American journal of physiology. Heart and circulatory physiology最新文献

{"title":"The 6-min walk test: improving the prognostic power.","authors":"Karen L Ball","doi":"10.1152/ajpheart.00846.2024","DOIUrl":"10.1152/ajpheart.00846.2024","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H187-H189"},"PeriodicalIF":4.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A comment on the physiological basis for longitudinal motion of the arterial wall.","authors":"Magnus Cinthio, Artturi Petäjä, Tobias Erlöv, Åsa Rydén Ahlgren","doi":"10.1152/ajpheart.00597.2024","DOIUrl":"10.1152/ajpheart.00597.2024","url":null,"abstract":"<p><p>The longitudinal motion and the intramural shear strain of the arterial wall increase dramatically in response to blood pressure, thereby impacting the vascular wall microenvironment. Exposure to a sedentary lifestyle has been identified as an independent risk factor for cardiovascular disease, but it has been shown that intermittent physical activity embedded into everyday life is enough to improve cardiovascular health. Marked changes in longitudinal motion already at a low workload may explain this finding. However, to understand the mechanism linking longitudinal motion and cardiovascular health, an understanding of the physiological basis for the longitudinal motion of the arterial wall is needed. The factors underlying the longitudinal motion of the arterial wall in vivo are numerous and intertwined. As a comment and complement to the recent review by Athaide et al. (<i>Am J Physiol Heart Circ Physiol</i> 322: H689-H701, 2022), we propose and discuss a comprehensive cardiovascular mechanical scenario based on the current literature. In this scenario, blood pressure, typically acting in the radial direction, also acts directly in the longitudinal direction through a tapered geometry. This complements ventricular contraction, ventricular-vascular coupling, arterial diameter change, arterial stiffness in both the radial and longitudinal directions, and prestretch of the arterial wall. In addition, we consider the geometry of the arterial tree and intramural friction of the arterial wall. Together, these important cardiovascular mechanical factors form the pattern of longitudinal motion of the arterial wall, indicating that the longitudinal motion of the arterial wall is important for cardiovascular health.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H190-H195"},"PeriodicalIF":4.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of oral contraceptive pill use on sympathetic transduction at rest in young females.","authors":"Andrew W D'Souza, Sarah L Hissen, Kazumasa Manabe, Takuro Washio, Meghan C Annis, Belinda Sanchez, Charlotte W Usselman, Qi Fu, J Kevin Shoemaker","doi":"10.1152/ajpheart.00623.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00623.2024","url":null,"abstract":"<p><p>Although previous work has demonstrated that oral contraceptive pill (OCP) use does not affect resting muscle sympathetic nerve activity (MSNA), growing evidence indicates that it attenuates neurogenic vasoconstriction. Despite these advances, it remains unknown how OCP use affects the ability of MSNA to dynamically control vascular tone and arterial blood pressure (BP) on a beat-by-beat basis. Thus, we tested the hypothesis that, compared with naturally menstruating females (MC), those using OCPs will exhibit attenuated sympathetic vascular transduction at rest. Forty-three females [MC: <i>n</i> = 21, 26 (4) yrs; OCP: <i>n</i> = 22, 24 (4) yrs; data are presented as means (SD)] completed 10 min of supine rest with continuous measurements of beat-by-beat BP, femoral artery blood flow (26 females; MC: <i>n</i> = 13, OCP: <i>n</i> = 13), and MSNA. Spike-triggered averaging was used to determine sympathetic transduction into leg vascular conductance (LVC) and BP for 12 cardiac cycles following MSNA bursts. Overall sympathetic-BP transduction (<i>P</i> = 0.293), as well as sympathetic-BP transduction of MSNA burst quartiles (<i>P</i> = 0.741) and burst firing patterns (<i>P</i> = 0.452) were not different between the MC and OCP groups. Conversely, sympathetic vascular transduction per unit MSNA burst amplitude (<i>P</i> = 0.026) and burst firing pattern (<i>P</i> = 0.014) were attenuated among females using OCPs. In addition, females using OCPs demonstrated progressively smaller leg vasoconstrictor responses as a function of MSNA burst firing pattern compared with MC females (<i>P</i> = 0.021). Collectively, these data indicate that, in premenopausal females, OCP use attenuates the leg vasoconstrictor responses to bursts of MSNA, particularly during periods of increased sympathetic neural drive, without affecting the transduction of MSNA bursts into beat-by-beat changes in BP.<b>NEW & NOTEWORTHY</b> This study investigated the impact of OCP use on the transduction of MSNA bursts into regional vasoconstriction and blood pressure in premenopausal females. We demonstrated that females using OCPs exhibit attenuated sympathetic transduction into LVC; however, this does not translate to reductions in sympathetic blood pressure transduction. Collectively, these data indicate that OCP use may alter the local vasoconstrictor response to bursts of MSNA; however, compensatory mechanisms may contribute to maintain sympathetic blood pressure transduction.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":"328 2","pages":"H271-H282"},"PeriodicalIF":4.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gestational arsenite exposure alters maternal postpartum heart size and induces Ca²⁺-handling dysregulation in cardiomyocytes.","authors":"Nicole Taube, Morgan Steiner, Obialunanma V Ebenebe-Kasonde, Raihan Kabir, Haley Garbus-Grant, Sarah-Marie Alam El Din, Emily Illingworth, Nadan Wang, Brian L Lin, Mark J Kohr","doi":"10.1152/ajpheart.00266.2024","DOIUrl":"10.1152/ajpheart.00266.2024","url":null,"abstract":"<p><p>Cardiovascular disease is the leading cause of mortality in the US. Studies suggest a role for environmental exposures in the etiology of cardiovascular disease, including exposure to arsenic through drinking water. Arsenic exposure during pregnancy has been shown to have effects on offspring, but few studies have examined impacts on maternal cardiovascular health. While our prior work documented the detrimental effect of arsenic on the maternal heart during pregnancy, our current study examines the effect of gestational arsenic exposure on the maternal heart postpartum. Timed-pregnant wild-type (C57BL/6J) mice were exposed to 0, 100 or 1000 µg/L sodium arsenite (NaAsO2) via drinking water from embryonic day 2.5 until parturition. Postpartum heart structure and function was assessed via transthoracic echocardiography and gravimetric measurement. Hypertrophic markers were probed via qRT-PCR and western blot. Isolated cardiomyocyte Ca²⁺-handling and contraction were also assessed, along with the expression of with Ca²⁺-handling and contractile proteins. Interestingly, we found that exposure to either 100 or 1000 µg/L sodium arsenite increased postpartum heart size at postpartum day 12 vs. non-exposed postpartum controls. At the cellular level, we found altered cardiomyocyte Ca²⁺-handling and contraction, along with expression changes of key contractile proteins, including α-Actin and cardiac myosin binding protein C (cMyBP-c). Together, these findings suggest that gestational arsenic exposure impacts the postpartum maternal heart, possibly inducing long-term cardiovascular changes. Furthermore, these findings highlight the importance of reducing arsenic exposure during pregnancy, and the need for more research on the impact of arsenic on maternal heart health and adverse pregnancy events.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated Frame Rates During Exercise Echocardiography Improve Speckle Tracking Success Rate and Augment Deformation Values.","authors":"Fabian Spahiu, Michelle Mook, Lars C Helbig, Eric J Stöhr","doi":"10.1152/ajpheart.00817.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00817.2024","url":null,"abstract":"<p><p><b>Background:</b> Although 2D speckle-tracking echocardiography (STE) is important for the clinical quantification of myocardial function it remains unknown whether increased frame rates during exercise STE augment tracking success and absolute deformation values. <b>Method:</b> 19 participants (15 male and 4 female; age 26.7±4.8) underwent step-wise exercise testing on a recumbent bicycle. Exercise started at 50 W, increasing by 30 W every 3 min until a target heart rate of 130-140 bpm was reached. During last 90 seconds of each exercise stage, echocardiographic sequences for offline quantification of longitudinal strain (LS), peak twist, untwisting velocity, basal rotation and apical rotation were acquired with high (HFPS), medium (MFPS), and low frame rates (LFPS). Differences in tracking success were determined using chi-square test and the impact of different frames rates on absolute deformation values were compared using mixed-model-analysis. <b>Results:</b> Utilization of HFPS significantly improved tracking success for parasternal short-axis images. LS acquired at HFPS was highest at baseline and across all exercise stages. Similar trends were observed for twist, peak untwisting velocity and apical rotation, while basal rotation showed no differences. Mixed model analysis revealed a significant effect of frame rate setting on LS (p<0.05) and untwisting velocity (p<0.05). <b>Conclusion:</b> In contrast to recommendations by leading organizations advocating for frame rates between 40 and 80 fps during resting conditions, with a proportional increase as heart rate rises, our findings suggest that consistently maintaining the frame rate at the highest feasible level is preferable for achieving optimal tracking success and accuracy in STE.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced vascular contraction induced by exposure to angiotensin II mediated by endothelin-1 biosynthesis following PKCβ activation.","authors":"Hirotaka Tajima, Nayu Morikita, Masashi Mukohda, Sho Nakamura, Mihiro Seki, Ryuya Imai, Fumiyo Saito, Risuke Mizuno, Hiroshi Ozaki","doi":"10.1152/ajpheart.00541.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00541.2024","url":null,"abstract":"<p><p>Protein kinase C (PKC) reportedly plays a role in the pathogenesis of many vascular dysfunction-related conditions. In this study, we investigated whether PKCβ is associated with vascular contractile changes induced by angiotensin II (Ang II) exposure. Long-term (24 h) treatment of rat aortae and mesenteric arteries in Ang II-containing culture medium enhanced 5-hydroxytrypatamine (5-HT)-induced vascular contraction in a dose-dependent manner, in association with enhanced phosphorylation of PKCβ S660. Increased contraction induced by Ang II treatment was also observed in endothelium-denuded aorta. Enhanced contraction induced by Ang II was markedly diminished by knockout of the PKCβ gene or treatment with LY333531 and CGP53353 (PKCβ inhibitors). Cycloheximide (protein synthesis inhibitor) blocked the Ang II-induced enhanced contraction. Gene expression profiling and real-time PCR analyses showed marked upregulation of endothelin-1 (ET-1) expression in Ang II-treated aorta, but was not observed in PKCβ-knockout aorta. Ang II increased the secretion of ET-1 peptide in endothelium-intact and -denuded aortae. Ang II-induced enhancement of vascular contraction was diminished by BQ-123 (ET_AR blocker). <i>In vivo</i> treatment with Ang II (250 ng/kg/min) for 7 days increased phosphorylation of PKCβ S660 in rat vascular tissue and increased the <i>in vitro</i> contractile responses to 5-HT and <i>in vivo</i> systolic blood pressure, but these changes were largely absent in PKCβ-knockout experiments. These data suggest that long-term exposure to Ang II increases vascular smooth muscle contraction and blood pressure elevation, mediated by activation of PKCβ and subsequent biosynthesis of ET-1 in vascular smooth muscle cells.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to prenatal hypoxia impairs the function and structure of the carotid arteries in the adult offspring.","authors":"Murilo E Graton, Amanda A de Oliveira, Aryan Neupane, Anita Quon, Raven Kirschenman, Floor Spaans, Sandra T Davidge","doi":"10.1152/ajpheart.00859.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00859.2024","url":null,"abstract":"<p><p>Prenatal hypoxia, a common pregnancy complication, can lead to vascular dysfunction, thereby increasing the risk of cardiovascular disease in the adult offspring. Carotid arteries are responsible for the majority of the blood flow to the brain/head, and carotid artery dysfunction is associated with life-threating cardiovascular events, such as stroke. However, whether prenatal hypoxia exposure impacts the function of the carotid arteries in the adult offspring is not known. We hypothesize that prenatal hypoxia impairs carotid artery function in the adult male and female offspring. Sprague Dawley rats were exposed to normoxia (21% O₂) or hypoxia (11% O₂) from gestational day (GD) 15 to 21 (term=22 days; n=9-11/group). Carotid arteries were isolated from the 4-month-old adult male and female offspring. Vasoconstrictor and vasodilatory properties were assessed by wire myography, and biomechanical properties (myogenic tone, circumferential stress and strain) by pressure myography. Collagen deposition (Masson's trichrome stain) and elastin density (Verhoeff stain) were measured in carotid artery cryosections. Prenatal hypoxia did not impact vasoconstriction or vasorelaxation responses in carotid arteries from both offspring. However, in males, prenatal hypoxia reduced carotid artery myogenic tone development and increased circumferential strain, which coincided with a lower collagen deposition and higher elastin density. In females, prenatal hypoxia tended to lower carotid artery circumferential strain (i.e., increased stiffness), without differences in myogenic tone or collagen/elastin density. Altogether, these data show that prenatal hypoxia exposure affects the carotid arteries of the adult offspring in a sex-specific manner, which may impact the blood flow regulation to the brain.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vivo Effects of Cardiomyocyte-Specific Beta-1 Blockade on Afterload- and Frequency-dependent Cardiac Performance.","authors":"Genri Numata, Yu Otsu, Shun Nakamura, Masayuki Toyoda, Hiroyuki Tokiwa, Yusuke Adachi, Taro Kariya, Kota Sueo, Mayo Shigeta, Takaya Abe, Tetsuo Sasano, Atsuhiko Naito, Issei Komuro, Eiki Takimoto","doi":"10.1152/ajpheart.00795.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00795.2024","url":null,"abstract":"<p><p>Pharmacologic beta-blockade is a well-established therapy for reducing adverse effects from sympathetic overactivity in cardiovascular diseases, such as heart failure. Despite decades of research efforts, in vivo cardiac functional studies utilizing genetic animal models remain scant. We generated a mouse model of cardiomyocyte-specific deletion of beta-1 adrenergic receptor (ADRB1) , the primary subtype expressed in cardiac myocytes, and demonstrated the role for ADRB1 in the maintenance of cardiac function at baseline and during exposure to increase in cardiac afterload by transient aortic occlusion and increasing heart rates (HRs) via atrial pacing. cKO hearts showed mildly depressed baseline left ventricular (LV) function, including slower HR, decreased contractility (dP/dtmax/IP) and prolonged relaxation (Tau) at baseline in both sexes. Exposure to increased LV afterload depressed LV function in either genotype similarly; however, the functional recovery following the removal of the afterload was severely impaired in cKO hearts, while cardiac function was immediately normalized in WT hearts. When HR was altered from 400 to 700bpm, cKO hearts were deficient in HR-dependent improvement of cardiac contractility and relaxation, known as positive force frequency relationship, that was evident in WT hearts. Enhanced phosphorylation of phospholamban by the HR increase was markedly blunted in cKO myocardium vs wild types, while CaMKII phosphorylation was comparable between the genotypes, suggesting the critical involvement of PKA. These results provide the first experimental evidence for the role of ADRB1 in cardiomyocytes for maintaining cardiac function at baseline and during acute stress, providing clinical perspective relating to the management of patients on beta-blockers.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P2 purinergic receptors at the heart of pathological left ventricular remodeling following acute myocardial infarction.","authors":"Ana Valéria Vinhais da Silva, Simon Chesseron, Oumnia Benouna, Jérôme Rollin, Sébastien Roger, Thierry Bourguignon, Stéphanie Chadet, Fabrice Ivanes","doi":"10.1152/ajpheart.00599.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00599.2024","url":null,"abstract":"<p><p>Pathological left ventricular remodeling is a complex process following an acute myocardial infarction, leading to architectural disorganization of the cardiac tissue. This phenomenon is characterized by sterile inflammation and the exaggerated development of fibrotic tissue, which is non-contractile and poorly conductive, responsible for organ dysfunction and heart failure. At present, specific therapies are lacking for both prevention and treatment of this condition, and no biomarkers are currently validated to identify at-risk patients. Physiopathological understanding of this process is limited, probably due to the combination of the multi-cellular responses involved that are initially necessary for tissue healing but may be detrimental on longer term. Current research focuses on understanding and modulating the inflammatory response, a key aspect of the tissue healing process. Inflammation is triggered by the release of inflammatory mediators from cardiomyocytes undergoing cell death in the context of ischemia-reperfusion injury. Among them, extracellular ATP is a strong mediator of inflammation through the activation of P2 purinergic receptors, regulating the behavior of all the cellular actors of the post-myocardial infarction response and impacting organ function and recovery. Rather than considering each cellular protagonist independently, this review provides an integrated overview of the inflammatory and tissue response to myocardial infarction by members of the P2 receptor family. Finally, it explores the possibility of reducing pathological left ventricular remodeling through the modulation of these receptors and their associated signaling pathways.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling Hidden Dangers: Quantitative Analysis of Ischemic Risks in High-Risk Patients with ASCVD and Dyslipidemia.","authors":"Shih-Hsien Sung, Min-Ji Charng","doi":"10.1152/ajpheart.00555.2024","DOIUrl":"https://doi.org/10.1152/ajpheart.00555.2024","url":null,"abstract":"<p><p>Cardiovascular disease is one of the foremost causes of morbidity and mortality worldwide, with low-density lipoprotein cholesterol (LDL-C) identified as a significant risk factor for subsequent ischemic events. Elevated LDL-C contributes to vascular injury and fibrosis by upregulating the expression of connective tissue growth factor and collagen IV, which leads to endothelial cell dysfunction that initiates the process of atherosclerotic diseases. Currently, there is an absence of clear, risk-defined criteria to identify patients who are in greater needs for intensive LDL-C reduction, particularly with PCSK9 inhibitors. The data of ischemic risk associated with different patient types are scattered across the sub-analyses of FOURIER and ODYSSEY OUTCOMES trials, as well as trials that analyzed the plaque morphology of high-risk patients. It would be helpful to highlight the use of clinical features and plaque morphology and identify the patient types at higher ischemic risk. This article aims to provide a clear visualization of the ischemic risk associated with various types of patients with atherosclerotic cardiovascular disease (ASCVD) and dyslipidemia, and its implications to improve risk stratification for patients with unveiling hidden dangers.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":4.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}