞分化为活性胶原混凝土肌成纤维细胞决定。RhoA/ROCK系统是血管紧张素II、血小板衍生生长因子、结缔组织生长因子和转化生长因子β等广泛分子效应物的最终途径,这些效应物总体上决定了钙失调和促纤维化重塑。在实验和临床研究中,RhoA/ROCK的激活与超氧化物离子的产生、纤维化重塑和连接蛋白重排有关,对AF的发病机制具有重要影响。因此,ROCK通路抑制可能是特殊AF亚组患者的治疗或预防靶点。
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引用次数: 0
Countermeasures for Maintaining Cardiovascular Health in Space Missions. 在太空任务中保持心血管健康的对策。
IF 2.4 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Pub Date : 2023-01-01 DOI: 10.2174/1573403X19666230330083225
Jhilam Pramanik, Akash Kumar, Lakshay Panchal, Bhupendra Prajapati

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.

在太空探索过程中,人体会受到改变的大气环境和重力、辐射、睡眠障碍和精神压力的影响;所有这些因素都是导致心血管疾病的原因。在微重力条件下,与心血管疾病相关的生理变化包括脑液转移、中心静脉压急剧下降、血液流变学和内皮功能变化、脑血管异常、头痛、视盘水肿、颅内高压、颈静脉充血、面部肿胀和味觉丧失。通常,(在太空任务期间和之后)有五种对策可用于保持心血管健康,包括防护、营养、药物、锻炼和人工重力。本文最后介绍了如何通过各种对策来减少太空任务对心血管健康的影响。
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Current Cardiology Reviews
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