Philipp Aigner, Theodor Abart, Thomas Schwab, Kamen Dimitrov, Erhan Urganci, Manar El-Shaer, Michael Roehrich, Daniel Zimpfer, Marcus Granegger
{"title":"Ventriculo-Arterial Coupling and Speed Modulations in Rotodynamic Blood Pumps.","authors":"Philipp Aigner, Theodor Abart, Thomas Schwab, Kamen Dimitrov, Erhan Urganci, Manar El-Shaer, Michael Roehrich, Daniel Zimpfer, Marcus Granegger","doi":"10.1152/ajpheart.00455.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00455.2026","url":null,"abstract":"<p><p>Clinical evidence indicates that myocardial recovery during left ventricular assist device (LVAD) therapy is influenced by mechanical unloading. Strategies restoring physiological ventriculo-arterial (VA) coupling may promote recovery. Therefore, this study investigated whether rotodynamic blood pumps (RBP) operated in modulated rotational speed can optimize ventriculo-pump-arterial (VpA) coupling and improve mechano-energetic performance. VpA coupling was assessed using a hybrid mock loop simulating a virtual 30-kg pediatric patient under moderate and end-stage heart failure (HF). Constant-speed operation, symmetric pulsatile profiles (sinusoidal and step), and an asymmetric step profile (30%/70% high/low speed duration) were tested at varying phase delays after systole onset. Key findings were validated in an isolated large-animal heart model, including analysis of VA/VpA coupling and cardiac efficiency. Constant speed LVAD support worsened VpA coupling (moderate HF: 1.50 to 1.79; end-stage HF: 4.19 to 7.67). In contrast, symmetric pulsatile profiles during copulsation improved coupling (moderate HF: sine/step 1.32/0.97; end-stage HF: sine/step 3.30/2.52) and arterial pressure pulsatility (moderate HF: sine/step +40%/+74%; end-stage HF: sine/step +132%/+225%) but caused significant diastolic backflow. The asymmetric step profile maintained improved matching (moderate/end-stage HF: 0.97/2.86) and arterial pulsatility (+58%/+174%) while reducing backflow. Isolated heart experiments confirmed improved coupling, arterial pulsatility and maximized cardiac efficiency at optimized phayse delays (70-90% delay). Cardiac cycle synchronized operation of RBPs in co-pulsation improves VpA coupling, cardiac efficiency and arterial pulsatility compared with constant-speed support. Tailoring pulsatile profiles to cardiac timing and residual function may enable more physiological support and promote recovery-oriented LVAD therapy.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148966190","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}
Takuro Washio, Sarah L Hissen, John D Akins, Ryosuke Takeda, Andrew W D'Souza, James P MacNamara, Satyam Sarma, Daniel W Trott, Kevin Lutz, Christopher M Hearon, Tony G Babb, Benjamin D Levine, Paul J Fadel, Qi Fu
{"title":"Sex-specific association between obesity and sympathetic nerve activity in HFpEF.","authors":"Takuro Washio, Sarah L Hissen, John D Akins, Ryosuke Takeda, Andrew W D'Souza, James P MacNamara, Satyam Sarma, Daniel W Trott, Kevin Lutz, Christopher M Hearon, Tony G Babb, Benjamin D Levine, Paul J Fadel, Qi Fu","doi":"10.1152/ajpheart.00214.2026","DOIUrl":"10.1152/ajpheart.00214.2026","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) is more prevalent in women than in men, and most patients with HFpEF are overweight or obese in the United States. However, whether the impact of obesity on autonomic dysregulation and inflammation differs by sex in HFpEF remains unknown. We investigated sex-specific associations between obesity, inflammation, and muscle sympathetic nerve activity (MSNA) in patients with HFpEF. In 57 HFpEF patients (mean ± SD; 71 ± 7 yr; 37 women, 20 men) and 69 non-HFpEF controls (70 ± 6 yr; 43 women, 26 men), body mass index (BMI), MSNA, and C-reactive protein (CRP) were measured during supine rest. A significant sex-by-BMI interaction was observed for the associations between BMI and MSNA (<i>P</i><sub>interaction</sub> = 0.047), as well as BMI and CRP (<i>P</i><sub>interaction</sub> = 0.012). The slopes of these associations were steeper in women than in men. Women with HFpEF had greater MSNA than men with HFpEF and control women (<i>P</i> < 0.05); however, MSNA was not different between men with HFpEF and control men (<i>P</i> = 0.727). The association between CRP and MSNA demonstrated a consistent trend toward sex-specificity (<i>P</i><sub>interaction</sub> = 0.060). In sex-stratified subgroup analyses of patients, MSNA and CRP were higher in women with high body fat assessed by dual-energy X-ray absorptiometry (DEXA) than in those with low body fat, but not in men. These findings identify a sex-specific association between obesity, inflammation, and sympathetic neural activity in HFpEF, characterized by a stronger obesity-related sympathetic activation in women. This pattern provides insight into the role of obesity-related inflammation as a key feature of disease expression in women with HFpEF.<b>NEW & NOTEWORTHY</b> Women with heart failure with preserved ejection fraction exhibit greater resting sympathetic neural activity than men with HFpEF. Furthermore, our findings suggest that obesity-related inflammation may contribute to sex-specific disease expression in heart failure with preserved ejection fraction and may help explain phenotypic differences observed in women.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H796-H805"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elio Salameh, Malak Hoballah, Elnaz Ebrahimihoor, Aysa Ostovaneh, Colin O Wu, Robyn L McClelland, Steven Shea, David A Bluemke, Bharath Ambale-Venkatesh, João A C Lima
{"title":"Integrated left ventricular mass and left atrial function for prediction of cardiovascular outcomes: the Multi-Ethnic Study of Atherosclerosis.","authors":"Elio Salameh, Malak Hoballah, Elnaz Ebrahimihoor, Aysa Ostovaneh, Colin O Wu, Robyn L McClelland, Steven Shea, David A Bluemke, Bharath Ambale-Venkatesh, João A C Lima","doi":"10.1152/ajpheart.00397.2026","DOIUrl":"10.1152/ajpheart.00397.2026","url":null,"abstract":"<p><p>Left ventricular (LV) mass and left atrial (LA) strain are physiologically coupled and individually predict adverse cardiovascular outcomes. Their imbalance may reflect early atrioventricular uncoupling and atrial myopathy before overt structural disease. We evaluated whether a cardiac magnetic resonance (CMR)-derived LV mass-to-LA strain ratio identifies early atrioventricular mechanical uncoupling and predicts cardiovascular events. Participants from the Multi-Ethnic Study of Atherosclerosis underwent CMR at <i>exams 1</i> (2000-2002) and <i>5</i> (2010-2012). The LV mass-to-LA strain ratio was calculated as indexed end-diastolic LV mass divided by peak LA strain. Classification and regression tree analysis identified cut points for baseline ratio and longitudinal change, defining low (<1.04), reference (1.04-3.26), and high (>3.26) groups, and lesser-(≤130%) versus greater-change (>130%) groups. Multivariable Cox models assessed associations with heart failure (HF), atrial fibrillation (AF), myocardial infarction (MI), and all-cause mortality. Among 4,232 participants (mean age 61.5 ± 10.1 yr; 52.8% female), the mean ratio was 1.95 ± 0.72. Over a median 18-yr follow-up, 6.0% developed HF, 5.2% MI, 18.7% AF, and 25.6% died. A high LV mass-to-LA strain ratio independently predicted HF [hazard ratio (HR) 2.85], AF (HR 2.00), MI (HR 1.96), and death (HR 1.70; all <i>P</i> ≤ 0.003). With repeat CMR, an increasing ratio also predicted cardiovascular events, including among individuals with normal LV mass and LA strain. Higher baseline ratios were associated with progression toward abnormal volumetric atrioventricular coupling over time. A higher LV mass-to-LA strain ratio and its increase independently predict cardiovascular events before overt chamber abnormalities, supporting impaired atrial adaptation as an early stage of atrial myopathy.<b>NEW & NOTEWORTHY</b> Left atrial failure underlies two of the most consequential conditions in cardiovascular medicine: atrial fibrillation, with predisposition to stroke and dementia, and heart failure with preserved ejection fraction, a leading cause of hospitalization and mortality. By examining the relationship between left ventricular hypertrophy and left atrial deformation at the population level, we demonstrate that the LV mass-to-LA strain ratio identifies a threshold beyond which adverse atrial remodeling independently predicts incident cardiovascular events-even within normal ranges.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H806-H816"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629313","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}
Jason R Carter, Nathaniel D M Jenkins, Jeremy A Bigalke, Austin T Robinson, Manda L Keller-Ross, Jody L Greaney, Ida T Fonkoue, Paul J Fadel, Vaughan G Macefield, Nisha Charkoudian, Benjamin D Levine, Michael J Joyner
{"title":"Guidelines for rigor and reproducibility of heart rate variability within human cardiovascular research.","authors":"Jason R Carter, Nathaniel D M Jenkins, Jeremy A Bigalke, Austin T Robinson, Manda L Keller-Ross, Jody L Greaney, Ida T Fonkoue, Paul J Fadel, Vaughan G Macefield, Nisha Charkoudian, Benjamin D Levine, Michael J Joyner","doi":"10.1152/ajpheart.00041.2026","DOIUrl":"10.1152/ajpheart.00041.2026","url":null,"abstract":"<p><p>Heart rate variability (HRV) is a widely utilized approach for investigating cardiovascular health and human performance. Methodological approaches, analyses, and interpretations of HRV can vary extensively, and scientific debates on HRV reliability and utility remain. These debates have been amplified in recent years by the rapid growth and ubiquity of wearable devices and their incorporation into scientific research studies. The present guidelines paper takes an evidence-based approach to propose more consistent and rigorous measurement and interpretation of HRV within human cardiovascular research and application. First, HRV has some utility as a cardiovascular risk stratification tool but is not appropriate to employ as a specific marker of cardiac sympathetic outflow or sympathovagal balance. Although time-domain and spectral analysis can more accurately reflect respiratory modulation of cardiac vagal (parasympathetic) activity, caution is necessary to avoid overinterpretation, particularly with respect to the concept of \"vagal tone.\" Numerous experimental, demographic, and environmental factors influence HRV assessment, interpretation, and reliability. Specifically, it is critical to account for nonmodifiable (age, sex, race/ethnicity, etc.) and modifiable (i.e., exercise, physical fitness, etc.) factors within participant samples. Furthermore, technical approaches such as the HRV input signal (e.g., electrocardiography vs. photoplethysmography), length of recording, location of recordings (i.e., laboratory vs. field), respiratory rate and depth, and analytical approaches (i.e., time vs. frequency domain) can all impact rigor, reliability, and study interpretations. Finally, with respect to the rapid advancements of HRV assessment using wearable technology, investigators should interpret and contextualize findings within the limitations outlined in this guideline review.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H918-H943"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13477148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148576799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Olufunto O Badmus, Sally Wahba, Gertrude Arthur, Landon D Parrow, Bentley S Montgomery, Isabela Cucolicchio, Karis McGowan, Erin B Taylor
{"title":"Gestational diabetes promotes future maternal cardiovascular disease through endothelin activation and suppressed NO/cGMP/PRKG and AMPK/SIRT1 signaling pathways.","authors":"Olufunto O Badmus, Sally Wahba, Gertrude Arthur, Landon D Parrow, Bentley S Montgomery, Isabela Cucolicchio, Karis McGowan, Erin B Taylor","doi":"10.1152/ajpheart.00871.2025","DOIUrl":"10.1152/ajpheart.00871.2025","url":null,"abstract":"<p><p>Women with gestational diabetes mellitus (GDM) are more likely to develop cardiovascular disease (CVD) within 3 to 10 yr following pregnancy. Despite a return to normoglycemia shortly after gestation, GDM mothers still possess an increased risk of future CVD. In this study, we use a novel preclinical hormonal model of GDM to examine the mechanisms underlying future vascular and cardiac dysfunction in mothers with a history of GDM. We treated 16-wk-old pregnant C57BL/6J mice with the insulin receptor antagonist (S961; 30 nmol/kg sc) from <i>gestational day 7</i> (second trimester of pregnancy) until delivery to induce GDM. GDM mice developed systolic and diastolic dysfunction, arterial stiffness, hypertension, increased cardiac mass, and exercise intolerance at 10 wk postpartum compared with saline-treated pregnant or S961-treated virgin mice. We also observed decreased plasma nitric oxide (NO) and increased endothelin-1 (ET-1) in GDM. The aorta of S961-induced GDM mice had increased pulse wave velocity, impaired vascular relaxation, remodeling, elevated reactive oxygen species (ROS) production and adhesion molecules, increased ET-1 type A receptor expression, and reduced sirtuin-1 (SIRT1) expression. The left ventricle of S961-induced GDM mice exhibited fibrosis, thickness, and increased ROS production. In addition, alterations in cardiac kinase activity in the nitric oxide/cyclic guanosine monophosphate/protein kinase G (NO/cGMP/PRKG) and AMP-activated protein kinase (AMPK) alpha pathways were observed at 10 wk postpartum using novel PamGene kinome technology. Thus, endothelin activation, suppressed NO/cGMP/PRKG signaling, impaired AMPK, and altered SIRT1 may be responsible for the development of vascular stiffness and cardiac dysfunction in mothers with a history of GDM.<b>NEW & NOTEWORTHY</b> Mechanisms underlying the future development of CVD in mothers with GDM were investigated using a mouse model of GDM that mimics the condition observed in human GDM. Examining the aorta in the later life of the GDM model reveals increased arterial stiffness and endothelin activation associated with vascular remodeling. In addition, kinome analysis reveals suppressed cardiac NO/cGMP/PRKG and impaired AMPK-SIRT1 signaling pathways, which corroborate the impaired ventricular relaxation observed in later life in GDM mothers.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H753-H773"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13564116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148652809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Somaya Y Ibrahim, Kyrilos Sadaka, Mary E Shepard, Ashim K Bagchi, Rushita A Bagchi
{"title":"Cardiac fibroblasts in extracellular matrix homeostasis and remodeling.","authors":"Somaya Y Ibrahim, Kyrilos Sadaka, Mary E Shepard, Ashim K Bagchi, Rushita A Bagchi","doi":"10.1152/ajpheart.00862.2025","DOIUrl":"10.1152/ajpheart.00862.2025","url":null,"abstract":"<p><p>Resident cardiac fibroblasts are indispensable regulators of myocardial homeostasis and key effectors of pathological cardiac remodeling. Formerly viewed as passive structural support cells, activated fibroblasts are now recognized as dynamic mediators of extracellular matrix (ECM) turnover, paracrine signaling, and electromechanical coupling within the heart. Fibroblast heterogeneity, defined by developmental origin and microenvironmental cues, further amplifies the complexity of their roles across physiological and pathological contexts. In response to stress or injury, cardiac fibroblasts undergo activation and transition into myofibroblasts, orchestrating wound repair but also driving maladaptive fibrosis when persistently stimulated. This activation is governed by an intricate network of signaling pathways, including transforming growth factor (TGF)-β/SMAD, renin-angiotensin-aldosterone system (RAAS), endothelin-1, RhoA-MRTF (Myocardin-Related Transcription Factor)-SRF (serum response factor), integrins, and inflammatory cytokine cascades, which collectively determine fibroblast phenotype and ECM remodeling outcomes. Their pleiotropic functions encompass ECM synthesis and degradation, regulation of angiogenesis, secretion of cytokines and growth factors, and modulation of cardiomyocyte electrophysiology. In this review, we synthesize current insights into the molecular and cellular mechanisms by which resident naive cardiac fibroblasts regulate cardiac ECM dynamics, with an emphasis on profibrotic signaling networks, transcriptional and developmental regulators, and intercellular cross talk. We also describe how recent lineage-tracing and transcriptomic studies redefine resident cardiac fibroblasts as the dominant drivers of ECM remodeling and fibrosis. We further identify unresolved questions surrounding fibroblast plasticity, their contributions to arrhythmogenesis, and cardiometabolic remodeling. Understanding the context-dependent functions of cardiac fibroblasts is essential to developing targeted antifibrotic interventions that preserve reparative processes while preventing adverse remodeling, ultimately improving outcomes in cardiovascular disease.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H779-H795"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148597376","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":"Fetal programming under hyperglycemic stress: the vascular system at risk.","authors":"Fabiano E Xavier","doi":"10.1152/ajpheart.00390.2026","DOIUrl":"10.1152/ajpheart.00390.2026","url":null,"abstract":"<p><p>Maternal hyperglycemia, arising from pregestational or gestational diabetes, affects approximately 19% of pregnancies worldwide. Beyond its immediate obstetric and neonatal consequences, it may leave a durable imprint on vascular development. Within the framework of the Developmental Origins of Health and Disease hypothesis, this review synthesizes current evidence linking an intrauterine hyperglycemic environment to persistent vascular dysfunction in the offspring. The analysis first focuses on the utero-fetoplacental interface, where impaired spiral artery remodeling, abnormal placental angiogenesis, and weakened endothelial barrier integrity may disturb maternal-fetal exchange and expose developing tissues to early stress. Clinical and experimental data indicate that these disturbances are followed by long-term alterations in vascular structure and reactivity, including a shift toward a proconstrictor phenotype, endothelial dysfunction, reduced nitric oxide bioavailability, oxidative stress, altered cyclooxygenase-2-derived prostanoid signaling, and enhanced neurovascular sympathetic influences. Structural remodeling, particularly in resistance arteries, may further increase peripheral vascular resistance and favor the later development of hypertension. The review also considers how epigenetic changes, including DNA methylation and histone modifications, may contribute to a persistent molecular memory of fetal hyperglycemic exposure. By integrating evidence from placental biology, vascular reactivity, arterial remodeling, and early cardiovascular phenotypes, this review outlines how maternal hyperglycemia may shape offspring cardiovascular risk through sustained alterations in vascular structure and function.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H842-H893"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668270","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":"Overlooked and ignored for too long: investigation of regional and sex-related differences in vascular reactivity along the murine aorta.","authors":"Andrew P Braun, Michael A Hill","doi":"10.1152/ajpheart.00627.2026","DOIUrl":"10.1152/ajpheart.00627.2026","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H914-H917"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148683208","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":"RORα-<i>Adra1a</i>: defining a new transcriptional axis in cardiomyocyte biology.","authors":"Caelan W Moreno, Caitlin C O'Meara","doi":"10.1152/ajpheart.00599.2026","DOIUrl":"10.1152/ajpheart.00599.2026","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H747-H749"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148629323","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":"Preserved diastolic carotid blood flow is associated with higher diastolic aortic pressure in lifelong female pearl divers.","authors":"Rintaro Sakamoto, Tsubasa Tomoto, Daisuke Hoshi, Marina Fukuie, Takashi Tarumi, Hirofumi Tanaka, Jun Sugawara","doi":"10.1152/ajpheart.00488.2026","DOIUrl":"10.1152/ajpheart.00488.2026","url":null,"abstract":"<p><p>Higher diastolic aortic pressure is associated with central arterial elastic recoil function and may help preserve peripheral perfusion. Japanese female pearl divers, called \"Ama,\" exhibit lower arterial stiffness as an adaptation to lifelong repeated diving, but whether this translates into enhanced diastolic blood flow remains unclear. This study investigated aortic and carotid hemodynamic profiles to determine whether female pearl divers demonstrate enhanced diastolic blood flow in association with diastolic aortic pressure. A total of 61 middle-aged and elderly female pearl divers (<65-yr group: <i>n</i> = 23, 53 ± 9 yr; ≥65-yr group: <i>n</i> = 38, 72 ± 4 yr, representing middle-aged and older groups, respectively) and 94 female nondivers (<65-yr group: <i>n</i> = 48, 53 ± 9 yr; ≥65-yr group: <i>n</i> = 46, 73 ± 5 yr) were studied. Aortic pressure was estimated from applanation tonometry of carotid arterial pressure waveforms via a general transfer function. Carotid blood flow was calculated from blood velocity and diameter of the common carotid artery. Diastolic aortic pressure-time integral and carotid flow volume were calculated as areas under the waveforms from the dicrotic notch to end-diastole. Compared with nondivers, pearl divers exhibited a higher diastolic aortic pressure-time integral (main effect of group, <i>P</i> < 0.01). Moreover, diastolic carotid blood flow volume was also greater in pearl divers than in nondivers (main effect of group, <i>P</i> < 0.01). Therefore, compared with female nondivers, lifelong female pearl divers may have lower central arterial stiffness that enhances diastolic aortic pressure, thereby preserving greater carotid blood flow during diastole.<b>NEW & NOTEWORTHY</b> This study indicated that, compared with female nondivers, lifelong female pearl divers exhibited higher diastolic carotid blood flow alongside higher aortic pressure during diastole. Therefore, lifelong repeated diving exposure may lead to decreased arterial stiffness, which can facilitate higher diastolic aortic pressure and thereby enhance distal arterial blood flow during diastole.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":"H1012-H1018"},"PeriodicalIF":3.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148787104","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}