Journal of the American Heart Association最新文献

Background: Chronic kidney disease (CKD) is prevalent in patients undergoing percutaneous coronary intervention for chronic total occlusion and is associated with worse outcomes due to impaired renal function. Understanding the outcomes and predictors of adverse events in this population is crucial.

Methods: A retrospective observational study was conducted on patients undergoing chronic total occlusion percutaneous coronary intervention at Houston Methodist DeBakey Heart and Vascular Center (2018-2023). Patients were categorized on the basis of kidney function: CKD (estimated glomerular filtration rate <60 mL/min per 1.73 m²) and non-CKD. The primary end point was procedural success. Secondary end points included 1-year all-cause death; clinically driven target-lesion revascularization at 1 year; target-lesion failure, defined as the composite of heart failure hospitalization, stroke, target-lesion revascularization, and myocardial infarction at 1 year; in-stent restenosis at 1 year, and in-hospital complications.

Results: A total of 492 patients were included, with 176 (35.8%) diagnosed with CKD. Patients with CKD were older and had a higher comorbidity burden. Patients with CKD had more complex disease, with higher rates of multivessel disease and graft vessel stenosis. Procedural success rates were high and similar between the groups (83.0% versus 83.4%). While 1-year all-cause death was comparable, patients with CKD exhibited higher rates of target lesion revascularization (hazard ratio, 2.41 [95% CI, 1.53-3.78]; P<0.001). Procedural complexity was not found as an independent predictor of death or target lesion revascularization.

Conclusions: Although chronic total occlusion percutaneous coronary intervention is associated with higher postprocedural outcomes in patients with CKD, procedural success was comparable between the groups. Further studies are needed to refine postprocedural management strategies.

Background: Understanding the transition from preclinical heart failure to its symptomatic stages, and its associated biomarker and Doppler echocardiographic changes, is crucial for prevention.

Methods: This was a retrospective cohort study using the STOP-HF (St. Vincent's Screening to Prevent Heart Failure) study. Median follow-up was 4.5 (interquartile range [IQR], 4.4-9.8) years. A total of 1425 participants were classified as stage A (at risk) or stage B (asymptomatic structural/functional abnormalities). Serial assessments included BNP (B-type natriuretic peptide), Doppler echocardiography, and cardiologist review. Progression to stage B required significant interval echocardiographic worsening, and regression required significant improvement. BNP levels and patient events between visits were recorded.

Results: At visit 1, 67% (n=959) of individuals were stage A and 33% (n=466) stage B. By visit 2, 22% (n=214) of stage A had progressed to stage B (4.4±0.3 per 100 person-years), while 10% of stage B had progressed to stage C (1.6±0.2 per 100 person-years). Stage A progressors had higher baseline BNP (26.4 [IQR, 12.7-53.2] pg/mL) versus nonprogressors (12.6 [IQR, 6.2-25.1] pg/mL; P<0.001). In stage B, 18% (n=86) regressed to stage A (3.1±0.3 per 100 person-years) with lower baseline BNP (21.6 [IQR, 9.2-52.7] pg/mL) versus progressors to stage C (83 [IQR, 50.7-166] pg/mL) and remainers in stage B (51.1 [IQR, 17.9-85.7] pg/mL) and more favorable Doppler echocardiographic features. Event rates increased with progression and were similar for stage B to stage A regressors and stage A remainers.

Conclusions: Preclinical heart failure exhibits a bidirectional trajectory, with evidence of regression/stability supporting prevention. Incorporating natriuretic peptide screening enhances risk stratification and effectiveness of preventative screening/intervention services.

Background: Clinical studies have shown that aortic arch pulse-wave velocity (PWV_aa), a measure of local aortic stiffness, is a strong independent predictor of subsequent white matter hyperintensity volume and white matter integrity, both associated with cognitive decline, elevated stroke risk, vascular dementia, and neurodegenerative diseases. Total arterial compliance (TAC), a measure of global arterial stiffness, has been recognized as a marker of preclinical vascular disease. This study introduces a smartphone-based method for the noninvasive measurement of PWV_aa and TAC using carotid pressure waveforms acquired via smartphone.

Methods: This method uses intrinsic frequency analysis of smartphone-acquired (iPhone) carotid pressure waveforms to assess PWV_aa and TAC. The method was trained, validated, and blind-tested on a cohort of 132 participants aged 20 to 90 years, including both healthy individuals and those with cardiovascular disease, all of whom underwent cardiac magnetic resonance imaging, tonometry, and iPhone waveform measurements.

Results: In the blind test set, our method achieved Pearson correlations of 0.81 and 0.80 for PWV_aa and TAC, with biases of -0.20 m/s and -0.06 mL/mm Hg and limits of agreement of -4.09 to 3.68 m/s and -0.52 to 0.40 mL/mm Hg, respectively. In the heart failure population, correlations were 0.81 for both, with a PWV_aa a bias of -1.07 m/s and TAC bias of -0.06 mL/mm Hg.

Conclusions: Our smartphone-based method enables accurate assessment of local and global arterial stiffness metrics (PWV_aa and TAC). It offers easy-to-use monitoring of vascular aging and arterial health, with important implications for identifying patients at higher risk of neurodegenerative and cardiovascular diseases.

Registration: URL: clinicaltrials.org; Unique Identifier: NCT02240979.

Background: Aortic dissection (AD) is a severe cardiovascular disease with high mortality and limited treatment options. Previous studies have shown that circular RNA and ferroptosis play significant roles in various cardiovascular diseases, regulating disease progression. However, there is little research on how circular RNA regulates ferroptosis in vascular smooth muscle cells during AD progression, and the specific molecular mechanisms remain a mystery.

Methods and results: In this study, we found that circTMEM71 is downregulated in AD and angiotensin II-induced human aortic smooth muscle cells and inhibits ferroptosis. Mechanistically, circTMEM71 can bind to IGF2BP3 (insulin-like growth factor II mRNA-binding protein 3) and inhibit its degradation via the ubiquitin-mediated proteasome pathway. Additionally, IGF2BP3 can bind to FSP1 (ferroptosis suppressor protein 1) mRNA, enhancing its stability and thus suppressing cellular ferroptosis. Finally, we also confirmed that circTMEM71 can alleviate symptoms of AD in Sprague-Dawley rats through in vivo experiments, including histopathologic changes and ferroptosis.

Conclusions: In summary, our study suggested that circTMEM71 is a potential therapeutic target for AD and highlights its role in inhibiting ferroptosis in vascular smooth muscle cells.

Background: Patients with hypertrophic cardiomyopathy (HCM) were excluded from pivotal trials comparing the efficacy and safety of direct oral anticoagulants (DOACs) and vitamin K antagonists.

Methods: Our retrospective cohort study using the TriNetX database compared adults with HCM-atrial fibrillation who initiated DOACs or vitamin K antagonists. The primary outcomes were all-cause mortality and ischemic stroke/systemic thromboembolism. Secondary outcomes included major bleeding, intracranial hemorrhage, gastrointestinal bleeding, and all-cause hospitalization. Subgroup analysis was conducted for obstructive HCM.

Results: Among 13 143 patients with HCM-atrial fibrillation (2963 matched pairs). DOAC use was associated with lower all-cause mortality (hazard ratio [HR], 0.82[ 95% CI, 0.73-0.93]; P<0.001), major bleeding (HR, 0.85 [95% CI, 0.73-0.99]; P=0.03), and intracranial hemorrhage (HR, 0.54 [95% CI, 0.36-0.79]; P=0.001) compared with vitamin K antagonists. No differences were observed in the rates of ischemic stroke (HR, 0.94 [95% CI, 0.73-1.2]; P=0.6) or the composite of stroke or systemic thromboembolism (HR, 0.87 [95% CI, 0.69-1.10]; P=0.25), gastrointestinal bleeding (HR, 0.97 [95% CI, 0.77-1.22]; P=0.82), or all-cause hospitalizations (HR, 1.07 [95% CI, 0.93-1.07]; P=0.051). In the subgroup with obstructive HCM, DOAC use was associated with a reduced risk of all-cause mortality (HR, 0.80 [95% CI, 0.66-0.99]; P=0.035) and major bleeding (HR, 0.76 [95% CI, 0.61-0.96]; P=0.02) without stroke or thromboembolic risk reduction (HR, 0.69 [95% CI, 0.47-1.01]; P=0.05).

Conclusions: Among patients with HCM-atrial fibrillation, DOACs were associated with lower mortality and bleeding risk compared with vitamin K antagonists, with no increased risk of stroke or systemic thromboembolism.

Background: Ischemic stroke in deep brain regions is commonly attributed to small vessel ischemic disease (SVID) or branch atheromatous disease (BAD). Differentiating these mechanisms is clinically important, as BAD is associated with progressive symptoms, early neurological deterioration, and poorer outcomes, whereas SVID typically follows a more stable course. Conventional imaging is limited in distinguishing these entities. High-resolution vessel wall imaging enables direct visualization of intracranial vessel wall pathology and may refine risk stratification.

Methods: We conducted a prospective, single-center study of patients with acute subcortical infarcts admitted between 2023 and 2025. Eligible patients underwent magnetic resonance imaging with high-resolution vessel wall imaging within 1 week of admission. SVID was defined as lacunar infarction without evidence of parent artery plaque or vessel wall enhancement. BAD was defined as infarction in the territory of a penetrating artery with associated parent artery enhancement. The primary outcome was differentiation of BAD from SVID based on vessel wall enhancement. Secondary outcomes included 90-day functional outcomes.

Results: Of 23 patients enrolled, 10 underwent magnetic resonance imaging with high-resolution vessel wall imaging. Vessel wall enhancement was observed in 5 patients (50%). Patients with enhancement were more often male (100% versus 40%) and had a higher prevalence of hyperlipidemia (100% versus 20%) compared with those without enhancement. Functional outcomes at 90 days were similar between the 2 groups.

Conclusions: High-resolution vessel wall imaging can identify parent artery pathology not evident on conventional imaging, helping to distinguish BAD from SVID. This differentiation is clinically meaningful, as BAD may require more intensive secondary prevention. Larger studies are needed to validate these findings.

Background: Risk assessment of patients with syncope does not consider a short PR interval despite its association with increased risk of atrial fibrillation and all-cause mortality. This study aimed to explore the association between the PR interval and all-cause mortality and recurrent syncope in patients admitted to the hospital with syncope.

Methods: We included patients with a diagnosis of syncope and an ECG recorded within 24 hours of hospital admission from the Danish Nationwide Electrocardiogram Cohort and divided patients into short (<120 ms), normal (120-200 ms), or long PR interval (>200 ms). Patients with ECG abnormalities or comorbidities influencing the PR interval or outcomes were excluded.

Results: A total of 52 038 patients were included. Adjusting for age, sex, and relevant covariates the highest hazard ratio (HR) was observed in patients with short PR interval with an HR of 1.50 (95% CI, 1.24-1.80, P<0.001). A long PR interval did not show an association with all-cause mortality (HR, 1.02 [95% CI, 0.97-1.08], P=0.3566). Adjusted 5-year cumulative incidence of all-cause mortality was 18% for short PR interval, 14% for normal PR interval, and 13% for long PR interval. Regarding recurrent syncope, a HR of 1.14 (95% CI, 1.09-1.20. P<0.001) was seen for long PR interval. Adjusted 5-year cumulative incidence of recurrent syncope was 23% in patients with a long PR interval.

Conclusion: In patients with syncope, a short PR interval was associated with higher risk of all-cause mortality; however, a long PR interval was associated with increased rate of recurrent syncope.

Background: Low-density lipoprotein cholesterol (LDL-C) and remnant cholesterol (RC) are risk factors for atherosclerotic cardiovascular disease (ASCVD). However, the extent to which differences in RC levels affect ASCVD risk in populations with varying degrees of LDL-C elevation remains unclear. This study aimed to investigate whether RC can provide additional risk stratification value across different sexes, ages, and elevated LDL-C statuses.

Methods: This study included 12 743 elevated LDL-C participants (LDL-C ≥3.4 mmol/L) and 50 073 age- and sex-matched non-elevated LDL-C controls from the Kailuan Study. Elevated LDL-C participants were categorized by RC levels into <0.5, 0.5 to <1.0, and ≥1.0 mmol/L subgroups. Kaplan-Meier curves and Cox proportional hazards models were used to assess the relationship between RC levels and ASCVD risk across different sexes, ages, and high LDL-C statuses.

Results: During a median follow-up of 12.8 years, 1686 elevated LDL-C participants (13.2%) and 5252 non-elevated LDL-C participants (10.5%) developed ASCVD. In the borderline-high LDL-C group (3.4 ≤ LDL-C < 4.1 mmol/L), those with the lowest RC levels showed no significant risk difference compared with controls (hazard ratio [HR], 1.03 [95% CI, 0.93-1.13]), and this pattern remained consistent across different sexes and ages. In contrast, in the high LDL-C group (LDL-C ≥4.1 mmol/L), even when RC was at the lowest level, ASCVD risk remained significantly higher than that of controls (HR, 1.20 [95% CI, 1.02-1.41]).

Conclusions: In the borderline-high LDL-C population, those with the lowest RC levels showed no significant risk difference compared with controls, and this pattern remained consistent across different sexes and age subgroups. In the high LDL-C population, even when RC was at the lowest level, ASCVD risk remained significantly higher than that of controls.

Background: Neutrophil extracellular traps are released from activated neutrophils and are involved in the pathogenesis of atherosclerotic lesions, atherothrombosis, and myocardial injury. We investigated the prognostic value of circulating neutrophil extracellular trap biomarkers in patients with suspected acute coronary syndrome (ACS).

Methods: A total of 1482 patients admitted with suspected non-ST-segment elevation ACS were included and followed for a median of 4.2 years. The primary end point was a composite of death from any cause, incident myocardial infarction and hospitalization for heart failure. Secondary end points were all-cause mortality, cardiovascular death, incident myocardial infarction, hospitalization for heart failure, and new-onset atrial fibrillation. Admission blood samples were analyzed for the neutrophil extracellular trap biomarkers double-stranded DNA (dsDNA), CitH3 (citrullinated histone H3), and myeloperoxidase-DNA.

Results: A doubling of dsDNA concentration was associated with a hazard ratio (HR) of 3.11 (95% CI, 1.61-5.98, P<0.001) for the primary end point after adjusting for traditional risk factors, cardiac troponin T and N-terminal pro-B-type natriuretic peptide. DsDNA served as a prognostic marker both in patients with (adjusted HR, 5.33 [95% CI, 1.67-17.06], P=0.005) and without ACS (adjusted HR, 2.86 [95% CI, 1.30-6.28], P=0.009). In contrast, CitH3 and myeloperoxidase-DNA showed no significant prognostic value.

Conclusions: In patients with suspected ACS, dsDNA emerged as a long-term prognostic marker for a composite outcome of death, incident myocardial infarction, or heart failure hospitalization, independent of conventional risk factors. DsDNA can independently from established risk factors identify high-risk patients with and without ACS who may benefit from risk reduction.

Background: Genetic risk scores may be useful for analyzing risks for coronary artery disease (CAD). However, comparisons between restricted and genome-wide scores have been underexplored, particularly for individuals at increased risk by one score but not the other. Here, we compared restricted polygenic risk scores with 181 high-confidence genetic variants (PRS₁₈₁) and genome-wide risk scores that encompass 6.6 million single-nucleotide polymorphisms (GRS_6.6M).

Methods: Data were from the RS (Rotterdam Study; n=11 001), MESA (Multi-Ethnic Study of Atherosclerosis; n=2685), and the Sanford Health study (n=25 166). We analyzed score associations with CAD (prevalent and incident), age at onset, and lipid medication use. Combined use of both scores was also examined.

Results: There were robust associations with CAD per SD of the scores for men (PRS₁₈₁: hazard ratio [HR], 1.19 [95% CI, 1.13-1.26]; GRS_6.6M: HR, 1.32 [95% CI, 1.26-1.39]) and women (PRS₁₈₁: HR, 1.24 [95% CI, 1.16-1.32]; GRS_6.6M: HR, 1.32 [95% CI, 1.25-1.40]). PRS₁₈₁ was more strongly associated with early-onset CAD in men (β=-0.93 [95% CI, -1.36 to -0.50]) and women (β=-0.76 [95% CI, -1.31 to -0.21]). Both scores correlated with lipid medication use, but the scores were also associated with CAD among nonusers. Individuals at high risk by both scores had the highest risk and the earliest age at onset.

Conclusions: PRS₁₈₁ and GRS_6.6M appear to identify different subsets of individuals. Use of both scores together may provide better association information on CAD risk and age at onset than each score alone.