Qiang Tu

Background: Acute aortic dissection (AAD) is among the most life‐threatening cardiovascular emergencies. Ambient exposure to fine particulate matter (PM _2.5 ) has been linked with AAD, particularly in urban areas. Yet the associations of key PM _2.5 components with specific AAD subtypes remain insufficiently understood. Methods: We used a time‐stratified case‐crossover design (2015–2023) in Hangzhou, China, investigating associations of major PM _2.5 components with AAD and its Stanford subtypes. Conditional logistic regression and weighted quantile sum models were applied to explore associations of single and joint exposure to PM _2.5 components with AAD, respectively. Stratified analyses based on age, sex, lifestyle factors, and existing comorbidities were performed. Results: At lag 0 to 1 days, black carbon, organic matter, and sulfate were significantly associated with AAD, especially type A, while positive but nonsignificant associations were observed for type B. An interquartile range increase in black carbon, organic matter, and sulfate was associated with a 42% (odds ratio, 1.42 [95% CI, 1.15–1.75]), 35% (odds ratio, 1.35 [95% CI, 1.10–1.64]), and 36% (odds ratio, 1.36 [95% CI, 1.09–1.69]) increased risk of type A AAD, respectively. The weighted quantile sum model revealed significant joint associations of coexposure to major PM _2.5 components with AAD and its type A, with black carbon contributing >50% to the joint associations. Age, smoking, alcohol consumption, and hypertension modified the PM _2.5 components–AAD associations. Conclusions: Precise regulation of ambient PM _2.5 components, particularly black carbon, is necessary to mitigate AAD risk. Tailored clinical management is critical for susceptible populations during high‐pollution periods.

Post-stroke cognitive impairment (PSCI) is a frequent and disabling consequence of stroke that limits long-term recovery and quality of life. Disruption of the hippocampal neurogenic niche may impair adult hippocampal neurogenesis (AHN), while exercise is increasingly recognized as a promising non-pharmacological strategy for cognitive rehabilitation. This review synthesizes evidence that exercise may shift the post-stroke hippocampal niche from a hostile to a permissive state through coordinated regulation of neuroinflammation, neurovascular integrity, and mitochondrial homeostasis. We distinguish increased progenitor proliferation from productive neurogenesis, defined by the survival, maturation, appropriate positioning, and functional integration of newborn neurons. Exercise may attenuate inflammatory signaling, support angiogenesis and blood–brain barrier repair, and improve mitochondrial biogenesis and quality control; however, much of the mechanistic evidence remains preclinical, and increases in early neurogenic markers do not by themselves establish functional neuronal integration or causality. Current clinical evidence supports cognitive benefits of exercise more strongly than it supports AHN as the indispensable mediator of those benefits. A productive-neurogenesis framework therefore provides a more rigorous basis for interpreting existing studies and designing future experiments that combine lineage tracing, temporally controlled neurogenesis ablation, circuit-level analysis, and domain-specific cognitive outcomes.

Background: Depression is a known risk factor for cardiovascular disease (CVD), but the impact of long‐term depressive symptom burden remains unclear. We examined the association between cumulative depression burden and risks of CVD and all‐cause death among adults aged ≥50 years in China and Mexico. Methods: Data were obtained from 2 nationally representative cohorts: CHARLS (China Health and Retirement Longitudinal Study) and MHAS (Mexican Health and Aging Study). Cumulative depression burden was quantified using 2 approaches: (1) the area under the curve of repeated depression scores and (2) the number of waves with depression. Multivariable Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% CIs for incident CVD and all‐cause death. Results: The analysis included 5277 CVD‐free participants from CHARLS and 4779 from MHAS. Higher cumulative depression burden was significantly associated with elevated risk of CVD. Compared with the lowest‐quartile group, participants in the highest‐quartile group had significantly greater CVD risk (CHARLS: HR, 1.723 [95% CI, 1.420–2.090]; MHAS: HR, 1.739 [95% CI, 1.347–2.245]). Dose–response associations were observed in both cohorts. Persistent depression was also linked to higher CVD risk compared with isolated or less frequent episodes. Associations with all‐cause death differed by cohort, with significant associations observed in CHARLS but not in MHAS. Conclusions: Long‐term cumulative depression burden is strongly associated with increased CVD risk among adults aged ≥50 years. Routine screening and sustained management of depressive symptoms should be considered integral to CVD prevention strategies.

BACKGROUND: This trial aimed to test the effectiveness of a data-driven quality improvement program in primary care on cardiovascular hospitalizations, major adverse cardiovascular events (MACE), risk factor profiles, and medication prescriptions at 24 months in people with coronary heart disease (CHD) compared with standard care. METHODS: A single-blind, cluster randomized controlled trial recruiting Australian primary care practices (2019–2022) was conducted. Practices using compliant data extraction software and having ≥200 adult patients annually with CHD were the units of randomization, and adults with CHD (who visited their general practitioner in the past 12 months) were the units of analysis. Practices were randomized to intervention (12-month data-driven quality improvement including benchmarking, monthly reporting, and improvement planning) or control (standard care). The primary outcome was the proportion of participants who had unplanned cardiovascular disease hospitalizations at 24 months. Secondary outcomes were MACE, medication prescriptions, risk factor targets, and management planning. Data were extracted from electronic records linked to administrative data. RESULTS: A total of 51 primary care practices participated, resulting in a patient cohort of 7864. The mean age of the patient cohort was 71.9 (±11.8) years, 68% were men, and 24% had a prior myocardial infarction. At 24 months, there was no significant difference between the groups for unplanned cardiovascular disease hospitalizations (relative risk, 0.91 [95% CI, 0.75–1.10]; MACE, 0.81 [95% CI, 0.61–1.07]; prescription of antiplatelet, 0.94 [95% CI, 0.79–1.13]), statin, 1.03 [95% CI, 0.97–1.09], angiotensin-converting enzyme or angiotensin receptor blocker, 1.00 [95% CI, 0.93–1.07]; risk factor targets for low-density lipoprotein cholesterol, 0.99 [95% CI, 0.86–1.13], systolic blood pressure, 0.97 [95% CI, 0.87–1.09], or smoking, 0.96 [95% CI, 0.57–1.59]; or management planning, 1.02 [95% CI, 0.64–1.63]). CONCLUSIONS: A primary care, data-driven quality improvement program did not improve unplanned hospitalizations, MACE, medication prescriptions, achievement of risk factor targets, or management planning for people with CHD. Robust evidence for the use of a data-driven, collaborative approach to improving care for people with CHD in primary care remains elusive. REGISTRATION: URL: https://www.anzctr.org.au ; Unique identifier: ACTRN12619001790134.

Intrinsic capacity (IC) serves as an integrative measure of biological reserve, and physical activity (PA) is a key modifiable determinant of cardiovascular health. The joint association of IC and PA with incident cardiovascular disease (CVD), and the mediating role of PA, remain unclear across populations. We analyzed 14,823 adults aged ≥ 60 years without baseline CVD from four longitudinal cohorts: CHARLS, ELSA, HRS, and MHAS. IC was assessed across five domains and classified as intact or impaired. PA was categorized as regular or inactive. Cox models estimated hazard ratios (HR) for incident CVD across four groups defined by IC and PA status. Interaction and mediation analyses evaluated combined effects, and random-effects meta-analysis pooled cohort estimates. Both impaired IC and inactivity were independently associated with higher CVD risk. Participants with both impaired IC and inactivity had the highest risk (CHARLS HR: 2.10; ELSA HR: 1.80; HRS HR: 1.62; MHAS HR: 1.68; pooled HR: 1.74, 95% CI: 1.57–1.93). Risk increased with the number of impaired IC domains, and within both PA groups, greater IC impairment was consistently associated with higher CVD risk. Mediation analysis suggested that PA accounted for part of the association between IC and CVD, with larger estimated proportions in ELSA (17.97%) and HRS (15.68%) than in CHARLS (5.29%) and MHAS (2.43%). Impaired IC and physical inactivity were jointly associated with higher CVD risk, with IC impairment consistently associated with elevated risk regardless of PA status. PA appeared to account for part of this association, although the magnitude varied across cohorts. The online version contains supplementary material available at 10.1186/s12877-026-07568-7.

Hypertension frequently co-exists with depression, leading to adverse health outcomes. This study aimed to examine the individual and joint effects of hypertension and depression on the risks of new-onset cardiovascular disease (CVD) and all-cause mortality among the middle-aged and older Chinese individuals. Data from the China Health and Retirement Longitudinal Study (CHARLS) during 2011–2020 were used. Participants were divided into four groups for comparison: hypertension alone, depression alone, both conditions, neither condition. Multivariate logistic regression models were established to compare the risks of all-cause mortality and CVD among the four groups. A total of 9178 participants without pre-existing CVD were included and followed for nine years. Compared with individuals with neither condition, the risk of all-cause mortality increased among individuals with hypertension alone (adjusted odds ratio [aOR]: 1.414, 95% confidence interval [CI]: 1.133–1.764), depression alone (aOR: 1.023, 95% CI: 0.795–1.317) and comorbid hypertension and depression (aOR: 1.524, 95% CI: 1.180–1.968). The aORs for CVD events in individuals with both conditions, hypertension alone, and depression only were 2.207 (95% CI: 1.885–2.584), 1.945 (95% CI: 1.702–2.222) and 1.572 (95% CI: 1.365–1.809), respectively. Furthermore, those with severe depressive symptoms were at higher risks of all-cause mortality and CVD, regardless of having hypertension. Hypertension with comorbid depression leads to higher risks of CVD and all-cause mortality than either condition alone. Screening and management of depression among individuals with hypertension are essential for the primary prevention of CVD and premature death.

Introduction Cardiac rehabilitation is known to reduce morbidity and improve quality of life in people living with heart disease, however, adherence, access and completion of these programmes is suboptimal. Peer support may offer an opportunity to close this service gap. The aim of the study is to determine whether the effectiveness of a digital peer support programme for people living with heart disease is effective in improving social connectedness, clinical and patient-reported outcomes and experience measures. Methods and analysis Heart2Heart is a community-based randomised controlled trial with 6 months follow-up for the primary outcome and 6 and 12 months for secondary outcomes. Approximately 752 adults with a diagnosis of heart disease in the past 12 months will be recruited from the general community and Australian cardiac rehabilitation programmes. Control group will participate in usual care, while intervention group will have access to a 6 months intervention that enables peer support via an interactive mobile application, in addition to usual care. The intervention includes online discussion groups, access to resources and facilitated conversations with health professionals. Primary outcome is social connectedness at 6 months follow-up. Secondary outcomes (6 and 12 months) will be all-cause/cardiovascular disease hospital admissions, all-cause mortality, lifestyle (sufficiently physically active, not smoking, sufficient fruit and vegetable consumption), proportion taking prescribed medications and health service utilisation (medical appointments, cardiac rehabilitation, participation in any other in-person peer support activities). Patient-reported outcome and experience measures including self-efficacy, quality of life, satisfaction and programme engagement will be analysed at 6 months. Process measures will include application analytics, barriers and facilitators to engagement with the intervention from participant’s perspective. An intention-to-treat analysis will be used. Ethics and dissemination Ethical clearance was obtained from Western Sydney Local Health District Ethics Committee. Heart2Heart has potential to improve social connectedness and provide a valuable addition to traditional cardiac rehabilitation. Trial registration number ACTRN12624000386538.

Objective: The study aimed to examine the individual and joint effects of hypertension and diabetes on cardiovascular diseases and all-cause mortality among the middle-aged and older Chinese population. Methods: A total of 9681 individuals without preexisting CVD from the China Health and Retirement Longitudinal Study (CHARLS) were included. Participants were classified into four different groups: hypertension alone, diabetes alone, both conditions, neither condition. Multivariate Cox proportional hazards models were performed to estimate the risks of all-cause mortality and CVD. Results: During the 7-year follow-up, 967 deaths and 1535 CVD events were documented. Compared to individuals without hypertension and diabetes, hypertension alone [adjusted hazard ratio (aHR) 1.571, 95% confidence interval (CI) 1.316–1.875, P < 0.001], diabetes alone (aHR 1.618, 95% CI 1.187–2.205, P < 0.01) and comorbid hypertension and diabetes (aHR 2.041, 95% CI 1.557–2.677, P < 0.001) increased risks of all-cause mortality. The aHRs for CVD events in individuals with both conditions, hypertension alone and diabetes only were 2.011 (95% CI 1.651–2.449, P < 0.001), 1.408 (95% CI 1.233–1.608, P < 0.001) and 1.036 (95% CI 0.808–1.327, P > 0.05), respectively. The risk of CVD among those with comorbid hypertension and diabetes exceeded the sum of the risks due to hypertension and diabetes alone (relative excess risk ratio = 0.567, 95% CI 0.136–0.999). Conclusion: Individuals with comorbid hypertension and diabetes had greater risks of CVD and all-cause mortality, beyond those associated with either condition alone. The synergistic interaction between hypertension and diabetes aggravated the risk of CVD.