搜索结果：Trends in cardiovascular medicine

Australia has previously experienced adverse trends in overweight- and obesity-related cardiovascular disease (CVD) mortality. Its obesity prevalence is relatively high, increasing and shows wide socio-economic inequalities. However, socio-economic inequalities in premature overweight- and obesity-related CVD mortality rate and their trends are unknown. This study measures recent trends in premature overweight- and obesity-related CVD mortality in Australia from 2007 to 2022 and their area-level socio-economic inequalities. Premature overweight- and obesity-related CVD mortality was measured as deaths at ages 35-74 years with a CVD reported with at least one (DKOLH-CVD) or two (DKOLH2-CVD) of diabetes, chronic kidney disease, obesity, lipidemias and hypertension. Age-standardised death rates (ASDR) from Australian death registration data were calculated. Inequalities were measured using the Index of Relative Socio-economic Advantage and Disadvantage (IRSAD) and analysed using rate ratios and the Relative Index of Inequality. Obesity prevalence data and their inequalities were also assessed using National Health Survey data. Premature overweight- and obesity-related CVD mortality, measured as the DKOLH-CVD ASDR, rose from 87.0 (95% confidence interval 84.6-89.5) per 100,000 in 2014 to 103.8 (101.1-106.5) in 2022 for males, or 19%, and from 44.6 (42.9-46.4) in 2013 to 50.5 (48.7-52.4) in 2022 for females, or 13%. When measured as DKOLH2-CVD ASDR, it increased by 37% for males and 21% for females from 2012 to 2022. DKOLH-CVD in ages 35-54 years rose by at least 45% from 2014 to 2022; average obesity prevalence since childhood or young adulthood of these age groups increased by approximately 50% from 2007 to 2022. The ratio of the male DKOLH-CVD ASDR of the most disadvantaged to the most advantaged IRSAD decile increased from 3.16 (2.93-3.41) in 2013-2015 to 3.51 (3.27-3.77) in 2020-2022 and for females from 4.55 (4.08-5.08) to 5.00 (4.51-5.54). Rate ratios were particularly high for DKOLH2-CVD and in ages 35-54 years. Similar socio-economic inequalities were found according to obesity prevalence. The recent rise in premature overweight- and obesity-related CVD mortality in Australia, especially among those aged 35-54 years and in the most disadvantaged socio-economic deciles, closely mirrors Australia's increasing obesity prevalence. Failure to effectively tackle Australia's high obesity prevalence may have a significant detrimental long-term impact on mortality.

High-sensitivity C-reactive protein (hsCRP) is gaining recognition as an important prognostic biomarker in cardiovascular diseases (CVDs), including atherosclerotic CVD (ASCVD), with and without chronic kidney disease (CKD), and heart failure (HF). Evidence suggests that systemic inflammation, measured by hsCRP, is prevalent in individuals with ASCVD, CKD, and HF, and is linked to increased risk of cardiovascular events. This review explores the interconnectedness of ASCVD, CKD, and HF within the cardiovascular-kidney-metabolic axis, with systemic inflammation emerging as a common underlying driver. Prevalence estimates show that systemic inflammation (hsCRP ≥ 2 mg/L) is found in 38% to 59% of patients with ASCVD, in 42% to 65% of those with both ASCVD and CKD, and in over 50% in various HF cohorts. Elevated levels of hsCRP are consistently associated with higher rates of major adverse cardiovascular events and mortality across these populations. Although hsCRP is frequently found to carry prognostic value independent of traditional biomarkers such as low-density lipoprotein cholesterol, its clinical adoption in practice is held back in part by guideline variability, lack of standardized cutoffs, and debate over how results may change clinical management with currently available therapies. The review calls for further research to define optimal hsCRP thresholds, examines the role of hsCRP in cardiovascular risk assessment, and reviews the ongoing development programs for emerging anti-inflammatory therapies. Addressing systemic inflammation could become a cornerstone of CVD management, potentially reducing residual risk beyond traditional targets.

Racial disparities in valvular heart disease are well-documented, yet evidence specific to mitral regurgitation (MR) remains fragmented. This study examined racial differences in mortality and treatment access among patients with moderate-severe MR within a universal healthcare system. This retrospective cohort study utilised digital health records from a South London tertiary centre using natural language processing (NLP), including demographic, clinical, echocardiographic and socioeconomic data. Adult patients with moderate or greater MR diagnosed between 2010 and 2023 were stratified by ethnicity (White, Black, Asian). Primary outcomes were all-cause mortality and surgical/transcatheter intervention rates. Multivariable Cox regression and competing risk analyses adjusted for demographics, MR characteristics, comorbidities and socioeconomic deprivation. The cohort (n=6665) comprised 5331 (80.0%) White, 958 (14.4%) Black and 376 (5.6%) Asian patients with under-represented minority proportions relative to local demographics. Black patients presented younger (65.4 vs 72.2 years; p <0.001) with greater socio-economic deprivation (median IMD decile 3 vs 5), higher comorbidity burden and predominantly secondary MR (91% vs 85%; p <0.001). Crude mortality rates were 103.8, 88.1 and 80.4 per 1000 person-years for White, Black and Asian patients respectively. After adjustment, ethnicity was not independently associated with mortality (Black vs White: HR 0.90; 95%&#x2009;CI 0.80 to 1.00; p=0.06) or intervention (OR 0.81; 95%&#x2009;CI 0.59 to 1.11; p=0.18). Socioeconomic deprivation was independently associated with mortality (HR 0.97/IMD decile increase; p <0.001) and intervention rates. Crude intervention rates were lower in Black than in White patients (6.9% vs 12.7%), this difference attenuated after adjustment for MR aetiology, comorbidities and socioeconomic deprivation and did not persist as an independent association (OR 0.81; 95%&#x2009;CI 0.59 to 1.11; p=0.18). MR appears under-detected among minority patients relative to local demographics and occurs at a younger age and with a greater prevalence of secondary MR and comorbidity. Once identified, clinical factors and socioeconomic deprivation rather than ethnicity itself drive outcomes and treatment access, with no statistically independent association between ethnicity and either mortality or intervention, although modest but clinically relevant differences cannot be excluded given the cohort sizes. These findings highlight the need for enhanced valve disease detection in diverse communities alongside strategies addressing socioeconomic determinants of cardiovascular health.

Social disconnection, both in the form of social isolation and loneliness, is increasingly recognized as a clinically significant but underappreciated risk factor for cardiovascular disease (CVD), affecting 16-25% of individuals. Population studies have consistently linked social disconnection to a higher risk of all-cause mortality, myocardial infarction, stroke, and cardiovascular death, yet routine screening for social disconnection is uncommon in everyday clinical practice. Even when identified, due to both lack of strong evidence-based interventions and awareness about them, meaningful clinical changes are seldom observed. In light of growing recognition by major health authorities, including the World Health Organization and the U.S. Surgeon General, and of the Harvard Study of Adult Development, showing that social integration and strong relationships are the most powerful predictors of healthy aging, we conducted a narrative literature review synthesizing current evidence on the relationship between social disconnection and CVD. The mechanism mediating social disconnection and cardiovascular events is still a matter of debate. We focus on cortisol-oxytocin imbalance and highlight that it is central in causing CVD through autonomic dysregulation, nutritional imbalance and gut microbiome alterations. Alongside psychosocial comorbidities, these factors may converge on endothelial dysfunction as an initiating mechanism of CVD. Our review also aims to foster discussion on how to recognize and address social disconnection in clinical practice, emphasizing the need for structured, multidisciplinary pathways as well as trials assessing their effect on improving both social disconnection and the associated CVD risk.

Pacemaker implantation rates are increasing worldwide, raising concerns about pacing-induced cardiomyopathy a complication of chronic right ventricular pacing (RVP). Pacing-induced cardiomyopathy results in adverse remodeling leading to left ventricular dysfunction and heart failure. pacing-induced cardiomyopathy treatment includes cardiac resynchronization therapy (CRT) and cardiac physiologic pacing upgrades, while preventative strategies include de novo implantation of CRT or cardiac physiologic pacing. Identification of patients who may be suitable for de novo CRT/cardiac physiologic pacing due to high risk for developing pacing-induced cardiomyopathy remains challenging, in part due to limited assessment of patient characteristics. A narrative review of pertinent literature was conducted to examine the definitions, pathophysiology, prevalence, risk factors, novel screening tools, and treatment options for pacing-induced cardiomyopathy in adult populations. Accurate assessment of pacing-induced cardiomyopathy prevalence is limited by center-to-center variability, as well as a variety of lead implantation sites and pacing options. Effective risk stratification, facilitated by a thorough collection and analysis of notable risk factors for pacing-induced cardiomyopathy, can help identify patients that may benefit from early use of cardiac physiologic pacing or CRT to prevent pathologic remodeling.

Parkinson's disease (PD) is a synucleinopathy best known for its motor symptoms, but emerging research shows it also impacts the cardiovascular system. In this paper, we explore the association between PD and cardiovascular disease (CVD), reviewing six key categories: cardiac dysautonomia, coronary artery disease, arrhythmias, cardiomyopathy, heart valve disease, and heart failure. We also discuss risk factors, epidemiology, and overlapping pathophysiology. Cardiac dysautonomia is the most frequently reported cardiovascular issue in PD and includes orthostatic hypotension, postprandial hypotension, supine hypertension, and nocturnal non-dipping blood pressure. PD also appears to be positively associated with coronary artery disease. Early-stage PD is linked to atrial fibrillation, but overall, there is no consistent increase in arrhythmias outside of certain PD medications. Structural and functional cardiac changes such as left ventricular hypertrophy and diastolic dysfunction have also been reported in PD, which may predispose to heart failure and cardiomyopathy. Dopamine agonists pergolide and cabergoline are associated with valve regurgitation, but this seems to be drug-related rather than caused by PD. Shared risk factors like aging, male sex, diabetes, and inflammation help explain the PD-CVD connection. However, some CVD risk factors like high LDL and smoking are associated with lower PD risk. Autonomic dysfunction, impaired lipid and glucose metabolism, and chronic inflammation may all contribute to disease overlap. Our review consolidates existing research to highlight the importance of recognizing cardiovascular manifestations in PD, which may present before motor symptoms. This has important implications for earlier diagnosis, better screening, and more effective management of PD.

As cannabis use accelerates globally with expanding legalization and availability of high-potency formulations, concerns regarding its cardiovascular safety have grown. However, the evidence remains unclear and often inconsistent. This narrative review aimed to summarize the current evidence on the cardiovascular effects of cannabis. We performed a narrative review of peer-reviewed studies on cannabis and cardiovascular outcomes, searching PubMed and Google Scholar for relevant human research published 2014-August 2025. Included evidence encompassed observational cohorts, randomized trials, meta-analyses, Mendelian randomization studies, and mechanistic investigations, supplemented by reference screening. Observational studies reveal mixed associations between THC use and myocardial infarction, stroke, and MACE, with many findings attenuated after adjustment for confounders. A stronger and more consistent association exists for atrial arrhythmias. Evidence for venous thromboembolism remains inconsistent. Interpretation of the available evidence is also hindered by exposure misclassification (e.g., dose, route, frequency), reliance on administrative coding, insufficient differentiation between medical and recreational use, residual confounding (e.g., tobacco, other substances), and limited translational data. Cannabis use is rising, and while mechanistic data suggest THC-related autonomic, endothelial, and platelet effects, overall cardiovascular evidence remains mixed with the most consistent signal seen for atrial arrhythmias. Risk appears influenced by dose, route, and co-use of substances, and current studies are limited by heterogeneity and exposure misclassification. Until higher-quality data emerge, clinicians should adopt a precautionary, harm-reduction approach, especially in patients with cardiovascular comorbidities.

Postoperative atrial fibrillation (POAF) is a common complication that can affect up to 20-44% of patients undergoing cardiac surgery. Evidence suggests that atrial fibrosis is a key factor in the development of POAF due to the disruption of the myocardial electric properties. This systematic review examines the correlation between pre-existing atrial fibrosis and the development of POAF after cardiac surgery. A systematic literature search was conducted in MEDLINE, Embase, and Google Scholar (2000 to March 2025) to identify studies that conducted comparative analysis of atrial fibrosis levels between those who did and did not develop POAF, using histological assessment methods. Extracted data, included study characteristics, histopathological staining methods and analysis findings, fibrosis quantification methods, and overall POAF incidence. Thirteen studies met the inclusion criteria, resulting in a total of 1222 patients, primarily undergoing coronary artery bypass surgery. The incidence of POAF ranged from 14%-42.4% (median 31.6%). In more than half of the studies (7/13), patients who developed POAF demonstrated statistically significant higher degrees of atrial fibrosis compared to those that remained in sinus rhythm postoperatively (four exhibited p < 0.001). Of the eight studies that conducted multivariate analyses, three identified atrial fibrosis as an independent POAF predictor. High heterogeneity precluded pooling of results into a meta-analysis. The current evidence examining the link between pre-existing atrial fibrosis and the development of POAF is restricted by methodological heterogeneity and inconsistent findings. Further efforts to standardize fibrosis quantification methods and POAF definitions are warranted before histopathological assessments can reliably inform POAF risk before cardiac surgery.

Background: Gastric cancer (GC) remains a major global health burden, yet US trends often obscure disparities hidden within national averages. Although incidence and mortality have declined overall, profound geographic, racial, and socioeconomic differences persist. Few studies have systematically examined how demographic composition and social determinants jointly shape GC burden across states. Methods: We analyzed Global Burden of Disease 2021 estimates for GC incidence, mortality, and disability-adjusted life years (DALYs) from 1990 to 2021 across 50 US states and the District of Columbia. Outcomes were stratified by age, sex, race/ethnicity, and sociodemographic index. Multivariable and mediation models assessed how income and education modified racial and ethnic disparities. Results: While national GC rates declined over three decades, the burden remained concentrated in states with large immigrant and low-income populations, including Hawaii, the District of Columbia, Mississippi, and New Mexico. States with higher Asian populations exhibited roughly fourfold greater incidence than those with larger Hispanic populations. Income and education together mediated 22%-31% of racial and ethnic disparities, demonstrating that socioeconomic position-not race alone-drives much of the observed heterogeneity. Conclusions: This state-level sociodemographic analysis reveals the structural underpinnings of US GC inequities within a broader global context of uneven early-life risk and population diversity. By linking racial composition, income, and education to disease burden, it identifies modifiable pathways for prevention and policy action. Viewed as a case study for migrant-receiving countries, these findings underscore the importance of equity-informed strategies-such as Helicobacter pylori screening, nutrition interventions, and targeted resource allocation-to address persistent GC disparities globally.

The COVID-19 pandemic disrupted healthcare systems, daily routines, and socioeconomic conditions, potentially increasing systolic blood pressure (SBP) at the population level. Understanding long-term SBP trends is critical to inform hypertension management and address pandemic-exacerbated disparities. We performed a retrospective study using interrupted time series analyses of&#xa0;electronic medical records from the Montefiore Health System (January 2017-August 2024). Adults with in-person outpatient visits were included in the primary analysis of comparing SBP trends post-onset of pandemic to pre-pandemic. Secondary analyses stratified by age, sex, race/ethnicity, and neighborhood-level socioeconomic indicators. Among 789,897 patients with 8,207,177 outpatient SBP measurements (55.0 &#xb1; 18.4 years old; 66.5% female), SBP increased by 1.69&#x2009;mmHg (95% CI, 1.59-1.78; P&#x2009;<&#x2009;0.001), and did not return to pre-pandemic levels until 16 months later. Racial/ethnic minorities experienced larger pandemic-related SBP increases (P&#x2009;<&#x2009;0.05). Patients from lower socioeconomic neighborhoods had greater SBP increases than residents of higher socioeconomic neighborhoods (P&#x2009;<&#x2009;0.05). The COVID-19 pandemic was associated with sustained population-level increases in SBP, disproportionately affecting racial/ethnic minorities and lower socioeconomic groups. These findings highlight the need for targeted interventions to mitigate long-term cardiovascular risks and reduce exacerbated health disparities.

Late presentation in ST-segment elevation myocardial infarction (STEMI) remains common and clinically challenging, as the duration of myocardial ischemia has traditionally been considered the main determinant of infarct size. However, the conventional 12-hour cut-off, derived from fibrinolytic-era evidence, no longer fully reflects contemporary understanding of ischemia pathophysiology, advances in percutaneous coronary intervention (PCI), and the ability to assess residual myocardial viability. The optimal management of late-presenting STEMI therefore remains debated, as reflected by divergent international guideline recommendations and the heterogeneity of available randomized clinical trials. While early studies failed to demonstrate a clear benefit of late reperfusion, more recent observational and imaging-based data suggest that selected patients may still experience myocardial salvage and improved outcomes even when revascularization is performed beyond traditional temporal thresholds. Collectively, these observations indicate that time from symptom onset represents an imprecise surrogate of myocardial infarct evolution. Focusing exclusively on symptom duration oversimplifies a complex pathophysiological process and risks denying reperfusion to patients who may still derive meaningful benefit. This state-of-the-art review critically appraises current evidence on late-presenting STEMI and proposes a physiology- and imaging-guided framework that integrates clinical presentation, electrocardiographic dynamics, biomarker kinetics, and cardiac imaging to support biologically informed decision-making beyond rigid time-based cut-off.

Artificial intelligence (AI) offers new opportunities in cardio-oncology for early detection, risk stratification, and personalized management of cardiovascular complications in cancer patients. By leveraging data from electronic health records, blood biomarkers, imaging tests such as echocardiography, electrocardiograms, and wearables, AI models can facilitate prediction, detection and response to treatment of cardiovascular disease entities, pre-existing and developing as a consequence of cancer therapy. Specific to the latter, referred to as cardiotoxicity, widespread adoption has been hindered by the limited availability of large datasets for model training, insufficient external validation, and challenges in integrating AI tools into routine clinical workflows. Future progress will depend on advancements in AI technologies, rigorous multi-center validation, development of explainable models, and seamless integration into clinical practice. Barriers, not only from a systems perspective, but also from a provider and most importantly from a patient perspective will need to be addressed for successful implementation. With a broad multidisciplinary perspective and patient focus, AI can advance cardio-oncology care and improve outcomes for patients with cancer.

Stretch-Induced Syncope is an uncommon form of situational syncope triggered by stretching upper-back, neck, and shoulder muscles. A review of 133 publications in PubMed, Embase, Scopus, Web of Science, Scielo, and Google Scholar, using search terms such as "stretch syncope," "syncope with stretch," and "stretch-induced syncope," identified 12 studies describing 30 patient cases (ages 5-26). Stretch-induced syncope episodes were triggered by neck hyperextension and upper-back stretching, producing brief loss of consciousness. Early reports attributed these events to vertebral artery compression or carotid baroreceptor stimulation. However, recent data from simulated stretch testing demonstrate a pronounced vasodepressor response with diminished compensatory tachycardia compared to the heart rate increment during an active standing maneuver in the same patient; these findings are best accounted for by a neural reflex-mediated mechanism rather than mechanical vascular obstruction. Diagnosis is best achieved through careful history taking in the clinic and symptom reproduction with simultaneous video-EEG and beat-by-beat blood pressure monitoring during autonomic testing. No pharmacologic therapy has proven effective; patient education and avoidance of provoking maneuvers remain the mainstays of management. Greater awareness of stretch-induced syncope may prevent misdiagnosis, reduce unnecessary testing, and guide future investigation into the autonomic mechanisms of this reflex.

With over 5 million attributed deaths per year, physical inactivity is a major global public health issue. Although the importance of physical activity is well recognized within the scope of obesity and cardiometabolic disease prevention and control, its broader benefits for the health of individuals and societies are yet to be fully harnessed. Furthermore, the role of active leisure, active transport and active labor-primary domains of physical activity-in supporting or hindering social and health equity has been largely overlooked. Here we (1) used a health equity lens to describe global domain-specific physical activity inequalities through an analysis of World Health Organization STEPwise approach to NCD risk factor surveillance (WHO STEPS) data from 68 countries; (2) summarized evidence linking physical activity with health outcomes beyond cardiometabolic disease, including immunity and infectious disease, depression and cancer; and (3) developed a new model reconceptualizing physical activity to better respond to 21st-century public health challenges. Our global, intersectional analysis of gender and socioeconomic physical activity inequalities revealed a 40-percentage-point gap in active leisure-the only domain consistently driven by choice-between historically privileged groups (wealthy men in high-income countries) and historically disadvantaged ones (poor women in low-income countries). Robust evidence supports the benefits of physical activity for immunity and infectious disease, depression and cancer. Our reconceptualized model recognizes the influence of social identities, norms, policies and structures on physical activity for health and wellbeing and emphasizes the urgent need to develop and roll out policies and programs that disseminate and harness the full benefits of physical activity for human, societal and planetary health.

Arrhythmogenic cardiomyopathy (ACM) is a genetically determined myocardial disease characterized by myocyte loss, fibro-fatty replacement, and electrical instability. In a subset of patients, episodes of chest pain with troponin release and electrocardiographic abnormalities occur in the absence of ischemic causes. These events, commonly referred to as "hot phases" (HP), often mimic acute myocarditis and raise important diagnostic and prognostic considerations. Among ACM-related genes, desmoplakin (DSP) variants are most frequently associated with HP, although episodes have also been observed in carriers of genes not classically associated with this presentation. Evidence suggests that HP presentation may vary across genotypes and ACM phenotypes, with DSP carriers more often exhibiting left sided or biventricular involvement. Growing data indicate that inflammation, autoimmunity, and innate immune activation play a central role in HP expression and ACM pathobiology, supported by findings of myocardial inflammatory infiltrates, circulating anti-desmosomal and anti-intercalated disc autoantibodies, and activation of NLRP3-inflammasome pathways. These mechanisms may contribute to disease progression and arrhythmic vulnerability. Therapeutic strategies remain empirical, but recent observations suggest that immunosuppressive therapy may modulate arrhythmic and heart-failure outcomes in DSP carriers. This review summarizes current knowledge on the clinical, genetic and immunologic features of HP in ACM, and discusses how these findings may refine the diagnostic approach and clinical interpretation of myocarditis-like presentations.

Pharmacological and electrical cardioversion of atrial fibrillation (AF) is associated with markedly increased (>10-fold) risk of thromboembolic events clustering within 7 days following sinus rhythm restoration. Current evidence indicates that post-cardioversion thrombus formation from atrial stunning, rather than preexisting thrombus, causes most thromboembolic complications. Risk factors include traditional CHA2DS2-VASc components (particularly heart failure), AF duration &#x2265;12 h, mitral valve stenosis, cardiac amyloidosis and hypertrophic cardiomyopathy. While placebo-controlled randomized trials are lacking, there is overwhelming observational evidence that oral anticoagulation (OAC) reduces post-cardioversion thromboembolism by 60-80 % to a residual risk of approximately 0.5 %. This benefit seems independent of CHA2DS2-VASc and AF duration (including <48 h). Current guidelines recommend OAC for &#x2265;3 weeks before and &#x2265;4 weeks after cardioversion, or to rule out intracardiac thrombus by imaging, with OAC immediately before cardioversion and for &#x2265;4 weeks. The safety of this strategy was validated in large prospective trials. However, alternative durations of pre-/post-cardioversion OAC have never been tested in randomized trials. The optimal duration of pre-cardioversion OAC remains unclear. Shorter pre-cardioversion delay is associated with increased success of cardioversion, reduced AF recurrence, reduced severity and duration of atrial stunning, and possibly reduced thromboembolic complications. Likewise, antiarrhythmic drug (AAD) pre-treatment improves cardioversion outcomes but is sometimes withheld by fear of early sinus rhythm restoration and associated thromboembolic risk. Randomized data from the ACUTE trial have shown that early AAD introduction was safe. Given the short-lived but dramatic increase in thromboembolic risk post-cardioversion, intensifying OAC immediately before cardioversion might further reduce risk, as suggested by observational studies.

Atrial fibrillation (AF) increases the risk of stroke and cognitive decline. While anticoagulation with vitamin K antagonists (VKAs) and direct oral anticoagulants (DOACs) prevents stroke, their role in reducing dementia risk in patients with AF remains unclear. To evaluate the effect of anticoagulation therapy on dementia incidence in patients with AF, comparing DOACs versus VKAs. We systematically reviewed PubMed, Scopus, Web of Science, Embase, and Cochrane. Systematic reviews and meta-analyses evaluating the effects of anticoagulation therapies on dementia were included. A total of 11 systematic reviews and meta-analyses were included in this umbrella review. Findings from 6 systematic reviews showed that OAC use was associated with a reduced risk of incident dementia in patients with AF, with effect estimates (RR/HR) ranging from 0.46 [0.28-0.78] to 0.79 [0.67-0.93]. For DOACs versus VKAs, most studies found a lower risk of dementia with DOACs, with effect sizes ranging from HR: 0.51 [0.37-0.71] to RR: 0.88 [0.82-0.94]. However, two studies found no significant difference between DOACs and warfarin in dementia risk (OR: 0.65 [0.34-1.25] and RR: 0.91 [0.75-1.12], respectively). Anticoagulation therapy, particularly with DOACs, may help reduce the risk of dementia in AF patients. The evidence remains of moderate to low certainty, and further high-quality, long-term randomized controlled trials are needed to confirm these findings and explore the neuroprotective mechanisms of OACs.

Plastics serve multiple functions in an industrialized society, including major applications in all aspects of healthcare such as single use syringes, coatings and implantable devices. Plastics break down into smaller particles called microplastics (MP; diameter smaller than five millimeters) and nanoplastics (NP; diameter smaller than one micrometer), which are resistant to degradation. Recent evidence suggest that the smallest of these particles may accumulate in the human body throughout multiple organ systems. There has been particular interest on the effects of MP and NP accumulation in the cardiovascular system. In this review, we will discuss MP/NP formation, describe the clinical evidence supporting cardiovascular effects of these particles, with also a discussion on the possible molecular mechanisms behind these interactions. Finally, we will discuss the major knowledge gaps and current controversies involving MP and NP research as they relate to cardiovascular disease. Current evidence linking MP/NPs to cardiovascular disease remains largely correlative, with limited mechanistic validation.

The 2025 European Society of Cardiology (ESC) guidelines and the 2024-2025 American College of Cardiology (ACC) consensus documents redefine the management of myocarditis and pericarditis, with notable convergence, yet key differences. Both emphasize early, accurate diagnosis, particularly through cardiac magnetic resonance (CMR), which now often supersedes immediate biopsy in stable, uncomplicated cases of acute myocarditis. The ESC introduces a unified "inflammatory myopericardial syndrome" (IMPS) framework encompassing myocarditis, pericarditis, and overlap syndromes, while the ACC provides separate pathways, including a novel four-stage clinical classification of myocarditis. Therapeutically, both endorse non-steroidal anti-inflammatory drugs (NSAIDs) and colchicine for pericarditis and myopericarditis, and heart failure-directed therapy for myocarditis, while reserving immunosuppression for select cases. Importantly, interleukin-1 (IL-1) blockade has emerged as a pivotal therapy in recurrent pericarditis, receiving a Class I recommendation in ESC guidelines and strong endorsement in ACC guidance. Prognostic assessment focuses on identifying high-risk features and structured follow-up with imaging and biomarkers. Divergences in terminology, staging, and diagnostic thresholds underscore opportunities for further harmonization. The ESC and ACC documents align in a patient-tailored, evidence-informed approach to management.