Journal of the American Heart Association最新文献

Background: Periodontitis is a chronic inflammatory condition with infectious origin that affects the tissues supporting the teeth. Increasing epidemiological evidence suggests that periodontitis is a risk factor for ischemic stroke with associated adverse outcomes. However, the underlying mechanism of this association remains incompletely elucidated.

Methods: We used a C57BL/6J mice model of ischemic stroke induced by transitory occlusion of the middle cerebral artery in the presence or absence of ligature-induced periodontitis using Porphyromonas gingivalis-soaked ligatures. Stroke severity was evaluated through infarct volume, sensorimotor deficit, blood-brain barrier (BBB) integrity, and markers of systemic and brain inflammation. The direct effect of P gingivalis on BBB endothelial cells was further explored in vitro.

Results: Mice with P gingivalis-associated periodontitis showed a significant exacerbation of stroke severity: larger infarct volume, more severe sensorimotor deficit, greater BBB disruption, and increased brain neutrophil infiltration compared with sham. Systemic inflammation was also markedly elevated. Intravenous administration of P gingivalis alone, without gingival injury, before transitory occlusion of the middle cerebral artery was sufficient to amplify brain inflammation and stroke lesions. In vitro P gingivalis, through its gingipain proteases, directly impaired BBB integrity by increasing endothelial permeability and disrupting tight-junction proteins.

Conclusions: Our findings demonstrate that P gingivalis-associated periodontitis worsens ischemic stroke outcome both indirectly by enhancing systemic and brain inflammation and directly via BBB disruption. These results highlight periodontitis as a modifiable risk factor and potential therapeutic target for improving stroke prognosis.

Background: Smartwatches are increasingly used for screening of tachyarrhythmias and for ECG recording. We therefore investigated possible mechanisms of magnet-mode induction of smartwatches in cardiac implantable electronic devices (CIED).

Methods: Fifteen CIED (5 pacemakers, 10 implantable cardioverter-defibrillators) from all manufacturers were implanted in a subcutaneous and submuscular location in an isolated porcine thorax and connected to an interactive heart simulator. Eight different smartwatches (3 Apple, 3 Samsung, 1 Huawei, 1 Withings) were placed on top of the implantation site in 3 different configurations, and signs of magnet mode induction were recorded.

Results: When the faces of smartwatches were placed on top of subcutaneously implanted CIED, only 1 instance of magnet mode induction was recorded in 120 measurements (<1%). When turning around the smartwatches and placing the backs on the implantation site, signs of magnet mode were recorded in 36 of 120 measured instances (30%). Smartwatches connected to respective chargers induced magnet mode in 28 of 120 measurements (23%). Magnet mode induction in submuscularly implanted CIED was seen in 5 of 360 measurements (1%). The smartwatch with physical charging connectors was the only one not to induce magnet mode in any CIED, resulting from a lower-than-average magnetic field strength likely due to its different charging mechanism.

Conclusions: ECG-capable smartwatches can induce magnet mode in CIED. Although the risk for patients wearing smartwatches on their wrist is low, patients should be discouraged from placing their watch close to their CIED. Smartwatch charging mechanism and CIED implantation depth influence the risk of magnet mode induction.

Background: Social determinants of health, including neighborhood deprivation measured by the Area Deprivation Index, are key drivers of disparities in health outcomes, including survival after cardiac surgery. We evaluated whether the association between neighborhood deprivation and survival differs across racial and ethnic groups undergoing coronary artery bypass grafting.

Methods: We conducted a retrospective study of 739 335 Medicare beneficiaries who underwent isolated coronary artery bypass grafting between 2008 and 2019. A flexible parametric survival model with time-dependent effects was implemented to estimate standardized (over demographics, clinical, and procedural characteristics) survival probabilities. Primary end points were differences in 30-day and 5-year standardized survival probabilities between beneficiaries from the lowest and highest quintiles of neighborhood deprivation (LDNs and HDNs), stratified by race and ethnicity.

Results: Unadjusted median survival was substantially higher among beneficiaries in LDNs compared with HDNs (10.65 [95% CI, 10.55-10.76] versus 9.20 [95% CI, 9.14-9.27] years). In our risk-adjusted model, the magnitude of this difference varied significantly by race and ethnicity. At 30 days, standardized survival differences between LDNs and HDNs were 1.49% [95% CI, 0.45-2.53] among Asian American or Native Hawaiian/Pacific Islander, 1.06% [95% CI, 0.94-1.19] among White, 0.94% [95% CI,0.583-1.31] among Black, and 0.56% [95% CI, 0.25-0.91] among Hispanic beneficiaries. At 5 years, Asian American or Native Hawaiian/Pacific Islander and White beneficiaries showed the largest standardized survival differences between LDNs and HDNs (8.07% [95% CI, 5.37-10.77] and 5.01% [95% CI, 4.62 -5.39], respectively), whereas Black and Hispanic beneficiaries had smaller differences (2.00% [95% CI, 0.71-3.28] and 1.15% [95% CI, 0.05-2.26], respectively).

Conclusions: Although LDN (compared with HDN) residence was associated with improved survival after coronary artery bypass grafting, these survival differences were not equally distributed across race and ethnicity. Policies aiming to reduce socioeconomic disadvantage may yield uneven outcomes unless tailored to the specific challenges faced by different racial and ethnic populations.

Background: Black Americans have greater coronary heart disease (CHD) burden than White Americans, disparities that are largely socially determined. Discriminatory societal practices that systematically disadvantage Black Americans are forms of structural racism but few studies have examined structural racism and incident CHD. We sought to determine associations between 3 validated measures of structural racism and incident CHD, hypothesizing that greater state-level structural racism is associated with incident CHD for Black but not White individuals.

Methods: We used data from the national REGARDS (Reasons for Geographic and Racial Differences in Stroke) cohort, which enrolled 30 239 Black and White community-dwelling adults between 2003 and 2007 who were contacted every 6 months with retrieval of medical records and expert adjudication of myocardial infarction and cause of death. Incident CHD was defined as myocardial infarction or death due to CHD. Structural racism variables included Black:White percentage living below the federal poverty line, Black:White percentage uninsured, and the Dissimilarity Index (DI), a measure of residential racial segregation. Structural racism variables were dichotomized at the median. Separate race-stratified Cox proportional hazards models examined associations between each measure of structural racism and incident CHD.

Results: The 24 533 participants free of CHD at baseline included 10 402 Black and 14 131 White participants. Mean age at baseline was 64 years, 59% were women, and 47% had an annual household income <$35 000. High DI was significantly associated with incident CHD and fatal CHD but not nonfatal CHD for Black but not White participants. High Black:White percentage poverty and high Black:White percentage uninsured were not significantly associated with any outcome. For fatal CHD, the hazard ratios (HRs) for high Black:White poverty were 1.19 (95% CI, 0.95-1.48) for Black participants and 0.92 (95% CI, 0.75-1.14) for White participants. For high Black:White uninsurance, the HRs were 1.16 (95% CI, 0.89-1.50) for Black participants and 1.00 (95% CI, 0.77-1.30) for White participants. For high DI, the HRs were 1.35 (95% CI, 1.08-1.68) for Black participants and 1.13 (95% CI, 0.92-1.40) for White participants. Results were similar for men and women and for older and younger individuals.

Conclusions: Racial residential segregation but not other structural factors were associated with higher incidence of fatal CHD for Black but not White individuals. If these associations are causal, changing or enforcing state level laws to reduce residential racial segregation could potentially lessen Black:White disparities in CHD.

Background: Guideline-directed medical therapy (GDMT) improves outcomes in heart failure with reduced ejection fraction, yet its adoption across Asia remains suboptimal. The American Heart Association launched the GWTG-HF A.S.I.A. (Get With The Guidelines-Heart Failure Adherence to Science, Implementation in Asia) program in 2021. We examined the association between program participation and GDMT implementation in Taiwan.

Methods: We analyzed 1991 patients with heart failure with reduced ejection fraction enrolled in the Taiwan Society of Cardiology HF Registry (2021-2024). Four hospitals participated in the GWTG-HF A.S.I.A. program (n=462) and 23 nonparticipating hospitals served as controls (n=1529). After propensity-score matching, prescription trends of 4-pillar GDMTs were compared using generalized estimating equations. Primary outcomes were patient-level and hospital-level GDMT prescription rates; secondary outcomes included echocardiographic remodeling, loss to follow-up, and 2-year mortality.

Results: Between 2021 and 2024, GDMT use increased in both groups, with greater gains in participating hospitals. Adjusted odds ratios (aOR) for program participation were 2.73 (95% CI, 2.23-3.34) for 4-pillar GDMTs, 1.59 (95% CI, 1.31-1.92) for angiotensin receptor-neprilysin inhibitors, 2.06 (95% CI, 1.72-2.47) for SGLT2 (sodium-glucose co-transporter 2) inhibitors, and 1.63 (95% CI, 1.34-2.00) for mineralocorticoid receptor antagonists (all P<0.001). After SGLT2 inhibitor reimbursement in 2022, the prescription gap widened. Participating hospitals showed greater left-ventricular reverse remodeling and lower loss-to-follow-up (0.5% versus 5.2%, P<0.001), and 2-year mortality was similar.

Conclusions: Participation in the GWTG-HF A.S.I.A. program was associated with higher GDMT prescription rates in Taiwanese hospitals. Structured quality improvement initiatives may help bridge the evidence-practice gap in Asia.

Background: Plasma biomarkers may aid Alzheimer disease (AD) diagnosis and prognosis. Cardiovascular risk contributes to cognitive decline in AD, but whether it modifies the relationship between plasma biomarkers and cognitive status has not been assessed in a large multisite cohort. We aimed to explore if cardiovascular risk moderates plasma AD biomarkers' relationship with cognitive status.

Methods: We included cognitively normal (n=301) participants and participants with mild cognitive impairment or probable AD (n=444) from the Bio-Hermes-001 study. Cardiovascular risk was quantified using the Atherosclerotic Cardiovascular Disease risk calculator. Logistic regression analyzed associations of cardiovascular risk and plasma biomarkers (amyloid beta 42/amyloid beta 40, phosphorylated tau [p-tau]181, p-tau217, apoE4 [apolipoprotein E]) with cognitive status. Moderation by cardiovascular risk was tested in each model.

Results: We included 745 participants (mean age=72.3 years; 423 [56.8%] female). Plasma biomarkers and cardiovascular risk were independently associated with cognitive status across models; the strongest association was with p-tau217 (odds ratio [OR], 2.33 [95% CI, 1.89-2.9]; P<0.001). Cardiovascular risk moderated only the relationships of p-tau181 and p-tau217 with cognitive status (P<0.05).

Conclusions: Plasma AD biomarkers and cardiovascular risk were independently associated with cognitive status, with cardiovascular risk moderating the p-tau181 and p-tau217 cognitive status relationships. If certain plasma biomarkers and cardiovascular risk independently contribute to dementia risk, cardiovascular risk assessment should complement other biomarker evaluations in cognitive screening. Results should be interpreted with caution as associations might be primarily driven by age and sex. Future research including education and genetic risk is needed to clarify the studied relationships.

Background: Hematoma expansion (HE) is a significant risk factor for poor prognosis in patients with intracerebral hemorrhage (ICH). Accurately predicting HE is crucial for determining optimal treatment strategies.

Methods: This study enrolled 452 patients with ICH from 10 hospitals. To predict HE, 28 clinical variables available on patient arrival (including medical history, ICH location, and ICH volume) and 1142 radiomics features extracted from noncontrast computed tomography images of the ICH regions were used. Clinical variables and radiomics features were selected using gradient boosting and the least absolute shrinkage and selection operator. Three HE prediction models were built on clinical variables alone, radiomics features alone, and a third combining both. The models were compared using 5-fold cross-validation, and the mean area under the receiver operating characteristic curve was calculated for each. Additionally, the important features of HE prediction in the combined model were explored.

Results: The combined model demonstrated the highest performance for predicting HE with a 5-fold mean area under the receiver operating characteristic curve of 0.77±0.05, compared with 0.70±0.06 for the clinical variables alone and 0.73±0.04 for the radiomics features alone. Permutation feature importance analysis suggested that anticoagulant treatment was the most predictive of HE.

Conclusions: A predictive model for HE was developed using the medical history, clinical features available on the patient's arrival, imaging, and radiomics features extracted from computed tomography images. This prediction model will assist non-stroke care specialists in making treatment decisions for ICH in emergency settings.

Background: Subclinical atrial fibrillation (SCAF) poses an increased stroke risk, but whether oral anticoagulation for SCAF prevents stroke is unclear. We sought to investigate the treatment effect of SCAF screening according to measures of cardiac structure and function.

Methods: This was an echocardiographic substudy of the LOOP (Atrial Fibrillation Detected by Continuous ECG Monitoring) study, which randomized older people at risk of stroke to usual care or an implantable loop recorder (ILR) with monitoring for SCAF and subsequent oral anticoagulation. A subset (24% of trial population) underwent echocardiography to measure left ventricular size and function, left atrial volume and strain, and valvular pathology. The primary outcome was a composite of stroke or systemic embolism.

Results: The study included 1422 participants (ILR: n=1001; control: n=421; mean age: 74 years; men: 54%). During follow-up, 354 (25%) were diagnosed with AF (ILR versus control: 30% versus 12%). During a median follow-up of 5.5 years (interquartile range, 4.9-5.9 years), 55 (4%) developed the primary outcome (ILR versus control: 3.9% versus 3.8%). No conventional measure of cardiac structure and function modified the treatment effect from randomization. However, left atrial contraction strain significantly modified the treatment effect (Pinteraction=0.003), such that a lower risk of the primary outcome was noted from ILR with lower left atrial contraction strain values (hazard ratio [HR], 0.38 [95% CI, 0.16-0.87], for participants with contraction strain<16.5%).

Conclusion: In a post hoc analysis of the LOOP study, conventional echocardiographic measures did not modify the effect of SCAF screening for stroke prevention. However, a significant stroke risk reduction was observed from ILR randomization among participants with reduced left atrial contraction strain.

Pediatric hemorrhagic stroke can lead to significant neurologic, cognitive, and behavioral morbidities that often emerge over time and can impede long-term academic, vocational, and socioemotional function. While many of the existing data stem from studies in arterial ischemic stroke, functional outcomes in hemorrhagic stroke, and particularly pediatric intracerebral hemorrhage, remain largely understudied. Extrapolating findings from ischemic stroke can be challenging, as there are notable differences in care and potentially in outcomes for hemorrhagic stroke. The primary goal of this consensus statement by a multidisciplinary group of stroke experts is to provide a review of the current literature on neurologic, cognitive, behavioral, and socioemotional outcomes after hemorrhagic stroke. Neurologically, children with pediatric intracerebral hemorrhage often experience motor deficits, including hemiparesis and coordination issues, as well as cognitive impairments affecting attention, memory, and executive function. Behavioral and emotional problems, such as depression, and social difficulties can also occur. Data on academic attainment are also presented, along with considerations regarding long-term outcomes and the transition to adulthood. We further examine a variety of key determinants predicting outcomes, including medical, demographic, familial, and socioeconomic factors, as well as current research on rehabilitation, with an emphasis on gold-standard guidelines for clinical interventions. Given the complexity of outcome measurement in pediatric hemorrhagic stroke and the lack of uniform tools for assessing outcomes across diverse populations, we propose guiding principles for outcome measurement, along with examples of domain-specific tools. Finally, we discuss the limitations of the current literature and outline goals for future clinical practice and research.