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

{"title":"Cognitive Impairment and Cerebral Haemodynamics in Individuals with Symptomatic Peripheral Artery Disease.","authors":"Beth L Cheshire, Yvonne J Sensier, Lucy C Beishon, Ronney B Panerai, Rob D Sayers, John S M Houghton","doi":"10.1152/ajpheart.00634.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00634.2026","url":null,"abstract":"<p><p>Peripheral artery disease (PAD) is highly prevalent in older adults. PAD is associated with cognitive impairment; however the underlying mechanisms are unclear. The brain's metabolic needs rapidly change in response to neuronal activity requiring adjustment of regional cerebral blood flow, termed neurovascular coupling (NVC). The microvascular endothelium contributes to NVC responses. Patients with PAD have endothelial dysfunction that may extend to the cerebral circulation, impairing NVC and cognitive function. The present study examined NVC responses to cognitive stimulation using Transcranial Doppler Ultrasonography (TCD) in older adults with PAD. Participants underwent bilateral TCD in the middle cerebral arteries during four recordings; baseline and tasks from Addenbrooke's-III Cognitive Examination and Digit Span. Mean absolute change in cerebral blood velocity (CBv) was measured at two time points (25-30s; 30-40s) from a 20s baseline. Nineteen patients with intermittent claudication and 20 age-matched controls (mean: 68.4 [8.1] years; female: 12) were included. CBv increased on all cognitive tasks, however no significant differences were observed between patients (range: 0.9-7.4 cm/s) and controls (range: 1.1-6.9 cm/s). Patients with PAD had significantly poorer working memory and global cognitive function. Older adults with PAD had similar NVC responses to age-matched controls. The lack of differences may be due to the low prevalence of cognitive impairment, disease severity, small sample size, or the relatively simple cognitive paradigms. Future studies examining NVC in patients with PAD during tasks with higher cognitive load, and in more advanced disease stages, are needed to further understand whether impaired NVC contributes to PAD-related cognitive impairment.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079509","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 Salt Sensitivity Index is a Pragmatic Advance in Detecting Salt-Sensitive Blood Pressure with Important Caveats.","authors":"Ida Tchuisseu Fonkoue, Austin T Robinson","doi":"10.1152/ajpheart.90104.2026","DOIUrl":"10.1152/ajpheart.90104.2026","url":null,"abstract":"","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079437","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":"Cardiac output and stroke volume dissociate during fluid loading in conscious sheep.","authors":"Terry O'Brien, Robert G Hahn","doi":"10.1152/ajpheart.90145.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.90145.2026","url":null,"abstract":"<p><p><b>Background.</b> A fluid challenge is judged by a rise in stroke volume or cardiac output, on the twin assumptions that the two report the same physiological effect and that either reflects circulatory benefit. We tested these assumptions across a fourfold crystalloid load in conscious sheep with intact autonomic reflexes. <b>Methods.</b> We performed a secondary analysis of 26 intravenous infusions of 0.9% saline (25, 50 or 100 mL·kg-1 over 20 min) in 13 conscious splenectomized sheep, a within-animal crossover. Cardiac output, arterial and central venous pressures and blood hemoglobin were recorded and mean systemic filling pressure was estimated by the Parkin analogue. <b>Results.</b> Stroke volume and cardiac output dissociated with dose. At 100 mL·kg^-1 cardiac output rose +75% carried entirely by heart rate (+143%) while stroke volume fell -25%; across the crossover cardiac output and heart rate scaled with dose, whereas stroke volume showed a non-significant monotonic decline (Friedman p = 0.22). Arterial pressure was the most defended variable, held to a ~16% ceiling by a load-scaled vasodilation (resistance -35% at the highest load). The flow gains barely raised oxygen delivery, which fell 8-14% below baseline by 180 min as hemoglobin was diluted. Filling pressure rose about threefold more than blood volume at every dose. <b>Conclusions.</b> In the conscious animal a fluid-induced rise in cardiac output can be carried entirely by an autonomic, Bainbridge-type tachycardia while stroke volume falls, and need not improve oxygen delivery or arterial pressure. A favorable stroke-volume reading is not a surrogate for systemic flow, and flow for oxygen delivery.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079506","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":"Test-Retest Reliability of Endothelial Ischemia-Reperfusion Injury in Healthy Young Adults.","authors":"Ethan J Hein, Kase J Pennartz, Ayrion W Moody, Alexander Fernandez, Joshua L Keller, Justin D Sprick","doi":"10.1152/ajpheart.90001.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.90001.2026","url":null,"abstract":"<p><p>Ischemia-reperfusion injury (IRI) describes the paradoxical phenomenon in which the restoration of blood flow to ischemic tissue can exacerbate damage during reperfusion. In humans, IRI can be modeled within the vascular endothelium by inducing 20 minutes of upper-arm ischemia and reperfusion. This approach transiently reduces flow-mediated dilation (FMD) of the brachial artery and is widely used to investigate mechanisms of vascular injury and evaluate cardioprotective therapies. Despite its widespread use, the test-retest reliability of this model has not been established. Therefore, we sought to quantify the inter-day reliability of IRI-induced reductions in FMD. Twenty healthy adults (10M/10F, age = 26 ± 7 years) completed two identical laboratory visits separated by no more than 7 (2 ± 2) days. During each visit, brachial artery FMD was assessed before and following IRI. Changes in FMD were analyzed using a two-way repeated measures ANOVA, and test-retest reliability was assessed via intraclass correlation coefficients (ICC_2,1). As expected, FMD was reduced following IRI in both visits (Visit 1: Pre = 7.3 ± 2.8%, Post = 4.4 ± 3.9%; Visit 2: Pre = 7.2 ± 2.8%, Post = 4.3 ± 3.6%, P < 0.001). The magnitude of this reduction (∆FMD) demonstrated excellent test-retest reliability (ICC = 0.88 [0.73-0.95]). Interestingly, a subset of participants demonstrated a resilient phenotype, characterized by preservation of FMD following IRI across both visits. These findings establish the test-retest reliability of the endothelial IRI model and support its use as a reliable tool for investigating mechanisms of vascular injury and evaluating potential therapies.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079512","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":"Alpha-Ketoglutarate Dehydrogenase and Citric Acid Cycle Flexibility in Heart Disease and Failure.","authors":"Nadia Martinez Naya, Abigail R Heath, Gustavo Adolfo Gámez de Armas, Keith A Webster, Lina A Shehadeh","doi":"10.1152/ajpheart.00428.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00428.2026","url":null,"abstract":"<p><p>Tricarboxylic acid cycle (TCA) enzymes, mitochondrial isocitrate dehydrogenase (IDH2), α-ketoglutarate dehydrogenase (AKGDH), and succinyl-CoA synthetase (SCS) catalyse the conversion of isocitrate to succinate generating reducing equivalents for mitochondrial complex I and ATP by substrate level phosphorylation. Because of their central roles in energy metabolism, TCA enzymes and their metabolites distribute extensively across cellular compartments coordinating intermediary metabolism, cellular redox, and nuclear gene expression. AKGDH activity is regulated by acylation, oxidation, energy charge, substrates, and product succinyl-CoA. Global TCA dysfunction is both a consequence and cause of the adverse metabolic remodelling that underlies contractile decline and ultimately heart failure (HF). This narrative review focuses on the potential for therapeutic enhancement of TCA function by augmenting AKG and/or AKGDH in the settings of cardiovascular disease and HF. The results support significant reversibility of TCA dysfunction and multiple clinical contexts wherein AKG supplementation confers benefit by mechanisms that include enhanced antioxidant defence as well as anaplerosis with improved bioenergetics and segmental TCA flux despite coincident dysfunction of other TCA enzymes. Elevated systemic AKG, recently identified as a biomarker of HF, is associated with worse outcomes of heart disease and, in preclinical models, with hypertrophy, fibrosis, and neurotoxicity, such that the success of therapeutic manipulation may be critically determined by the disease stage and context.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079515","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":"AFM Force-to-Signal Assay Uncovers Glypican-1 and TRP Channel Roles in Endothelial Mechanotransduction.","authors":"Matthew A Dragovich, Xaymara I Rivera Gonzalez, X Frank Zhang","doi":"10.1152/ajpheart.90228.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.90228.2026","url":null,"abstract":"<p><p>The endothelial surface glycocalyx (ESG) is a dense, carbohydrate-rich mesh of glycoproteins, proteoglycans, and glycosaminoglycans (GAGs) that coats the surface of endothelial cells (ECs). Mechanical cues, such as shear stress, at the ESG can be rapidly translated into biochemical signals. An impairment in this mechanosignaling pathway is linked to cardiovascular complications, such as diabetes, stroke, sepsis, and atherosclerosis, due to the decrease in the potent vasodilator, nitric oxide (NO). ESG plays a role in this pathway; however, the receptor-level pathways remain obscure. We present an atomic force microscopy (AFM) force-to-signal assay that delivers real-time, pico- to nano-newton, receptor-targeted mechanical inputs to a single live EC while simultaneously recording NO production via fluorescence. We apply controlled pulling forces to ESG components on mouse brain ECs to investigate which ESG elements are relevant to mechanosensing and which transient receptor potential (TRP) ion channels support Ca²⁺-dependent NO production. Our key findings are the following: (1) heparan sulfate (HS) and glypican-1 act as proximal mechano-sensors that trigger rapid NO signaling. (2) Pharmacological perturbation with SKF96365 markedly suppressed the mechanically evoked NO response, whereas a smaller but significant response persisted in the presence of amiloride. Together, our findings highlight glypican-1 engagement and the potential involvement of TRP-channel-associated Ca²⁺ entry in the ESG-mediated mechanosignaling pathway. Additionally, by directly coupling a molecule-specific mechanical input to a quantitative fluorescent readout, this technique provides a direct, single-cell map of endothelial mechanotransduction from receptor to downstream signal, enabling exploration of relevant targets for cardiovascular pathologies associated with glycocalyx dysfunction.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073193","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 reduction in blood pressure required to reduce arterial stiffness components in SPRINT: A randomized controlled trial.","authors":"Theodore M DeConne, Jordan Tanley, Ryan Pewowaruk, Deepika Laddu, Cecilia Peterson, Adam D Gepner, Timothy M Hughes, Mark A Supiano","doi":"10.1152/ajpheart.00578.2026","DOIUrl":"10.1152/ajpheart.00578.2026","url":null,"abstract":"<p><p><b>Background:</b> We previously demonstrated that intensive blood pressure (BP) control reduces total pulse wave velocity (T-PWV), through a load-dependent (LD-PWV), but not structural mechanism (S-PWV). We examined the extent to which changes in supine systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP) influence T-PWV, S-PWV, and LD-PWV (per m/s) in participants enrolled in the SPRINT (Systolic Blood Pressure Intervention Trial). <b>Methods:</b> SPRINT was a multicenter randomized controlled trial that enrolled participants with baseline SBP ≥130 mmHg. Participants were randomized to intensive (SBP<120 mmHg) or standard (SBP<140 mmHg) BP interventions. We leveraged supine carotid-femoral PWV in a subset data from SPRINT-PWV ancillary (N=516). Our analysis examined the effect of changes in BP on changes in T-PWV, S-PWV, and LD-PWV over one year, adjusting for baseline covariates. <b>Results:</b> Decreases in SBP, DBP, and MAP were associated with reductions in T-PWV and LD-PWV (all p<0.001), but not S-PWV. Participants with reductions in T-PWV (≥1 m/s) had adjusted SBP, DBP, and MAP reductions that were 11.0, 5.4, and 7.2 mmHg greater, respectively, than participants who did not. For LD-PWV, progressively larger reductions in SBP, DBP, and MAP were observed across categories of LD-PWV change, with the greatest reductions occurring with LD-PWV decreases of ≥1.0 m/s. <b>Conclusions:</b> BP lowering significantly reduces T-PWV through LD-PWV, but not S-PWV. Clinically meaningful reductions in T-PWV were accompanied by reductions in LD-PWV, whereas no BP reduction was associated with changes in S-PWV. Further evaluation of existing or novel therapies to reduce S-PWV are needed.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149035905","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":"Peripheral oxygen extraction and central determinants of exercise capacity in adults with Fontan circulation.","authors":"Hannah Van Belle, Alexander Van De Bruaene, Yogesh N V Reddy, C Charles Jain, Alexander C Egbe, Kathryn F Larson, Werner Budts, Heidi M Connolly, William R Miranda","doi":"10.1152/ajpheart.00411.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00411.2026","url":null,"abstract":"<p><p><b>Aims:</b> Altered central hemodynamics impair exercise tolerance post-Fontan procedure. However, the prevalence of peripheral impairment and its contribution to peak O₂ consumption (pV̇O₂) in this population are unknown. <b>Methods:</b> Exercise catheterization data in 52 adults with Fontan circulation [age 32 (24;36) years] were compared with patients with heart failure with preserved ejection fraction (HFpEF) and non-cardiac dyspnea (NCD) at 1:1 ratio. <b>Results:</b> Peak heart rate [108 (85;126) vs 108 (95;125) bpm] and indexed stroke volume [46 (39;54) vs 45 (40;53) ml/m²] were similar in the Fontan and HFpEF groups but lower compared to NCD [126 (108;141) bpm, p>0.001 and 51 (45;59) ml/m², p>0.001]. Peak peripheral O₂ extraction post-Fontan procedure was comparable to HFpEF [12 (10;14) vs 11 (10;13) ml/dl, p=0.17] but higher than in NCD [10 (9;12) ml/dl, p>0.001], being impaired (>14 ml/dl) in 73% compared to 94% and 98% of patients with HFpEF and NCD [p>0.001]. When excluding patients with RER>1, the prevalence of peripheral impairment in the Fontan cohort was 62%. Correlates of pV̇O₂ post-Fontan in multivariable regression were peak O₂ extraction [β 0.5±0.1 per ml/dl; p>0.001], mPAP [β -0.2±0.05 per mmHg; p=0.002], heart rate [β 0.03±0.01 per bpm; p=0.01], and systolic arterial blood pressure [β 0.03±0.01 per mmHg; p=0.02]. Thirty-one percent of adults with Fontan circulation had both reduced cardiac output reserve (>80% predicted) and inappropriate peripheral O₂ extraction. <b>Conclusions:</b> Impaired O₂ extraction is prevalent amongst adults post-Fontan and co-exists with central hemodynamic abnormalities. Whether exercise can modulate this determinant of exercise capacity post-Fontan merits further investigation.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149035895","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":"Impaired mitochondrial proteostasis underlies cardiomyocyte bioenergetic dysfunction in a murine 3-hit model of heart failure with preserved ejection fraction.","authors":"Xuan Li, Yiling Fu, Jussara M do Carmo, Alexandre A da Silva, Alan J Mouton, Ana C M Omoto, Lucas Wang, John E Hall, Zhen Wang","doi":"10.1152/ajpheart.00304.2026","DOIUrl":"10.1152/ajpheart.00304.2026","url":null,"abstract":"<p><p>Heart failure with preserved ejection fraction (HFpEF) predominantly affects older individuals with multiple comorbidities. Although mitochondrial dysfunction appears to be a major contributor to diastolic dysfunction, the mechanisms underlying it during HFpEF remain unclear. We used a clinically relevant two-hit HFpEF model in aged mice to investigate remodeling of cardiomyocyte mitochondrial proteins and to determine whether mitochondrial dysfunction reflects impaired biogenesis or defective mitochondrial proteostasis. HFpEF was induced in aged (15-month-old) male and female mice using a high-fat diet combined with chronic nitric oxide synthase inhibition (L-NAME). This model recapitulated key features of human HFpEF, including preserved ejection fraction with diastolic dysfunction and impaired cardiac reserve in both sexes. Consistent with impaired energy reserve, mitochondrial respiratory capacity measured by high-resolution respirometry (Oroboros) was significantly reduced in left ventricular muscle fibers. To examine cardiomyocyte-intrinsic mechanisms, mitochondria were isolated from cardiomyocytes using Langendorff perfusion and analyzed by proteomics and pathway enrichment analysis. Proteomic profiling revealed broad suppression of mitochondrial proteins that support oxidative metabolism and organelle maintenance, including those involved in oxidative phosphorylation, carbohydrate metabolism, and the TCA cycle. In contrast, key regulators of mitochondrial biogenesis were preserved. Notably, mitochondrial chaperones and proteases for protein quality control were reduced, leading to increased accumulation of ubiquitinated mitochondrial proteins and impaired mitochondrial proteostasis. Together, these findings indicate that mitochondrial dysfunction in a 3-hit HFpEF model is characterized by reduced respiratory capacity and impaired mitochondrial proteostasis, rather than defective biogenesis, suggesting that impaired mitochondrial protein quality control may contribute to reduced cardiac reserve in HFpEF.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057186","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":"Robust Quantification of Intraventricular Flow Using Ultrafast Vector Doppler Imaging in a Murine Model of Dilated Cardiomyopathy.","authors":"Geraldi Wahyulaksana, Colin K L Phoon, Ashmit K Pal, Glenn I Fishman, Jeffrey A Ketterling","doi":"10.1152/ajpheart.00313.2026","DOIUrl":"https://doi.org/10.1152/ajpheart.00313.2026","url":null,"abstract":"<p><p>Accurate assessment of cardiac mechanics and hemodynamics is important for understanding cardiac dysfunction and disease progression. However, conventional echocardiographic metrics primarily reflect global mechanical performance and provide limited insight into intraventricular flow dynamics. Ultrafast vector Doppler imaging (VDI) enables contrast-agent-free quantification of intracardiac flow, but acquisition-related reproducibility is difficult to isolate clinically because physiological conditions, acoustic windows, and probe orientation may vary simultaneously. Murine imaging permits repeated acquisitions under standardized conditions, enabling controlled assessment of cycle-to-cycle and imaging-plane variability, and providing a platform for systematic evaluation of VDI in the heart. We established a standardized framework for intraventricular flow quantification using ultrafast VDI and evaluated its reproducibility in a cardiomyocyte-specific Tafazzin knockout (Taz-cKO) murine model of dilated cardiomyopathy (DCM). Nine male mice (n = 3 Taz-cKO and n = 6 controls), aged 12-13 months, were studied. Cycle-to-cycle variability (beat-to-beat variation) averaged ~17.5%, whereas between-acquisition variability was higher (~25.5%), reflecting differences in imaging-plane orientation. Despite this variability, VDI-derived parameters differentiated control and DCM mice, with reduced kinetic energy and vector concentration, increased flow angle difference, and reduced vorticity magnitude during systole. Correlations with conventional echocardiographic indices ranged from weak to strong and varied by parameter, region, and cardiac phase, reflecting heterogeneous associations across metrics. These findings indicate that VDI-derived parameters capture complementary aspects of intraventricular flow not fully reflected by conventional measures of cardiac function. Overall, these results establish the reproducibility and physiological relevance of ultrafast VDI and support its potential for longitudinal and translational studies of cardiac flow dynamics.</p>","PeriodicalId":7692,"journal":{"name":"American journal of physiology. Heart and circulatory physiology","volume":" ","pages":""},"PeriodicalIF":3.9,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149057194","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}