Ischemic heart disease (IHD) remains a leading cause of mortality and disability worldwide. Using Global Burden of Disease (GBD) 2021 estimates, this study provides an integrated assessment of IHD burden across the Middle East and North Africa (MENA) region from 1990 to 2021, highlighting temporal trends, inter-country heterogeneity, sociodemographic index (SDI)-related patterns, and attributable risk factors by sex and age.

We conducted a secondary analysis of GBD 2021 estimates for the 21 countries and territories in MENA. We assessed prevalence, deaths, and disability-adjusted life years (DALYs), reporting counts and age-standardized rates per 100,000 population with 95% uncertainty intervals (UIs). This framework allowed direct comparison of temporal change, cross-country variation, development-related gradients, and modifiable risk attribution within a single regional analysis.

In 2021, the age-standardized prevalence of IHD in MENA was 6404.8 per 100,000 (95% UI: 5872.0-7041.1), with an age-standardized mortality rate of 202.8 (95% UI: 180.6-223.7) and DALY rate of 4023.2 (95% UI: 3581.7-4507.5). Although age-standardized death and DALY rates declined from 1990 to 2021, the burden remained substantial and unevenly distributed. Kuwait had the highest age-standardized prevalence [7806.4 (95% UI: 7141.6-8556.3)] and Turkey the lowest [5365.9 (95% UI: 4895.5-5874.7)]. Saudi Arabia had the largest increase in age-standardized prevalence [17.1% (95% UI: 11.4-23.0)], whereas Turkey had the largest decrease [-11.9% (95% UI: -17.3 to -6.9)]. DALY rates increased progressively with age for both sexes, and IHD burden showed an inverse, non-linear relationship with SDI. The leading contributors to IHD DALYs were elevated systolic blood pressure [49.6%], elevated LDL cholesterol [39.6%], and exposure to ambient particulate matter pollution [28.2%].

Despite reductions in age-standardized mortality and DALY rates, IHD remains a major public health challenge in MENA, with substantial cross-country variation and a large contribution from modifiable risks. By integrating temporal trends, inter-country heterogeneity, SDI-related patterns, and attributable risk factors, this study provides novel evidence for prioritizing prevention efforts across the region. These findings support context-specific prevention strategies prioritizing hypertension control, lipid management, and improved access to cardiovascular prevention and treatment, alongside action to reduce air pollution exposure; implementation should be tailored to national risk profiles, disease trends, and health-system capacity.

Cardiovascular-kidney-metabolic (CKM) Stage 4 is defined by established cardiovascular disease in the setting of kidney and/or metabolic dysfunction. Despite the high risk carried by this condition, simple tools for refining prognosis are limited. The neutrophil-to-lymphocyte ratio (NLR), derived from routine differential blood counts, has been linked to outcomes in cardiovascular, renal, and critically ill populations. Whether it is prognostically informative in critically ill adults with CKM Stage 4 is not established. We investigated the relationship between NLR and all-cause mortality in this population.

Using the Medical Information Mart for Intensive Care IV (MIMIC-IV), we assembled a retrospective cohort of adults who met CKM Stage 4 criteria. For patients with multiple intensive care unit (ICU) admissions, analysis was restricted to the earliest stay. Admission NLR was derived from the first valid paired neutrophil and lymphocyte measurements recorded within 24 h. Patients were classified by NLR quartile. The prespecified primary endpoints were 30-day and 365-day all-cause mortality, with 90-day and 180-day mortality as secondary endpoints. Associations were examined using multivariable Cox regression, restricted cubic splines, subgroup analyses, sensitivity analyses, and mediation analysis.

Among 13,602 eligible patients, mortality rose progressively across NLR quartiles at all assessed time points. After full adjustment, the hazard ratio (HR) for Q4 compared with Q1 was 2.142 (95% confidence interval [CI], 1.858-2.469) for 30-day mortality. The corresponding 365-day HR was 1.708 (95% CI, 1.543-1.891). Associations at 90 and 180 days were similar. Restricted cubic splines indicated nonlinear relationships. Results were generally stable in subgroup and sensitivity analyses. Adding NLR improved established ICU severity scores, and blood urea nitrogen (BUN) partially mediated the observed association.

Admission NLR was independently related to higher all-cause mortality during both short- and long-term follow-up in critically ill adults with CKM Stage 4. Because it is routinely available, NLR may provide complementary information for risk stratification in this population.

Pregnancy is regarded as a crucial window period for the assessment and management of cardiovascular health (CVH). This study investigated the relationship between the gestational CVH metrics of Chinese women and adverse pregnancy outcomes.

Six separate CVH metrics (smoking status, body mass index, blood pressure, total cholesterol, fasting blood glucose, and sleep health) were measured at 24-28 gestational weeks and categorized as ideal (2 points), intermediate (1 point), or poor (0 point) to generate a gestational CVH score. Total gestational CVH was categorized as high (all ideal metrics), moderate (no poor metrics), or low (one or more poor metric). Associations between gestational CVH and adverse pregnancy outcomes were evaluated using Poisson regression.

Among the 2,775 pregnant women included, 36.07%, 36.11%, and 27.82% had high, moderate, and low CVH, respectively. Each one-point increase in the CVH score was significantly associated with 7% and 4% lower risk of adverse maternal and neonatal outcomes (relative risk [RR], 0.93 and 0.96; 95% confidence interval [CI], 0.90-0.95 and 0.93-0.98). Compared with low CVH, high CVH was associated with 21% and 12% lower risk of adverse maternal and neonatal outcomes (RR, 0.79 and 0.88; 95% CI, 0.72-0.87 and 0.80-0.96). Individual CVH metrics also showed associations with adverse pregnancy outcomes, in which ideal body mass index, fasting blood glucose and sleep health were particularly important.

High gestational CVH was significantly associated with a considerably lower risk of adverse pregnancy outcomes, but approximately two-thirds of pregnant Chinese women do not achieve a high level of CVH.

Objective: To understand the potential parent-of-origin effect (POE) of imprinted gene KCNQ1 on the risk for hypertension by using a family-based design. Methods: Probands and their relatives in 9 rural areas in Fangshan District, Beijing, were included in this study. Mixed-effects model was used to evaluate the association between single nucleotide polymorphisms (SNPs) in the KCNQ1 gene and hypertension. The POE effects were evaluated by adopting log-linear model, and the interactions between POE and environmental factors, including smoking, alcohol consumption, were analyzed by using Wald χ² test. The POE was assessed by the ratio of maternal relative risk to paternal relative risk (RR_m/RR_f). Results: A total of 195 SNPs in the KCNQ1 gene were included in the analysis after quality control. The association analysis in 1 261 study participants identified 13 loci in the KCNQ1 gene associated with hypertension (all P<0.05). POE analysis, involving 167 study participants from 54 core families, identified 6 loci that showed possible POE with hypertension (all P<0.05). The most significant locus was rs231879, with an RR_m/RR_f of 3.46 (95%CI: 1.36-8.57, P=0.009), indicating that the relative risk of inheriting the risk allele from mother was 3.46 times higher than that from father. Analysis on the interactions between POE and environmental exposure revealed that sleep duration might potentially modify the POE of rs170786 (interaction for P=0.023). Conclusion: The imprinted gene KCNQ1 might be associated with the risk for hypertension through POE.

Hypertension is a major contributor to cardiovascular morbidity and mortality, largely driven by oxidative stress, mitochondrial dysfunction, endothelial injury, and chronic vascular inflammation. Emerging evidence suggests that targeting vascular bioenergetics may provide complementary therapeutic strategies beyond conventional antihypertensive drugs. This review explores the mitochondrial protective mechanisms of Piper retrofractum and its major bioactive compounds in the context of hypertension and oxidative vascular injury. The phytochemical profile of P. retrofractum, particularly piperine, piplartine, pipernonaline, and retrofractamides, demonstrates significant antioxidant, anti-inflammatory, and metabolic regulatory activities. Mechanistically, these compounds may attenuate mitochondrial reactive oxygen species (mtROS), restore endothelial nitric oxide synthase (eNOS) coupling, activate AMPK-SIRT1-PGC-1α signaling, induce Nrf2-HO-1 antioxidant pathways, and modulate mitochondrial dynamics and mitophagy. Collectively, these effects contribute to improved endothelial function, reduced vascular remodeling, suppression of inflammatory cascades, and enhanced mitochondrial resilience. In addition, emerging omics technologies, network pharmacology, and AI-assisted nutraceutical discovery offer new opportunities to elucidate multitarget mechanisms and optimize P. retrofractum-based interventions. Despite promising preclinical evidence, important limitations remain, including insufficient clinical studies, limited mitochondrial-specific investigations, and challenges related to bioavailability and standardization. Overall, P. retrofractum represents a promising mitochondria-centered nutraceutical candidate for hypertension management and vascular protection, warranting further translational and clinical investigation.

Staphylococcus aureus (S. aureus) is a leading cause of bacteraemia and infective endocarditis worldwide, posing significant public health challenges in resource-limited low- and middle-income countries (LMICs). However, whether specific genomic factors influence the development of S. aureus infective endocarditis (SAIE) during S. aureus bacteraemia (SAB) remains unclear. Thus, the study aimed to determine whether clinical SAIE isolates were genomically distinguishable from SAB isolates originating from public hospitals in Gauteng, South Africa. Seventy-seven (54 SAB, 23 SAIE) bloodstream isolates were characterised to assess antimicrobial susceptibility (VITEK®2 system), biofilm formation (crystal violet assay), virulence genes (multiplex-polymerase chain reactions) and genetic relatedness (pulsed-field gel electrophoresis), while 12 representative isolates underwent whole-genome sequencing. A higher SAIE (29.9%) prevalence than previously reported in South Africa was observed, with cases linked to young male persons who inject drugs (P < 0.01). While the SAB and SAIE groups did not differ in virulence profiles, SAB isolates demonstrated higher resistance rates to gentamicin and clindamycin than SAIE isolates (P < 0.05). The endemic Panton-Valentine leukocidin-positive sequence type (ST) 152, clonal complex (CC) 152 lineage predominated in SAIE isolates, while the pandemic CC8, encompassing ST239 and ST612, was exclusive to SAB isolates. Overall, SAB and SAIE isolates were not clearly distinguished by the markers assessed, suggesting that SAIE development may reflect the combined effects of bacterial traits, host susceptibility and exposure-related risk factors, rather than a distinct SAIE-specific genomic profile. These findings highlight the need for continued genomic surveillance of circulating S. aureus lineages to inform targeted infection-control strategies.

Tachycardia-induced cardiomyopathy secondary to persistent tachycardia in children is a distinct form of cardiomyopathy caused by sustained or frequent tachyarrhythmias. It is characterized by cardiac enlargement, impaired cardiac function, and heart failure and is clinically reversible with early and standardized treatment. Herein, we report a challenging pediatric case presenting with recurrent intermittent dyspnea and palpitations for 1 year. The final diagnoses were as follows: (a) paroxysmal atrial tachycardia and (b) tachycardia-induced cardiomyopathy. Under the guidance of a three-dimensional electroanatomical mapping system, an intracardiac electrophysiological study accurately localized the focal atrial tachycardia to the posterior margin of the right upper pulmonary vein, followed by successful radiofrequency ablation. The patient's clinical symptoms improved significantly postoperatively, and the patient was discharged uneventfully. During the 8-month follow-up period, no recurrence of atrial tachycardia was documented. Follow-up echocardiography confirmed normalization of cardiac dimensions and function.

Myeloperoxidase (MPO), a key enzyme involved in neutrophil extracellular trap formation and other inflammatory processes, has emerged as an attractive therapeutic target for cardiovascular, central nervous system, respiratory, and autoimmune diseases. To date, four irreversible MPO inhibitors have entered clinical trials; however, none have reached the market, highlighting the challenges of MPO drug discovery.

This review provides an overview of MPO biology, its pathological roles in inflammatory diseases, and recent advances in MPO drug discovery. It then systematically summarizes patent literature published between 2020 and 2026, identified through Espacenet, Google Patents, and SciFinder, comprehensively covering the structural optimization and pharmacological characterization of emerging MPO inhibitors, including small molecules, peptides, and antibodies.

Patent analysis indicates that MPO drug discovery remains heavily dependent on legacy thioxanthine/deazathioxanthine scaffolds. Current efforts are primarily focused on overcoming historical liabilities through improving target selectivity and pharmacokinetic properties. In parallel, non-thioxanthine chemotypes are emerging, although most still exhibit suboptimal potency and therefore require further optimization. The development of dual- or multi-target MPO inhibitors may represent a promising strategy for addressing complex inflammatory networks.

Chronic kidney disease (CKD) represents a significant public health problem. Patients with CKD have high morbidity and mortality, mainly due to cardiovascular diseases. As CKD progresses, impaired renal clearance leads to the progressive accumulation of uremic toxins, culminating in deleterious effects on multiple organ systems. Uremic toxins contribute to cardiovascular disease by inducing inflammation, oxidative stress, and endothelial barrier dysfunction, thereby promoting atherosclerotic processes. They are also potentially implicated in neurological impairment, bone disorders, and sarcopenia. Some uremic toxins originate from dietary components and gut microbiota metabolism, which are key mechanisms and pathways in uremic toxicity. Current dialysis therapies only partially mitigate uremic toxicity, highlighting the need for strategies that reduce uremic toxin generation as well as more efficient dialysis modalities. Given the importance of uremic toxins in CKD progression, this review provides a comprehensive overview of uremic toxicity, focusing on its pathophysiological mechanisms, its relationship with the gut microbiota, and emerging interventions to mitigate its deleterious effects.