Journal of the American Heart Association最新文献

Background: Limited data are available comparing clinical outcomes between patients with small and large annuli following transcatheter aortic valve replacement using balloon-expandable valves. This study sought to investigate 5-year clinical outcomes in patients with severe aortic stenosis with a small annulus compared with those with a large annulus following transcatheter aortic valve replacement with newer-generation balloon-expandable valves.

Methods: A total of 3182 patients with aortic stenosis treated with balloon-expandable valves were divided into small-annulus (≤430 mm²) and large-annulus (>430 mm²) groups. A 1:1 propensity-matched analysis was performed to adjust baseline differences. The primary end point was all-cause death at 5-year follow-up. Secondary end points included heart failure hospitalization, bioprosthetic valve failure, and aortic valve reintervention.

Results: Among 533 matched pairs, compared with the large-annulus group, the small-annulus group had higher rates of aortic valve mean gradients ≥20 mm Hg (14.1% versus 2.9%; P<0.001) and severe prosthesis-patient mismatch (9.8% versus 5.2%; P=0.019). At 5 years, there were no significant differences in all-cause death (hazard ratio, 0.75 [95% CI, 0.52-1.09]; P=0.13). The incidence of heart failure rehospitalization, bioprosthetic valve failure, and aortic valve reintervention were similar between groups. Both groups achieved similar sustained improvements in New York Heart Association functional class and Kansas City Cardiomyopathy Questionnaire-Overall Summary scores.

Conclusions: Despite higher transvalvular gradients and a greater rate of severe prosthesis-patient mismatch, 5-year clinical outcomes in patients with a small annulus were comparable to those with a large annulus following transcatheter aortic valve replacement using newer-generation balloon-expandable valves.

Background: Novel risk factors for stroke, such as occupation, are increasingly under exploration. We investigate if specific occupational exposures and settings increase the risk of developing small-vessel disease (SVD), including SVD-related strokes.

Methods: We performed a systematic review on stroke-occupation associations and then analyzed data from patients presenting to Lothian stroke services with mild ischemic stroke (modified Rankin Scale score ≤2). We performed magnetic resonance imaging and inquired about occupational status. We assessed relationships between high-risk occupations (per Control to Substances Hazardous to Health guidelines) and standard occupational classifications (per Standard Occupational Classifications criteria) against white matter hyperintensity volumes, SVD score, and stroke subtype.

Results: Our systematic review identified 37 papers assessing occupations/broad occupational classifications (n=13), psychosocial work-related factors (n=11), and occupational exposure to hazardous substances (n=13). We then analyzed data from 414 participants and found, after adjustment for age, hypercholesterolemia, socioeconomic status, years of education, hypertension, diabetes, and smoking history, that high-risk occupations were associated with higher SVD scores (odds ratio, 1.64 [95% CI, 1.07-2.54]; n=357; P=0.02) but not for lacunar stroke subtype (odds ratio, 1.03 [95% CI, 0.64-1.67]; n=358; P=0.90) or white matter hyperintensity volume (% intracranial volume) (β=-0.003 [95% CI, -0.015 to 0.008]; n=357; P=0.60). Examples of high-risk occupations include drivers, engineers, and skilled trade workers. No associations were found for standard occupational classifications.

Conclusions: This systematic review shows limited data on stroke-occupation associations. Our analysis showed that high-risk occupations are associated with higher SVD scores but not stroke subtype.

Registration: URL: www.crd.york.ac.uk/PROSPERO; Unique Identifier: 42024466671.

Complex bidirectional interactions between the nervous and cardiovascular systems are integrated through the heart-brain axis, a physiological pathway that governs both neural regulation of cardiovascular function and cardiovascular influences on brain health. Emerging evidence indicates that even in the absence of overt disease, subclinical changes in the heart, aortic arch, and extracranial arteries contribute to brain injury and cognitive vulnerability. This review synthesizes current knowledge on how subclinical heart-brain axis dysfunction affects brain structure and function, highlighting the roles of central and autonomic neural pathways as well as hormonal signaling in driving neurological decline. Key biomarkers linked to silent brain injury, cognitive decline, and dementia are discussed, emphasizing their potential for early risk stratification and as targets for preventive interventions. We also outline mechanistic pathways connecting subclinical heart-brain axis dysfunction to adverse brain outcomes, identify major gaps in current evidence, and propose priorities for future research and clinical trials aimed at early detection and risk reduction to preserve brain health.

Background: Inadequate self-care is reported among people with heart failure (HF), contributing to poor prognosis. Nurse-led HF self-care interventions underpinned by the Common-Sense Model of Self-Regulation may promote behavior change and improve health outcomes; however, their effectiveness has yet to be established.

Methods: A randomized controlled trial was conducted at a hospital in China from March to August 2023. Patients with HF were randomly assigned to either the intervention or control group (N=69 per group). Participants in the intervention group received a 6-week, nurse-led Common-Sense Model of Self-Regulation-based HF self-care program in addition to usual care, whereas the control group received only usual care. The primary outcomes were illness perceptions and self-care behaviors and secondary outcomes included self-care self-efficacy, health-related quality of life, depression, anxiety, symptom burden, sleep quality, health care service use, and mortality. Data were collected at baseline, 6 weeks (T1), and 3 months (T2) after enrollment. Intervention effects were estimated using generalized estimating equations or the Mann-Whitney U test.

Results: Of the 138 participants, 97 (70.3%) were male, and the mean±SD age was 63.95 (11.91) years. Participants in the intervention group revealed significant improvements in illness perceptions, self-care behaviors, self-care self-efficacy, health-related quality of life, depression, symptom burden, and sleep quality compared with the control group at T1 and T2. The intervention group also demonstrated a significant reduction in the number of HF-related unscheduled outpatient department visits at T2.

Conclusions: This care model was effective in promoting behavior change and improving health outcomes among patients with HF during vulnerable phases of the condition.

Registration: URL: https://www.chictr.org; Unique Identifier: ChiCTR2300067270.

Background: Intracranial arteriosclerosis (large- and small-vessel disease) is considered a risk factor for major neurological disorders, such as stroke, cognitive impairment, and dementia. While most studies investigating intracranial arteriosclerosis include individuals from industrialized populations, the prevalence and clinical meaning of intracranial vascular calcifications in populations with a subsistence lifestyle is unknown.

Methods: In this population-based study evaluating data collected between 2017 and 2019 from Tsimane and Moseten people, 2 indigenous populations of forager-horticulturalists living in the Bolivian Amazon, we used computed tomography to determine the prevalence of vascular calcifications in the intracranial internal carotid arteries, vertebral arteries, and lenticulostriate arteries within the basal ganglia, and their association with demographic characteristics, brain atrophy, cognitive performance, and clinical factors.

Results: Our analysis included 1232 individuals who underwent a head computed tomography scan. Intracranial vascular calcifications were found in most individuals (>90%) and their prevalence was higher than that reported for age-equivalent industrialized populations. These calcifications were significantly associated with higher age, brain atrophy, worse cognitive performance, and parkinsonian symptoms.

Conclusions: Despite the physically active subsistence lifestyle and the low rates of typical cardiovascular risk factors and coronary artery disease, intracranial vascular calcifications are common in these Bolivian Amerindian people, suggesting that alternative factors may contribute to intracranial arteriosclerosis and a novel dementia phenotype.

Background: This study evaluated the long-term outcomes of asplenia syndrome with single ventricle palliation, hypothesizing that total anomalous pulmonary vein connection (TAPVC), pulmonary atresia (PA), and greater than or equal to moderate atrioventricular valve regurgitation increase mortality risk.

Methods: This retrospective review analyzed 151 patients with asplenia syndrome who underwent single ventricle palliation between 1990 and 2024. The primary end point was mortality, with risk factors assessed by Cox regression analysis over a mean follow-up of 9.3 years.

Results: The median age at initial operation was 35 days, including 70 neonates (46%). Overall, 62 (41%) patients died, whereas 66 (44%) patients are alive post-Fontan completion. Survival probabilities at 1 and 20 years were 75.7% (95% CI, 67.9-81.8) and 53.7% (95% CI, 44.5-62.0), respectively. TAPVC (P=0.014), PA (P=0.007), and greater than or equal to moderate atrioventricular valve regurgitation (P=0.040) emerged as independent risk factors for mortality in the overall cohort. In the TAPVC cohort, independent risk factors for mortality included PA (P=0.019), infracardiac TAPVC (P=0.045), and neonatal TAPVC repair (P=0.018). When stratified by the risk factors of TAPVC, PA, or greater than or equal to moderate atrioventricular valve regurgitation, survival probabilities did not differ between patients with none or 1 of these conditions (P=0.181) but were significantly lower in those with ≥2 risk factors (P<0.001, at 15 years: 0, 72.9%; 1, 59.1%; ≥2, 32.8%).

Conclusions: Survival after single ventricle palliation for asplenia syndrome remains suboptimal, particularly when TAPVC, PA, and greater than or equal to moderate atrioventricular valve regurgitation are present in combination rather than in isolation. Improved strategies or surgical techniques are required for this complex asplenia syndrome cohort.

Background: Historical data indicate men develop coronary heart disease (CHD) 10 years before women. However, whether this sex gap persists in a contemporary sample amid changing cardiometabolic risk profiles, and whether differences exist for other cardiovascular disease (CVD) subtypes (ie, stroke, heart failure), is not known.

Methods: Data are from the CARDIA (Coronary Artery Risk Development in Young Adults) study, a prospective multicenter cohort study. US adults aged 18 to 30 years enrolled in 1985 to 1986 and were followed through August 2020. Sex differences in the cumulative incidence functions of premature CVD (onset <65 years), overall and for each subtype (CHD, heart failure, stroke), were compared using Gray's test.

Results: Among 5112 participants (54.5% female, 51.6% Black) with a mean age of 24.8 years (SD: 3.7) at enrollment and a median follow-up of 34.1 years (interquartile range, 33.8-35.7), men had a significantly higher cumulative incidence of CVD, CHD, and heart failure (P<0.05 for all), with no difference in stroke (P=0.63). Men reached 5% incidence of CVD 7.0 years earlier than women (50.5 versus 57.5 years, P<0.001). CHD was the most frequent CVD subtype, and men reached 2% incidence 10.1 years earlier than women (P<0.001). Men and women reached 2% stroke and 1% heart failure incidence at similar ages. Ten-year CVD event rates diverged at an index age of 35.

Conclusions: Men developed CVD earlier than women, with the greatest difference observed for CHD. Sex differences in CVD risk emerged at age 35, persisted through midlife, and were not attenuated by accounting for cardiovascular health.

Background: Effective cardiovascular disease (CVD) risk management is essential for optimal diabetes care. Here, we estimated the prevalence and determinants of CVD risk factor control among individuals with diagnosed diabetes in Mexico.

Methods: We analyzed data from individuals ≥20 years with diagnosed diabetes from 2016 to 2023 Mexican National Health and Nutrition Surveys. We estimated the prevalence of glycemic, blood pressure, noncurrent smoking, low-density lipoprotein cholesterol, and combined CVD risk factor control. We estimated use of blood pressure-lowering, cholesterol-lowering, and glucose-lowering medication and explored determinants of control achievement using logistic regression.

Results: We analyzed data from 2916 participants, representing 43.2 million adults with diagnosed diabetes during 2016 to 2023. In 2023, glycemic control was 29% (95% CI, 21%-38%), blood pressure control 22.9% (95% CI, 14%-31%), and noncurrent smoking 89% (95% CI, 81%-96%). The prevalence of high or very-high CVD risk using Systematic Coronary Risk Evaluation 2-Diabetes increased from 59.8% (95% CI, 52.1%-67.0%) in 2016 to 68.4% (95% CI, 55.6%-78.9%) in 2023, representing ~5.1 million adults. Low-density lipoprotein cholesterol control increased from 2.8% (95% CI, 1.2%-4.4%) in 2016 to 6.6% (95% CI, 1.9%-11.2%) in 2023 and statin use from 5.5% in 2016 to 63% in 2023. Combined risk factor control achievement was low due to suboptimal low-density lipoprotein cholesterol control and was more likely achieved in women, younger individuals, and those with college education or living in states with higher socioeconomic position.

Conclusions: Despite increasing CVD risk during this period, glycemic and CVD risk factor management for adults with diabetes in Mexico remains suboptimal. Our findings suggest a need for strategies to improve CVD risk management to reduce diabetes-related mortality and complications.

Background: Lipoprotein(a) (Lp(a)) is a highly atherogenic lipoprotein and the target of investigational therapies. Using a Mendelian randomization study design, we aimed to clarify associations between genetically predicted Lp(a) levels and cerebrovascular disease outcomes and related phenotypes.

Methods: We obtained genetic associations with Lp(a) levels (n=343 681), ischemic stroke subtypes (≤62 100 cases), intracranial hemorrhage subtypes (≤15 400 cases), and 12 related cerebrovascular phenotypes. Lp(a) was proxied using 2 LPA genetic variants (rs10455872 and rs3798220) that explain 36% of the variance in Lp(a) levels. We performed Mendelian randomization analyses to estimate the association of a genetically predicted 100 nmol/L increase in Lp(a) levels on each outcome.

Results: Genetically predicted Lp(a) levels associated with significantly increased risk of all-cause ischemic stroke (odds ratio [OR], 1.04 [95% CI, 1.02-1.07], P=2.05×10^-4) and large artery atherosclerotic stroke (OR, 1.23 [95% CI, 1.14-1.33], P=3.54×10^-7). There was a nominal association with cardioembolic stroke (OR, 1.07 [95% CI, 1.01-1.13], P=0.02), and no evidence for association with small vessel stroke (OR, 0.98 [95% CI, 0.91-1.06], P=0.60). Associations with early-onset stroke were similar, though with a greater magnitude of association for large artery atherosclerotic stroke (OR, 1.37 [95% CI, 1.15-1.64], P=5.58×10^-4). Analyses of secondary outcomes paralleled these findings, including significant associations of genetically predicted Lp(a) with carotid plaque and atrial fibrillation, nominal associations with lobar hemorrhage and autopsy-confirmed microinfarcts, and null associations with cerebral small vessel disease phenotypes.

Conclusions: Elevated Lp(a) is primarily associated with ischemic stroke due to large artery atherosclerosis, while showing no link to cerebral small vessel disease. These findings support prioritization of patients with atherosclerotic cerebrovascular disease in Lp(a)-lowering stroke prevention trials.

Background: Mitral annular calcification (MAC) is common and associated with increased cardiovascular risk and, when severe, mitral stenosis (MS). MAC-related MS differs anatomically and hemodynamically from rheumatic MS (RMS), challenging standard diagnostic methods. This study compares structural and flow characteristics, including  kinetic energy losses, across MAC-related MS, RMS, and normal mitral valves, and evaluates the applicability of conventional diagnostic metrics in MAC.

Methods: Three-dimensional transesophageal echocardiographic data sets from 70 patients (22 normal mitral valves, 26 RMS valves, 22 MAC valves) were used to obtain linear, area, and volumetric measurements for valve comparison. Representative valves from each group were converted into 3-dimensional silicone models for in vitro testing in a heart flow simulator. Transmitral flow was assessed with particle image velocimetry, flow energetics were quantified, and coefficients of contraction were derived from geometric and effective orifice areas.

Results: Compared with RMS, MAC-related MS had smaller anteroposterior dimensions, reduced valve volume, and lower coefficients of contraction. MAC demonstrated the highest transmitral velocities and energy dissipation in vitro. Unlike the normal model, neither MAC nor RMS produced a consistent transmitral vortex ring. Despite having a larger geometric orifice, MAC MS produced a greater pressure drop than RMS, likely due to increased flow disruption and lower coefficients of contraction.

Conclusions: MAC-related MS represents a unique pathophysiological entity, characterized by distinct structural and hemodynamic features. These findings underscore the necessity for disease-specific diagnostic frameworks and multimodality imaging strategies to inform clinical decision making and guide emerging therapeutic approaches.