Pub Date : 2023-01-01DOI: 10.4103/hm.hm-d-23-00039
Yong-Jian Geng
Atherosclerotic vascular diseases have two life-threatening complications, namely myocardial and cerebral infarcts. The development of the two pathological conditions involves interplays between genetic, epigenetic, and environmental factors. Mental stress is an independent factor that contributes to the pathogenesis of atherosclerotic heart and brain diseases. Increased mental stress is linked to heightened vascular stiffness, inflammation, atherosclerosis, and hypertension. Neuroendocrinological impacts of stress include the involvement of the renin-angiotensin system and its active peptides, particularly angiotensin II (Ang II), in stress-related disorders. In a circadian manner, Ang II and its two subtypes of receptors exist in the stress-responsive brain hypothalamus–adrenal–pituitary axis. Mental stress can cause broken heart syndrome or stress cardiomyopathy. Stress resilience is an important factor that regulates the susceptibility to stress-associated cardiovascular dysfunction and the development of adverse events. Preventive and therapeutic approaches are developed on multiple fronts aimed at mitigating the stress-associated vascular responses and development of atherosclerotic vascular disorders.
{"title":"Mental stress contributes to the pathogenesis of atherosclerotic heart and brain diseases: A mini-review","authors":"Yong-Jian Geng","doi":"10.4103/hm.hm-d-23-00039","DOIUrl":"https://doi.org/10.4103/hm.hm-d-23-00039","url":null,"abstract":"Atherosclerotic vascular diseases have two life-threatening complications, namely myocardial and cerebral infarcts. The development of the two pathological conditions involves interplays between genetic, epigenetic, and environmental factors. Mental stress is an independent factor that contributes to the pathogenesis of atherosclerotic heart and brain diseases. Increased mental stress is linked to heightened vascular stiffness, inflammation, atherosclerosis, and hypertension. Neuroendocrinological impacts of stress include the involvement of the renin-angiotensin system and its active peptides, particularly angiotensin II (Ang II), in stress-related disorders. In a circadian manner, Ang II and its two subtypes of receptors exist in the stress-responsive brain hypothalamus–adrenal–pituitary axis. Mental stress can cause broken heart syndrome or stress cardiomyopathy. Stress resilience is an important factor that regulates the susceptibility to stress-associated cardiovascular dysfunction and the development of adverse events. Preventive and therapeutic approaches are developed on multiple fronts aimed at mitigating the stress-associated vascular responses and development of atherosclerotic vascular disorders.","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135838569","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}
Pub Date : 2023-01-01DOI: 10.4103/hm.hm-d-23-00036
Yuchuan Ding, Fengwu Li, Xiaokun Geng
INTRODUCTION As we delve into the complexities of the human body, we often find ourselves facing formidable adversaries, many of which remain unknown. Heart disease and stroke are two such adversaries, claiming millions of lives each year.[1] According to the World Health Organization,[2] ischemic heart disease was the leading cause of death worldwide in 2019, responsible for 8.9 million fatalities, while stroke was the second leading cause, accounting for 6.1 million deaths. The inextricable links between heart disease and stroke are obvious, as 30% of strokes are complicated by heart attacks and the mortality rate soars as high as 54%. Furthermore, symptoms of cardiovascular disease, such as atrial fibrillation and heart failure, can exacerbate the inflammatory response after a stroke, leading to worsened functional outcomes. These facts emphasize the need to address both diseases concomitantly and highlight the importance of a multi-pronged approach in our battle against them. This Special Issue of Heart and Mind aimed to shine a light on these entwined conditions and their ongoing battle against humanity. THE CHALLENGE OF PREVENTION The magnitude of the challenge at hand cannot be overstated, and as such, we must focus on reducing the global impact of heart disease and stroke. A key part of this battle is the prevention of common risk factors,[3,4] which include: (1) High blood pressure: A leading cause of both heart disease and stroke, hypertension damages blood vessels and increases the risk of plaque buildup in arteries, which can lead to heart attacks and strokes. (2) High cholesterol: Elevated levels of low-density lipoprotein cholesterol contribute to the formation of plaque in blood vessels, increasing the risk of heart disease and stroke. (3) Diabetes: High blood sugar levels can damage blood vessels and nerves, increasing the risk of heart disease and stroke. (4) Smoking and secondhand smoke exposure: Tobacco use and exposure to secondhand smoke can damage blood vessels and increase the risk of heart disease and stroke. (4) Obesity: Excess weight puts a strain on the heart and can lead to high blood pressure, high cholesterol, and diabetes, all of which increase the risk of heart disease and stroke. (4) Unhealthy diets: Diets high in saturated fats, trans fats, cholesterol, and sodium can contribute to heart disease and stroke. (5) Physical inactivity: Sedentary lifestyles increase the risk of heart disease and stroke by contributing to obesity, high blood pressure, and high cholesterol. (6) Mental stress: Chronic stress has been linked to an increased risk of heart disease and stroke due to its effects on blood pressure and inflammation. Addressing these risk factors may help reduce health disparities and improve outcomes for individuals across geographic, racial, ethnic, and socioeconomic divides. COMPREHENSIVE EXPLORATION Currently, we encompass a comprehensive exploration of heart disease and stroke prevention, diagnosis, treatme
{"title":"Unraveling the complex web: Heart disease and stroke","authors":"Yuchuan Ding, Fengwu Li, Xiaokun Geng","doi":"10.4103/hm.hm-d-23-00036","DOIUrl":"https://doi.org/10.4103/hm.hm-d-23-00036","url":null,"abstract":"INTRODUCTION As we delve into the complexities of the human body, we often find ourselves facing formidable adversaries, many of which remain unknown. Heart disease and stroke are two such adversaries, claiming millions of lives each year.[1] According to the World Health Organization,[2] ischemic heart disease was the leading cause of death worldwide in 2019, responsible for 8.9 million fatalities, while stroke was the second leading cause, accounting for 6.1 million deaths. The inextricable links between heart disease and stroke are obvious, as 30% of strokes are complicated by heart attacks and the mortality rate soars as high as 54%. Furthermore, symptoms of cardiovascular disease, such as atrial fibrillation and heart failure, can exacerbate the inflammatory response after a stroke, leading to worsened functional outcomes. These facts emphasize the need to address both diseases concomitantly and highlight the importance of a multi-pronged approach in our battle against them. This Special Issue of Heart and Mind aimed to shine a light on these entwined conditions and their ongoing battle against humanity. THE CHALLENGE OF PREVENTION The magnitude of the challenge at hand cannot be overstated, and as such, we must focus on reducing the global impact of heart disease and stroke. A key part of this battle is the prevention of common risk factors,[3,4] which include: (1) High blood pressure: A leading cause of both heart disease and stroke, hypertension damages blood vessels and increases the risk of plaque buildup in arteries, which can lead to heart attacks and strokes. (2) High cholesterol: Elevated levels of low-density lipoprotein cholesterol contribute to the formation of plaque in blood vessels, increasing the risk of heart disease and stroke. (3) Diabetes: High blood sugar levels can damage blood vessels and nerves, increasing the risk of heart disease and stroke. (4) Smoking and secondhand smoke exposure: Tobacco use and exposure to secondhand smoke can damage blood vessels and increase the risk of heart disease and stroke. (4) Obesity: Excess weight puts a strain on the heart and can lead to high blood pressure, high cholesterol, and diabetes, all of which increase the risk of heart disease and stroke. (4) Unhealthy diets: Diets high in saturated fats, trans fats, cholesterol, and sodium can contribute to heart disease and stroke. (5) Physical inactivity: Sedentary lifestyles increase the risk of heart disease and stroke by contributing to obesity, high blood pressure, and high cholesterol. (6) Mental stress: Chronic stress has been linked to an increased risk of heart disease and stroke due to its effects on blood pressure and inflammation. Addressing these risk factors may help reduce health disparities and improve outcomes for individuals across geographic, racial, ethnic, and socioeconomic divides. COMPREHENSIVE EXPLORATION Currently, we encompass a comprehensive exploration of heart disease and stroke prevention, diagnosis, treatme","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135838821","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}
Pub Date : 2023-01-01DOI: 10.4103/hm.hm-d-23-00045
Meiyan Liu, BarryA Franklin, Icey Zhang
In the interview, Prof. Barry A. Franklin discussed his perspectives on physical activity, cardiorespiratory fitness, and cardiovascular health. He also unraveled how soft skills can empower superachievers. His major viewpoints are: (a) exercise benefits cardiac patients; yet, too much exercise may be risky, (b) exercise prescription should be scientifically based and varies by different objectives for each individual, (c) patients’ motivation to change their behaviors matters during cardiac rehabilitation, (d) physical activities could play a protective role for dementia prevention, (e) technology and virtual approaches enable more patients to participate in cardiac rehab programs, (f) patients with heart failure may benefit even more from exercise training than other patient populations, (g) psychosocial stressors may partially explain some cardiac events, (h) novel risk factors help identify people at increased risk of cardiovascular disease, such as genetics, coronary calcium score, air pollution, and inflammation, and (i) soft skills are needed by all people, regardless of their field.
在访谈中，Barry A. Franklin教授讨论了他对身体活动、心肺健康和心血管健康的看法。他还揭示了软技能是如何赋予超级成功者力量的。他的主要观点是:(a)运动对心脏病患者有益;然而，过多的运动可能是有风险的，(b)运动处方应该有科学依据，并且因人而异，(c)患者改变行为的动机在心脏康复过程中很重要，(d)体育活动可以起到预防痴呆的保护作用，(e)技术和虚拟方法使更多的患者参与心脏康复计划，(f)心力衰竭患者可能比其他患者群体从运动训练中获益更多，(g)心理社会压力因素可能部分解释一些心脏事件，(h)新的风险因素有助于识别心血管疾病风险增加的人群，如遗传学、冠状动脉钙评分、空气污染和炎症，以及(i)所有人都需要软技能，无论他们从事什么领域。
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The favorable risk factor profiles and superb cardiac performance of elite long-distance runners, as well as the anti-aging effects of exercise, have likely contributed to the escalating number of adults worldwide who have embraced the notion that “more exercise is invariably better.≵ Nevertheless, vigorous-to-high-intensity physical activity (PA), particularly when unaccustomed, appears to be a trigger for acute cardiac events in individuals with known or occult atherosclerotic cardiovascular disease or structural cardiovascular abnormalities, most notably, hypertrophic cardiomyopathy. Although regular endurance exercise and moderate-to-vigorous PA provide established cardioprotective benefits, high-volume, high-intensity exercise training regimens appear to induce maladaptive cardiac remodeling in some individuals. These potential adverse cardiac adaptations include accelerated coronary artery calcification (CAC), elevated cardiac biomarker release, myocardial fibrosis, and atrial fibrillation (AF), which may be described by a reverse J-shaped curve. However, the risk for acute cardiovascular events is lower in fit/active persons compared to their unfit/inactive counterparts with the same CAC scores. Similarly, the risk of AF is the highest in habitually sedentary older adults, decreases with light-to-moderate intensity regular PA but increases with high-volume, high-intensity exercise regimens (i.e., reverse J-shaped curve). This review examines these relations and more, with specific reference to the World Health Organization exercise intensity and duration recommendations for optimal health, as well as the thresholds for other research-based exercise metrics, including steps/day and the concept of metabolic equivalents-minutes/week. The primary beneficiaries of exercise training programs and long-term goal training intensities, based on age, sex, and “good≵ fitness, are also discussed. In summary, the benefits of regular moderate-to-vigorous PA and the associated improvements in cardiorespiratory fitness far outweigh the risks for most individuals.
{"title":"A narrative review on exercise and cardiovascular disease: Physical activity thresholds for optimizing health outcomes","authors":"Barry A. Franklin, Thijs H Eijsvogels","doi":"10.4103/hm.hm_1_23","DOIUrl":"https://doi.org/10.4103/hm.hm_1_23","url":null,"abstract":"The favorable risk factor profiles and superb cardiac performance of elite long-distance runners, as well as the anti-aging effects of exercise, have likely contributed to the escalating number of adults worldwide who have embraced the notion that “more exercise is invariably better.≵ Nevertheless, vigorous-to-high-intensity physical activity (PA), particularly when unaccustomed, appears to be a trigger for acute cardiac events in individuals with known or occult atherosclerotic cardiovascular disease or structural cardiovascular abnormalities, most notably, hypertrophic cardiomyopathy. Although regular endurance exercise and moderate-to-vigorous PA provide established cardioprotective benefits, high-volume, high-intensity exercise training regimens appear to induce maladaptive cardiac remodeling in some individuals. These potential adverse cardiac adaptations include accelerated coronary artery calcification (CAC), elevated cardiac biomarker release, myocardial fibrosis, and atrial fibrillation (AF), which may be described by a reverse J-shaped curve. However, the risk for acute cardiovascular events is lower in fit/active persons compared to their unfit/inactive counterparts with the same CAC scores. Similarly, the risk of AF is the highest in habitually sedentary older adults, decreases with light-to-moderate intensity regular PA but increases with high-volume, high-intensity exercise regimens (i.e., reverse J-shaped curve). This review examines these relations and more, with specific reference to the World Health Organization exercise intensity and duration recommendations for optimal health, as well as the thresholds for other research-based exercise metrics, including steps/day and the concept of metabolic equivalents-minutes/week. The primary beneficiaries of exercise training programs and long-term goal training intensities, based on age, sex, and “good≵ fitness, are also discussed. In summary, the benefits of regular moderate-to-vigorous PA and the associated improvements in cardiorespiratory fitness far outweigh the risks for most individuals.","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46546282","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}
Jing Zhou, Min-Lin Fang, Tuo Han, Jiajia Wang, Honghong Li, Zhile Li
{"title":"College students' awareness of the epidemic and their mental health during the COVID-19 outbreak","authors":"Jing Zhou, Min-Lin Fang, Tuo Han, Jiajia Wang, Honghong Li, Zhile Li","doi":"10.4103/hm.hm_47_22","DOIUrl":"https://doi.org/10.4103/hm.hm_47_22","url":null,"abstract":"","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70736594","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}
Pub Date : 2023-01-01DOI: 10.4103/hm.hm-d-23-00014
Eduard Guasch, Gemma Sangüesa, Montserrat Batlle
Dear Editor, We have read with great interest the most recent issue of Heart and Mind addressing the relationship between exercise, heart, and cognition.[1,2] Dr. Jenna Taylor excellently summarized the intertwine between cardiovascular and brain health and how regular moderate and vigorous exercises positively impinge the cardiovascular-cognition connection.[1] The growing core of evidence supporting exercise as a promising tool to blunt cardiovascular risk factors, but also cognitive impairment, is exhaustively reviewed. However, while the benefits of regular moderate exercise are undoubted and convincingly supported by preclinical and clinical data, the consequences of long-term strenuous exercise are still uncertain. In fact, emerging evidence shows that the relationship between training load and cardiovascular and brain health is not linear (the more exercise, the more benefit), but rather U-shaped. In recent years, long-term strenuous exercise has shown to increase the risk of cardiovascular disease, particularly cardiac arrhythmias , in certain populations. Atrial fibrillation risk is heightened in male endurance athletes, exercise is central to the pathophysiology of the arrhythmogenic cardiomyopathy in some patients, and the (formerly considered) physiological athlete’s bradycardia could evolve into clinically relevant sinus node dysfunction.[3] Moreover, recent data also suggest aortic tunica media damage in heavily trained animals[4] and more intense coronary atherosclerosis in male master marathon runners.[5] Could these negative effects extend to the brain? The robustness of clinical trials assessing long-term exposures is jeopardized by confounding factors and the lack of control groups. Although caution is needed when translating the conclusions of animal work to humans, preclinical studies restrict confounding factors and enable a more precise comparison between exercise loads. In an animal model, we have recently shown that high-intensity exercise could not replicate many of the moderate exercise-induced benefits on cerebrovascular and connectivity efficiency enhancement, both underlying improved learning capacity.[6] These results suggest that the maximal benefit of exercise in brain health is obtained at moderate doses while very high loads yield limited effects, thereby supporting the existence of a “sweet spot” for exercise intensity and duration on cognition.[7] Clinical studies confirm this notion, including a large epidemiological trial in which former professional athletes (i.e., soccer players) had a higher risk of neurodegenerative disease than the general population.[8] The pathophysiology behind many of the deleterious effects of strenuous exercise is only partially understood. The reduced cerebral blood flow occurring in an animal model after long-term strenuous training[6] would link the unexpected cognitive effects to recently demonstrated exercise-induced vascular damage.[4,5] Each strenuous bout of exercise super
亲爱的编辑:我们怀着极大的兴趣阅读了最近一期的《心与心》杂志，讨论了运动、心脏和认知之间的关系。[1,2]詹娜·泰勒博士出色地总结了心血管和大脑健康之间的相互关系，以及有规律的适度和剧烈运动如何积极地影响心血管和认知之间的联系。[1]越来越多的核心证据支持运动是一种有希望的工具，可以降低心血管风险因素，也可以降低认知障碍。然而，尽管定期适度运动的好处是毋庸置疑的，并且有临床前和临床数据令人信服地支持，但长期剧烈运动的后果仍不确定。事实上，新出现的证据表明，训练负荷与心血管和大脑健康之间的关系不是线性的(运动越多，益处越多)，而是u形的。近年来，长期剧烈运动已显示出在某些人群中增加心血管疾病，特别是心律失常的风险。男性耐力运动员房颤风险增高，运动是部分患者致心律失常性心肌病病理生理学的核心，(以前认为的)生理性运动员心动过缓可能演变为临床相关的窦房结功能障碍。[3]此外，最近的数据还表明，在训练有素的动物中存在主动脉中膜损伤[4]，而男性马拉松大师运动员的冠状动脉粥样硬化更为严重[5]。这些负面影响会延伸到大脑吗?评估长期暴露的临床试验的稳健性因混杂因素和缺乏对照组而受到损害。虽然在将动物实验的结论转化为人类实验时需要谨慎，但临床前研究限制了混杂因素，并使运动负荷之间的比较更加精确。在动物模型中，我们最近表明，高强度运动不能复制许多中等强度运动引起的脑血管和连接效率增强的好处，这两者都是学习能力提高的基础。[6]这些结果表明，运动对大脑健康的最大益处是在中等剂量下获得的，而非常高的负荷产生的效果有限，从而支持运动强度和持续时间对认知的“最佳点”的存在。[7]临床研究证实了这一观点，包括一项大型流行病学试验，其中前职业运动员(即足球运动员)患神经退行性疾病的风险高于一般人群。[8]剧烈运动的许多有害影响背后的病理生理学只是部分被理解。在长期剧烈训练后的动物模型中出现的脑血流量减少[6]将意想不到的认知影响与最近证实的运动引起的血管损伤联系起来。[4,5]每次剧烈运动都会对心血管系统施加血液动力学和生化压力，这可能导致一过性右心室功能障碍[9]。同样，大脑中短暂的氧化应激和线粒体能量的改变可以介导观察到的高强度运动的益处逆转。[6]在剧烈运动后进行的人体实验支持短暂的认知能力下降和脑流量调节受损。最后，运动本身以外的因素也可以解释这些有害的影响。正如最近提出的那样，反复的脑震荡不仅会在激烈的身体接触运动中导致大脑健康恶化，而且在足球等运动中也会导致大脑健康恶化。[10]总之，动物模型和人体试验表明，定期运动所促进的认知益处可能高度依赖于运动强度和持续时间;矛盾的是，剧烈和长期的运动形式可能显示出有害。然而，这些数据需要在大型和精心设计的研究中得到证实。O 'Keefe等人在他们的社论[2]中恰当地指出，“对心脏有益的东西对大脑也有益。”我们是否也应该宣称“对心脏有害的东西也对大脑有害?”本研究得到了西班牙卡洛斯三世研究所(PI19/00443和PI22/00953)、CERCA项目/Generalitat de Catalunya、CIBERCV(16/11/00354)、Consejo Superior de Deportes (EXP_75119)和欧洲区域发展基金(FEDER)的部分资助。edward Guasch博士是Heart and Mind杂志的编辑委员会成员。这篇文章遵循了该杂志的标准程序，同行评议独立于爱德华·瓜施博士和研究小组进行。没有利益冲突。
{"title":"What is bad for the heart is bad for the brain?","authors":"Eduard Guasch, Gemma Sangüesa, Montserrat Batlle","doi":"10.4103/hm.hm-d-23-00014","DOIUrl":"https://doi.org/10.4103/hm.hm-d-23-00014","url":null,"abstract":"Dear Editor, We have read with great interest the most recent issue of Heart and Mind addressing the relationship between exercise, heart, and cognition.[1,2] Dr. Jenna Taylor excellently summarized the intertwine between cardiovascular and brain health and how regular moderate and vigorous exercises positively impinge the cardiovascular-cognition connection.[1] The growing core of evidence supporting exercise as a promising tool to blunt cardiovascular risk factors, but also cognitive impairment, is exhaustively reviewed. However, while the benefits of regular moderate exercise are undoubted and convincingly supported by preclinical and clinical data, the consequences of long-term strenuous exercise are still uncertain. In fact, emerging evidence shows that the relationship between training load and cardiovascular and brain health is not linear (the more exercise, the more benefit), but rather U-shaped. In recent years, long-term strenuous exercise has shown to increase the risk of cardiovascular disease, particularly cardiac arrhythmias , in certain populations. Atrial fibrillation risk is heightened in male endurance athletes, exercise is central to the pathophysiology of the arrhythmogenic cardiomyopathy in some patients, and the (formerly considered) physiological athlete’s bradycardia could evolve into clinically relevant sinus node dysfunction.[3] Moreover, recent data also suggest aortic tunica media damage in heavily trained animals[4] and more intense coronary atherosclerosis in male master marathon runners.[5] Could these negative effects extend to the brain? The robustness of clinical trials assessing long-term exposures is jeopardized by confounding factors and the lack of control groups. Although caution is needed when translating the conclusions of animal work to humans, preclinical studies restrict confounding factors and enable a more precise comparison between exercise loads. In an animal model, we have recently shown that high-intensity exercise could not replicate many of the moderate exercise-induced benefits on cerebrovascular and connectivity efficiency enhancement, both underlying improved learning capacity.[6] These results suggest that the maximal benefit of exercise in brain health is obtained at moderate doses while very high loads yield limited effects, thereby supporting the existence of a “sweet spot” for exercise intensity and duration on cognition.[7] Clinical studies confirm this notion, including a large epidemiological trial in which former professional athletes (i.e., soccer players) had a higher risk of neurodegenerative disease than the general population.[8] The pathophysiology behind many of the deleterious effects of strenuous exercise is only partially understood. The reduced cerebral blood flow occurring in an animal model after long-term strenuous training[6] would link the unexpected cognitive effects to recently demonstrated exercise-induced vascular damage.[4,5] Each strenuous bout of exercise super","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135844259","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}
Hanin Abdullah, J. Beckmann, Caroline Andonian-Dierks
{"title":"Empirical findings on associations between anxiety, depression, and congenital heart disease in adults – A systematic review and meta-analysis","authors":"Hanin Abdullah, J. Beckmann, Caroline Andonian-Dierks","doi":"10.4103/hm.hm_2_23","DOIUrl":"https://doi.org/10.4103/hm.hm_2_23","url":null,"abstract":"","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70736471","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}
Pub Date : 2023-01-01DOI: 10.4103/2468-6476.374491
S. Abohashem, Ahmad Gill, W. Aldosoky, MatthewB H. Ong, Tanveer Mir, Tawseef Dar
{"title":"A narrative review on mental stress and cardiovascular disease: Evidence, mechanisms, and potential interventions","authors":"S. Abohashem, Ahmad Gill, W. Aldosoky, MatthewB H. Ong, Tanveer Mir, Tawseef Dar","doi":"10.4103/2468-6476.374491","DOIUrl":"https://doi.org/10.4103/2468-6476.374491","url":null,"abstract":"","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70623906","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}
Objective: The objective of this study was to provide data on implantable loop recorder (ILR)-based atrial fibrillation (AF) rates, recurrent stroke rates, and predictors of AF in patients with cryptogenic stroke (CS) after 1, 6, 12, 24, and 36 months of follow-up. Methods: We searched MEDLINE/PubMed, Cochrane Central Register of Controlled Trials, EMBASE, Web of Science, and reference lists of retrieved reports, which were published by April 30, 2023, which was the date of our last search. We utilized random-effects meta-analysis for detection rates, and meta-regression analysis, t-test (for normally distributed variables), and Mann-Whitney (for skewed variables) for predictor factors. Results: Thirteen studies were analyzed, which included data from 3,377 patients with CS or embolic stroke of undetermined source. The ILR-based AF rates in patients with CS were 4.73% (95% confidence interval [CI] 3.91–5.71) at 1 month, 13.45% (95% CI 12.19–14.81) at 6 months, 17.5% (95% CI 16.25–18.82) at 12 months, 20.69% (95% CI 19–22.49) at 24 months, and 25.98% (95% CI 23.21–28.58) at 36 months. Age and CHA2DS2-VASc score were positively associated with AF detection. Specifically, the mean difference of age and CHA2DS2-VASc score in the group with AF versus the group without AF was 7.47 (95% CI 4.58–10.36, P < 0.001) and 0.75 (95% CI 0.22–1.28, P = 0.01), respectively. Finally, AF detection was positively associated with recurrent strokes with an estimated risk ratio of 1.27 (95% CI 0.69–2.31). Conclusions: There is a correlation between AF detection rate and ILR monitoring duration. One out of eight patients was diagnosed with AF after 6 months of follow-up and about one quarter after 3 years. Our results demonstrate the critical use of ILRs, especially in older patients, and in patients with high CHA2DS2-VASc scores.
目的:本研究的目的是在随访1、6、12、24和36个月后，提供基于植入式环路记录仪(ILR)的隐源性卒中(CS)患者房颤(AF)发生率、卒中复发率和房颤预测因素的数据。方法:检索MEDLINE/PubMed、Cochrane Central Register of Controlled Trials、EMBASE、Web of Science和检索报告的参考文献列表，检索日期为2023年4月30日，即我们最后一次检索的日期。我们对检出率采用随机效应元分析，对预测因子采用元回归分析、t检验(正态分布变量)和Mann-Whitney检验(偏态变量)。结果:我们分析了13项研究，其中包括3377例来源不明的CS或栓塞性卒中患者的数据。CS患者基于ilr的AF发生率在1个月时为4.73%(95%可信区间[CI] 3.91-5.71)， 6个月时为13.45% (95% CI 12.19-14.81)， 12个月时为17.5% (95% CI 16.25-18.82)， 24个月时为20.69% (95% CI 19-22.49)， 36个月时为25.98% (95% CI 23.21-28.58)。年龄和CHA2DS2-VASc评分与房颤检测呈正相关。其中，房颤组与非房颤组年龄和CHA2DS2-VASc评分的平均差值分别为7.47 (95% CI 4.58 ~ 10.36, P < 0.001)和0.75 (95% CI 0.22 ~ 1.28, P = 0.01)。最后，房颤检测与卒中复发呈正相关，估计风险比为1.27 (95% CI 0.69-2.31)。结论:AF检出率与ILR监测时间存在相关性。1 / 8的患者在随访6个月后被诊断为房颤，约1 / 4的患者在随访3年后被诊断为房颤。我们的研究结果证明了ILRs的关键作用，特别是在老年患者和CHA2DS2-VASc评分高的患者中。
{"title":"The role of implantable loop recorder in patients with cryptogenic stroke: A systematic review and meta-analysis","authors":"KonstantinosA Gatzoulis, Kiriaki Mavromoustakou, Symeoni Katzouridi, Stergios Soulaidopoulos, Ioannis Doundoulakis, Achilleas Papadopoulos, Petros Arsenos, Skevos Sideris, Polychronis Dilaveris, Dimitris Tsiachris, Athanasios Kordalis, Konstantinos Tsioufis","doi":"10.4103/hm.hm-d-23-00030","DOIUrl":"https://doi.org/10.4103/hm.hm-d-23-00030","url":null,"abstract":"Objective: The objective of this study was to provide data on implantable loop recorder (ILR)-based atrial fibrillation (AF) rates, recurrent stroke rates, and predictors of AF in patients with cryptogenic stroke (CS) after 1, 6, 12, 24, and 36 months of follow-up. Methods: We searched MEDLINE/PubMed, Cochrane Central Register of Controlled Trials, EMBASE, Web of Science, and reference lists of retrieved reports, which were published by April 30, 2023, which was the date of our last search. We utilized random-effects meta-analysis for detection rates, and meta-regression analysis, t-test (for normally distributed variables), and Mann-Whitney (for skewed variables) for predictor factors. Results: Thirteen studies were analyzed, which included data from 3,377 patients with CS or embolic stroke of undetermined source. The ILR-based AF rates in patients with CS were 4.73% (95% confidence interval [CI] 3.91–5.71) at 1 month, 13.45% (95% CI 12.19–14.81) at 6 months, 17.5% (95% CI 16.25–18.82) at 12 months, 20.69% (95% CI 19–22.49) at 24 months, and 25.98% (95% CI 23.21–28.58) at 36 months. Age and CHA2DS2-VASc score were positively associated with AF detection. Specifically, the mean difference of age and CHA2DS2-VASc score in the group with AF versus the group without AF was 7.47 (95% CI 4.58–10.36, P < 0.001) and 0.75 (95% CI 0.22–1.28, P = 0.01), respectively. Finally, AF detection was positively associated with recurrent strokes with an estimated risk ratio of 1.27 (95% CI 0.69–2.31). Conclusions: There is a correlation between AF detection rate and ILR monitoring duration. One out of eight patients was diagnosed with AF after 6 months of follow-up and about one quarter after 3 years. Our results demonstrate the critical use of ILRs, especially in older patients, and in patients with high CHA2DS2-VASc scores.","PeriodicalId":34653,"journal":{"name":"Heart and Mind","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135838564","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}
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