Heart failure is a risk factor for adverse events such as sudden cardiac arrest, liver and kidney failure and death. The gut microbiota and its metabolites are directly linked to the pathogenesis of heart failure. As emerging studies have increased in the literature on the role of specific gut microbiota metabolites in heart failure development, this review highlights and summarizes the current evidence and underlying mechanisms associated with the pathogenesis of heart failure. We found that gut microbiota-derived metabolites such as short chain fatty acids, bile acids, branched-chain amino acids, tryptophan and indole derivatives as well as trimethylamine-derived metabolite, trimethylamine N-oxide, play critical roles in promoting heart failure through various mechanisms. Mainly, they modulate complex signaling pathways such as nuclear factor kappa-light-chain-enhancer of activated B cells, Bcl-2 interacting protein 3, NLR Family Pyrin Domain Containing inflammasome, and Protein kinase RNA-like endoplasmic reticulum kinase. We have also highlighted the beneficial role of other gut metabolites in heart failure and other cardiovascular and metabolic diseases.

Hypertensive heart disease (HHD) is characterized by pressure overload-induced cardiac remodeling, in which mitochondrial dysfunction has emerged as a central contributor to pathophysiology. Mitochondria occupy roughly one-third of the volume of a cardiomyocyte and serve as the primary source of ATP for the constantly active heart, while also regulating calcium homeostasis, redox balance, and apoptotic signaling. Chronic hypertension imposes energetic and oxidative stress on cardiomyocytes, disrupting mitochondrial structure and function. Key mitochondrial quality control processes including organelle fusion–fission dynamics, biogenesis, and mitophagy become dysregulated in HHD, leading to impaired energy production and heightened cell injury. This unstructured review discusses the physiological roles of mitochondria in cardiac muscle and examines how altered mitochondrial dynamics contribute to hypertensive cardiac damage. We detail mechanisms of mitochondrial dysfunction in HHD, such as excessive fission, cristae disruption, and oxidative stress, and how these changes are exacerbated by aging. Age-related mitochondrial remodeling such as loss of cristae and decreased organelle volume may synergistically worsen hypertensive cardiac injury. We further integrate findings from recent studies in animal and human models, including advanced three-dimensional ultrastructural analyses and molecular investigations that illuminate new aspects of mitochondrial network organization, the mitochondrial contact site and cristae organizing system (MICOS), cristae maintenance complex, and quality control pathways in HHD. Understanding mitochondrial dysfunction in HHD reveals potential therapeutic avenues targeting mitochondrial quality and dynamics to preserve cardiac function in hypertension.

Background: Hypertension has in the recent past surfaced as one of the conditions that has a significant impact on workforce productivity in emerging economies. Zambia is no different and has in the recent past recorded increasing cases. Despite the impact of hypertension being of great importance in regards to productivity, we have scarcity of data and studies on hypertension-related Productivity-Adjusted Life-Years (PALYs) in Zambia and Africa at large. This study assessed the impact of hypertension on PALYs lost and socioeconomic factors associated with nonadherence to antihypertensive medication (NATAM). Methods: This was a cross-sectional study of 198 participants from Livingstone University Teaching Hospital and Maramba Clinic situated in Livingstone, Zambia. Structured questionnaires were used to collect data. Productivity index multiplied by years lived was used to calculate PALYs and descriptive statistics were used to summarize sociodemographic, clinical and economic variables. Multivariable logistic regression was used to determine factors associated with NATAM. Results: The participants had a median age (interquartile range (IQR)) of 49 years (41, 59) and 60.1% (n = 119) were females while 39.9% (n = 79) were male. Our estimated PALYs lost per person due to hypertension were 0.2 (IQR 0.0, 2.7). Cumulative PALYs value lost due to the burden of hypertension was estimated to be at $871,239.58 in gross domestic product (GDP). The prevalence of NATAM was 48% (n = 95). The factors that were significantly associated with NATAM were age (odds ratio (OR) 0.94; 95% confidence interval (CI) 0.90, 0.98), female sex (OR 2.52; 95%CI 1.18, 5.40), self-employment (OR 2.57; 95%CI 1.02, 6.45) and absenteeism from work (OR 3.60; 95%CI 1.16, 11.22). Conclusions: Findings in our study highlight a high economic loss of PALYs due to hypertension with a potential to impact GDP negatively. We also found that NATAM reduced productivity and income among individuals of working age further impacting PALYs lost due to hypertension. The factors associated with NATAM were age, sex, employment status and absenteeism from work. This study underscores the need for interventions targeting young people, females, self-employed individuals, and absentees at work to improve adherence to antihypertensive drugs in order to reduce PALYs lost due to hypertension.

Hypertension remains a significant global public health challenge affecting billions of adults and remains a risk factor for adverse cardiovascular outcome

Background: The inflammatory pathophysiology of hypertension involves interactions between innate and adaptive immune pathways. While interleukin‐6 (IL‐6) and tumor necrosis factor‐alpha (TNF‐α) have established roles, the contributions of specific T cell–derived cytokines, especially interferon‐γ (IFN‐γ), interleukin‐17A (IL‐17A), and interleukin‐1 (IL‐1), remain less defined in age‐stratified human populations. The aging immune system undergoes characteristic shifts that may differentially engage these pathways in regulating blood pressure, with this immune senescence being notably accelerated in people living with HIV (PLWH). Therefore, this study aimed to investigate age‐stratified associations between key cytokines and systolic blood pressure (SBP) and to determine how these relationships interact with metabolic factors in both PLWH and non‐PLWH. Methods: We conducted a cross‐sectional analysis of 332 adults, stratified into two age groups: < 45 years ( n = 121) and ≥ 45 years ( n = 211). Of the participants, 241 were living with HIV (PLWH) and 91 were HIV‐negative. Multiple linear regression models, adjusted for demographics, HIV status, LDL cholesterol, and smoking, assessed associations between SBP and plasma levels of IFN‐γ, IL‐17A, IL‐6, IL‐1, and TNF‐α. Analyses were performed separately for each age group. In secondary analysis, we evaluated the cytokine–SBP associations using multilinear regression within the HIV + subgroup and in a pooled model including both PLWH and HIV‐negative participants to assess consistency across HIV serostatus. Results: The older cohort had significantly higher median SBP, BMI, and LDL cholesterol (all p < 0.001). Regression models revealed distinct, age‐dependent drivers of SBP. In adults < 45 years, only IFN‐γ ( β = 0.00107, p = 0.018) and chronological age ( β = 0.487, p = 0.047) showed significant positive associations with SBP. In contrast, for adults ≥ 45 years, body mass index (BMI) was the dominant and consistent predictor across all models ( β range: 1.95–2.08, all p < 0.001). In this older group, IL‐17A was additionally significant in its specific model ( β = 0.00322, p = 0.0448). Systemic levels of IL‐6, IL‐1, and TNF‐α were not significantly associated with SBP in either cohort. Secondary analysis showed consistent cytokine–SBP relationships by HIV status, with a slight reduction in effect size seen in IL‐17A after adding HIV‐negative participants: HIV+ ( β = 0.0029, p = 0.035) to the combined cohort ( β = 0.0027, p = 0.048). IFN‐γ remained stable with near‐identical effect sizes (HIV+: β = 0.0010, p = 0.011; combined: β = 0.0010, p = 0.010). Conclusion: The regulation of blood pressure appears to undergo a fundamental pathophysiological transition with advancing age. In younger adults (< 45 years), SBP is associated with adaptive immune activity, mainly the Th1‐associated IFN‐γ. After midlife (≥ 45 years), this relationship is superseded by a model dominated by adiposity, within which the Th17‐associated IL‐17A acts as a contributing inflammatory mediator. These age‐stratified cytokine–blood pressure relationships were consistent across PLWH and HIV‐negative individuals, suggesting that this pathophysiological succession operates independently of HIV serostatus. Collectively, these findings advocate for age‐tailored, mechanism‐based approaches to the understanding and managing blood pressure–related risk.

Background: Hypertensive disorders of pregnancy (HDP) are a leading cause of maternal and perinatal morbidity, yet data on their burden among adolescent mothers in Sub‐Saharan Africa are limited. This study aimed to determine the prevalence of HDP and their association with birth outcomes among adolescent mothers at Livingstone University Teaching Hospital (LUTH) in Zambia. Methods: We conducted a retrospective cross‐sectional study of 405 medical records of adolescent pregnancies (aged 10–19 years) at LUTH from January 2023 to December 2024. HDP was defined as systolic/diastolic blood pressure ≥ 140/90 mmHg after 20 weeks of gestation. Data were abstracted using REDCap and analyzed with StatCrunch. Univariable and multivariable logistic regression identified factors associated with HDP. Bivariate analyses examined associations with birth outcomes. Statistical significance was set at p < 0.05. Results: The prevalence of HDP was 16.8% (68/405). In multivariable analysis, increasing age (AOR = 1.31 per year, 95% CI: 1.06–1.63, p = 0.012), a previous history of hypertension (AOR = 1.77, 95% CI: 1.19–2.62, p = 0.005), and a positive family history of chronic hypertension (AOR = 3.89, 95% CI: 1.03–14.61, p = 0.044) were independent predictors. HDP was significantly associated with adverse birth outcomes ( p = 0.014), particularly fetal death (46.2% vs. 16.1% among normotensive). Hypertensive adolescents had higher rates of preeclampsia (86.4% vs. 12.8%, p < 0.001), eclampsia (100% vs. 16%, p < 0.001), and fetal complications, including asphyxia (34.5% vs. 14.6%, p = 0.013) and prematurity (23.5% vs. 14.6%). Conclusions: HDP affect nearly one in six adolescent mothers at a Zambian tertiary hospital and are strongly associated with adverse birth outcomes. Older age, prior hypertension, and family history of chronic hypertension are independent predictors. Enhanced antenatal risk assessment, including detailed personal and family history, age‐stratified monitoring, and routine proteinuria screening, is urgently needed to improve maternal and neonatal outcomes in this high‐risk population.