Search Results (1,946)

Background: The Semipalatinsk Nuclear Test Site (SNTS) represents a unique example of long-term population exposure to ionizing radiation. This study aimed to assess the health status of individuals from three generations permanently residing in territories affected by radioactive contamination resulting from nuclear weapons testing at the SNTS, based on the findings of a population screening examination. Materials and Methods: A cross-sectional screening study was conducted among 2802 adults aged 18 years and older. The exposed group consisted of residents of the Abay and Beskaragai districts of the Abay Region and their descendants (n = 1358). The control group included residents of Arshaly village in the Akmola Region with no history of radiation exposure (n = 1444). All participants underwent a structured questionnaire survey, clinical examination, biochemical and hematological testing, and assessment of thyroid function. Individual radiation doses were obtained from the State Scientific Automated Medical Registry of Persons Exposed to Radiation (SSAMR). Results: Arterial hypertension (p < 0.001), chronic ischemic heart disease (p < 0.001), thyroid disorders (p < 0.001), malignant neoplasms (p = 0.003), renal diseases, and respiratory diseases were significantly more prevalent in the exposed population than in the control group. Exposed individuals also demonstrated significantly higher levels of total cholesterol, triglycerides, and the triglyceride-glucose (TyG) index, indicating increased insulin resistance. After adjustments, the only outcome that retained a statistically significant association with radiation dose was thyroid disorders (adjusted OR per 10 mSv increase = 1.017; 95% CI: 1.009–1.025; p < 0.001). ROC analysis demonstrated a moderate discriminative ability of radiation dose with respect to arterial hypertension (AUC = 0.715), chronic ischemic heart disease (AUC = 0.735), and ischemic stroke (AUC = 0.711). Conclusions: The findings suggest long-term adverse health effects associated with radiation exposure among populations residing near the SNTS. Continued epidemiological surveillance and medical monitoring of exposed individuals and their descendants are warranted. Full article

Background/Objectives: Frailty is a clinically significant syndrome in older patients with ischemic heart disease, associated with adverse outcomes including hospitalization, disability, and mortality. This study aimed to evaluate the association of potentially inappropriate medication (PIM) and the Geriatric Nutrition Risk Index (GNRI) with the incidence of frailty among elderly patients with ischemic heart disease (IHD). Methods: This retrospective cohort study enrolled elderly patients with IHD between January 2018 and March 2024. Patients were grouped by PIM use and GNRI levels (<92 vs. ≥92). Cox proportional hazards models assessed the associations of PIM and GNRI with the incidence of frailty. Subgroup and sensitivity analyses evaluated the consistency and robustness of these findings. Results: PIM use was associated with a significantly higher risk of frailty (HR = 3.01, 95% CI = 2.48–3.65) than non-use. Similarly, lower GNRI increased the risk of frailty compared to higher GNRI (HR = 1.31, 95% CI = 1.12–1.54). Patients with both PIM and lower GNRI may have a higher risk of frailty, with an adjusted aHR of 4.09. Subgroup analyses showed significant interactions between GNRI and hypertension. Sensitivity analyses indicated that PIM (aHR = 2.65) and lower GNRI (aHR = 1.14) remained significantly associated with frailty, even after including those with pre-existing frailty. Conclusions: For elderly patients with IHD, both PIM and lower GNRI were significantly associated with the incidence of frailty. These findings suggest that PIM exposure and low GNRI may serve as clinically accessible markers for identifying older IHD patients at elevated risk of frailty. Full article

Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality in the elderly worldwide. Over the past two decades, there has been a wealth of evidence of a close relationship between autonomic nervous system activity and cardiovascular mortality, including sudden cardiac death. Heart rate variability (HRV), derived from photoplethysmographic (PPG) signals, is increasingly recognized as a promising non-invasive digital marker for evaluating autonomic nervous system function and stratifying CVD risk. The application of machine learning algorithms to PPG-derived HRV analysis offers a promising approach for improving CVD risk stratification and facilitating the development of personalized medicine strategies. Background/Objectives: To evaluate the potential of heart rate variability indicators in predicting the risk of developing CVD in individuals aged 65 years and older. Methods: The study involved individuals aged 65 years and older, divided into two groups: those with a risk of developing CVD (n = 54) and those without risk (n = 46). The first stage included a questionnaire as well as anthropometric and hemodynamic measurements. At the second stage, a PPG was performed using the Eldar computer photoplethysmograph and Eldar-Vario software, followed by an analysis of time-domain and spectral HRV parameters. Statistical data analysis was conducted using the SPSS Statistics 22.0 software package, focusing on the evaluation of associations between HRV indicators and the presence of CVD. Interpretable machine learning models were developed using logistic regression and a random forest algorithm within a nested cross-validation framework. In addition to the discriminatory characteristics, Brier score, LogLoss, calibration analysis, error matrices, permutation importance, and SHAP interpretation were analyzed in the study. Results: In patients with cardiovascular diseases, a statistically significant decrease in heart rate variability was revealed: SDNN by 2 times (26 [Q1–Q3: 15, 35] ms), pNN50 by 3.5 times (4 [3, 5]%), TINN by 5 times (31 [20, 51] ms), and HRV by 2.5 times (6 [4, 8.7]). In addition, a decrease was seen in the spectral components of VLF by one-fold (2450 [Q1–Q3: 2450, 4500] ms²), LF by four-fold (750 [750, 1500] ms²) and HF by five-fold (450 [450, 750] ms²) (p < 0.05). At the same time, there was a significant increase in the VLF/HF and LF/HF ratios, which indicates a predominance of sympathetic activity. According to the results of the correlation analysis, statistically significant associations of HRV indicators with age, physical activity level, body mass index and systolic blood pressure were revealed. The results of machine learning also revealed the association of HRV with arterial hypertension, physical activity and BMI. The best final results were demonstrated by a random forest model with a combined set of clinical and HRV signs of HF and RMSSD (ROC-AUC was 0.9988). The signs of heart rate variability obtained by photoplethysmography demonstrated additional prognostic value in relation to clinical signs. PPG-derived HRV features demonstrated additional discriminatory value for cardiovascular risk stratification. Conclusions: The obtained data demonstrate a close association between the risk of developing cardiovascular disease and autonomic nervous system dysfunction. The decrease in heart rate variability is most pronounced in elderly individuals with existing cardiovascular disease and can be considered a potential tool for developing diagnostic, prognostic, and risk stratification strategies. The use of machine learning demonstrated that heart rate variability features obtained using photoplethysmography improve diagnostic prognostication and classification of cardiovascular diseases compared to models based solely on clinical data. Full article

Background: Type 2 diabetes mellitus (T2DM) is associated with subclinical myocardial dysfunction, which may occur despite preserved left ventricular ejection fraction. Left ventricular global longitudinal strain (LV GLS) is a sensitive marker of early systolic impairment and may detect subtle changes in myocardial function before conventional echocardiographic parameters become abnormal. The effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) on LV GLS in adults with T2DM remains incompletely defined. Objective: To synthesize the available evidence on the effects of SGLT2i therapy on LV GLS or LV strain in adults with T2DM. Methods: Original full-text human studies evaluating SGLT2i therapy in adults with T2DM and reporting LV GLS or LV strain were included. LV GLS was assessed primarily by speckle-tracking echocardiography, while one study used cardiac magnetic resonance feature-tracking. Reviews, conference abstracts, protocols, animal-only studies, and studies without LV strain assessment were excluded. Risk of bias was assessed using RoB 2 for randomized studies and ROBINS-I for non-randomized studies. Results: Twenty-six studies involving more than 2300 participants were included. The studies evaluated dapagliflozin, empagliflozin, ertugliflozin, canagliflozin, or mixed SGLT2i regimens across heterogeneous clinical populations, including patients with preserved ejection fraction, pre-heart failure, diabetes-related cardiomyopathy, chronic heart failure, coronary artery disease, hypertension, non-alcoholic fatty liver disease, and cardio-oncology risk. Most observational and before–after studies reported favorable changes in LV GLS after SGLT2i therapy, whereas randomized and controlled studies showed more variable findings. Several studies also reported improvements in LV remodeling, diastolic function, left atrial function, myocardial work indices, NT-proBNP, cardiometabolic parameters, or epicardial adipose tissue thickness. However, the certainty of evidence was limited by methodological heterogeneity, differences in comparator groups, variable follow-up duration, non-standardized imaging protocols, and risk of bias, particularly in non-randomized and single-arm studies. Conclusions: SGLT2i therapy may be associated with favorable changes in LV GLS in adults with T2DM, suggesting a potential beneficial effect on subclinical left ventricular systolic function. However, current evidence does not definitively establish a consistent treatment effect across all populations. Larger randomized controlled trials with standardized strain imaging protocols, predefined LV GLS endpoints, and clinically relevant follow-up are needed to determine whether SGLT2i-related improvements in LV GLS reflect true myocardial benefit and translate into improved cardiovascular outcomes. Full article

Background/Objectives: Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide. Individuals with hypertension (HTN) and type 2 diabetes mellitus (T2DM) are at particularly high risk; however, awareness of cardiovascular risk within the broader community and among high-risk subgroups remains suboptimal. This study aimed to assess CVD risk awareness and its correlates among adults in the Northern Border Region of Saudi Arabia, with a particular focus on individuals with HTN and/or T2DM. Methods: A descriptive, quantitative, cross-sectional survey was conducted among adults aged 18–50 years residing in the Northern Border Region of Saudi Arabia. An anonymous online questionnaire was distributed via social media between October 2025 and January 2026. The survey incorporated a 22-item scale assessing HTN knowledge, T2DM knowledge, and CVD risk awareness (Heart Disease Fact items). Participants were categorized according to self-reported diagnosis (no diagnosis, HTN, T2DM, or both). Descriptive statistics, non-parametric tests, and multivariable regression analyses were used to evaluate knowledge scores and predictors of CVD risk awareness. Results: A total of 458 participants completed the survey. Overall knowledge was moderate (mean 12.40/22; 56.4%), with relatively higher scores for HTN (73.2%) and T2DM knowledge (68.8%), but markedly lower CVD risk awareness (30.8%). Fewer than half of participants correctly answered key CVD items, particularly those related to asymptomatic disease progression and lipid (HDL) concepts. Only 21.6% achieved good awareness (≥75%). In multivariable analyses, higher educational level, positive family history of cardiometabolic disease, and the presence of HTN and/or T2DM were independent predictors of higher awareness. Conclusions: CVD risk awareness is suboptimal among adults in the Northern Border Region, including those with established HTN and T2DM. The observed gap between disease-specific knowledge and CVD risk awareness highlights the need for targeted, structured risk communication strategies in primary care, particularly for individuals with lower educational attainment and no family history of CVD. Full article

Atrial fibrillation (AF) and diabetes mellitus frequently coexist and together define a high-risk cardiometabolic phenotype. Diabetes is associated with an increased incidence of AF, although this relationship is strongly influenced by obesity, hypertension, chronic kidney disease (CKD), heart failure (HF), sleep-disordered breathing, and broader metabolic risk clustering. Once AF develops, diabetes is associated with greater thromboembolic and HF risk, impaired quality of life, cognitive vulnerability, and excess mortality. These adverse outcomes may be partly explained by a multidimensional atrial substrate, described here within the conceptual framework of diabetic atrial cardiomyopathy, in which hyperglycaemia, insulin resistance, glycaemic variability, oxidative stress, inflammation, autonomic dysfunction, microvascular disease, lipotoxicity, and epicardial adipose tissue dysfunction may contribute to atrial fibrosis, electrical heterogeneity, impaired calcium handling, mitochondrial injury, and mechanical dysfunction. Collectively, these abnormalities may facilitate AF initiation, persistence, progression, and recurrence after rhythm-control interventions. Management should therefore extend beyond rhythm control and anticoagulation alone. In individuals at increased risk of AF, priorities include cardiometabolic optimization, treatment of obesity, hypertension, CKD, HF, and sleep apnoea, lifestyle intervention, and selective rhythm surveillance. In subclinical AF, decisions regarding anticoagulation should account for AF burden, thromboembolic and bleeding risk, renal function, frailty, and patient preference. In established AF, stroke prevention, symptom-directed rate or rhythm control, cardiometabolic therapy, and longitudinal reassessment remain central. This narrative review integrates the epidemiology, mechanisms, and management of AF in diabetes across the continuum from AF risk to subclinical and clinical disease. Full article

Thrombospondin-2 (TSP-2) is an extracellular matrix glycoprotein involved in angiogenesis, vascular remodeling, cell adhesion, and tissue repair. Its expression is induced by pathological stimuli, including mechanotransduction, hypoxia, and TGF-β signaling, and has been associated with several cardiovascular diseases (CVDs), such as heart failure, coronary artery disease, abdominal aortic aneurysm, and hypertension. Elevated circulating TSP-2 levels, particularly in combination with NT-proBNP, as well as alterations in THBS2 and its regulatory non-coding RNAs, have been linked to disease severity and adverse cardiovascular outcomes. This review summarizes current evidence on the role of TSP-2 in cardiovascular pathophysiology and its involvement in cardiovascular homeostasis. Although accumulating data suggest that TSP-2 may have diagnostic, prognostic, and therapeutic relevance, its clinical utility as a biomarker or therapeutic target has not yet been established. Further large-scale studies and standardized assessment methods are required to validate its potential and support future clinical translation. Full article

Heart failure (HF) with preserved ejection fraction (HFpEF) is increasingly prevalent and now recognized as a systemic syndrome with diverse clinical phenotypes and multiorgan involvement. The predominant clinical phenotype has evolved from patients with isolated hypertensive heart disease to individuals with cardiometabolic (CM) abnormalities [obesity, insulin resistance, increased waist circumference (a surrogate for visceral adiposity), dyslipidemia, type 2 diabetes, and hypertension] that result in metabolic alterations leading to CM-HFpEF. Indeed, CM-HFpEF and metabolic dysfunction-associated fatty liver disease are recognized as two sides of the same coin. Chronic systemic inflammation is a defining pathophysiologic feature of CM-HFpEF, with visceral adipose tissue serving as a central driver. In this regard, lifestyle changes, including diet and exercise, are crucial for managing HFpEF. Several recent studies have shown that exercise training (aerobic and resistance combined) with or without calorie restriction is an effective therapeutic management strategy for improving exercise capacity, physical function, and quality of life in patients with clinically stable HFpEF. Also, the pharmacologic interventions that have proven beneficial in HFpEF so far (sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists) are effective due to their metabolic protective effects. In this review, we outline the current available evidence on lifestyle interventions in HFpEF management and therapeutics, discussing their modalities and potential mechanisms. Full article

Background: Pulmonary arterial hypertension (PAH) is a rare and progressive disorder characterized by increased pulmonary vascular resistance and vascular remodeling. Genetic polymorphisms, epigenetic modifications, and ion channel dysregulation are increasingly recognized as key contributors to disease pathogenesis. Anoctamin-1 (ANO1/TMEM16A), a calcium-activated chloride channel, plays a critical role in vascular tone regulation. Objective: This study aimed to investigate the association between ANO1 gene polymorphisms (rs7127129 and rs2509153), promoter methylation status, and serum chloride levels in patients with idiopathic pulmonary arterial hypertension (IPAH), congenital heart disease (CHD), and chronic thromboembolic pulmonary hypertension (CTEPH). Methods: A total of 106 IPAH patients, 40 CHD patients, and 30 CTEPH patients, together with 125 healthy controls, were included. The control group had a comparable age distribution, with a balanced sex ratio, whereas females predominated in all three PH groups. Genotyping was performed using TaqMan-based real-time PCR. Promoter methylation was analyzed using bisulfite conversion followed by quantitative real-time PCR. Serum chloride levels were measured using an ion-selective electrode method. Results: No significant association was observed between rs7127129 and rs2509153 polymorphisms and IPAH or CTEPH (p > 0.05). However, rs7127129 showed a significant association with CHD (p < 0.05). After excluding hypertensive patients, both polymorphisms remained significantly associated with CHD. Serum chloride levels differed significantly among groups (p < 0.001), with higher levels observed particularly in the CTEPH and CHD groups compared to controls, while IPAH patients exhibited intermediate but still elevated levels relative to controls. In contrast, promoter methylation levels were significantly lower in all patient groups compared to controls. An inverse relationship between chloride levels and methylation status was observed. Conclusions: ANO1 polymorphisms are not major determinants of IPAH or CTEPH but may contribute to CHD susceptibility. Increased serum chloride levels, together with decreased promoter methylation, suggest a potential mechanistic link between ion channel dysregulation and epigenetic alterations in pulmonary hypertension. Further large-scale and functional studies are warranted. Full article

Environmental exposure to persistent and non-persistent endocrine-disrupting chemicals (EDCs), including per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), polycyclic aromatic hydrocarbons (PAHs), dioxins, phthalates, and bisphenols, has been increasingly associated with elevated cardiovascular disease (CVD) risk. Emerging evidence suggests the importance of gene–environment interactions in modulating individual susceptibility to EDC-related cardiovascular effects. This review summarizes current knowledge by synthesizing the main classes of EDCs, evaluating the evidence linking them to cardiovascular outcomes, and highlighting how genetic variability may modulate EDC-induced cardiovascular risk. Across the studies analyzed, the most extensively investigated genetic polymorphisms involve pathways related to oxidative stress regulation, xenobiotic metabolism and detoxification, hormone signaling, and lipid homeostasis. Variants in antioxidant defense genes, such as CAT, eNOS, and PON1, have been associated with increased hypertension risk and vascular dysfunction following exposure to bisphenols and PAHs. Polymorphisms in GSTP1, CYP2C19, CYP1A2, CYP2E1, ABCB1, and MTHFR may influence susceptibility to cardiometabolic alterations and congenital heart defects, whereas variants in ESR2, FTO, LEPR, and INSIG2 have been linked to obesity, dyslipidemia, and hypertension associated with PFAS, PBDEs, and bisphenols. A deeper understanding of gene–environment interactions is essential to advance preventive cardiology and mitigate the cardiovascular impact of environmental pollutants. Full article

Cardiovascular diseases (CVDs) remain the leading global cause of morbidity and mortality, imposing an increasing clinical and socioeconomic burden. Despite significant therapeutic advances, optimal control of risk factors and long-term outcomes remain challenging, particularly in patients with complex comorbidities. This narrative review provides a comprehensive and up-to-date synthesis of pharmacological options across major cardiovascular domains, with a specific focus on hypertension, heart failure, arrhythmias, and hypertrophic cardiomyopathy, conditions in which hemodynamic, neurohormonal, and electrophysiological pathways play central roles. We summarize mechanisms of action, clinical evidence, safety profiles, and guideline-based indications of established therapies, highlighting their relevance to vascular tone regulation, neurohormonal modulation, endothelial signaling, and myocardial function, the mechanistic axes that intersect with pathways implicated in pulmonary vascular disease (PVD). In addition, we discuss emerging therapeutic targets and innovative agents such as renin-angiotensin-aldosterone system silencers, endothelin pathway modulators, SGLT2 inhibitors, soluble guanylate cyclase stimulators, myosin inhibitors, and other mechanism-based approaches. Current challenges and unmet clinical needs are examined in the context of translational relevance for PVD and the broader goal of advancing individualized pharmacotherapy. Continued therapeutic innovation targeting shared vascular, metabolic, and neurohormonal pathways holds promise for improving outcomes across both systemic and pulmonary vascular diseases. Full article

Hypertension is the leading risk factor for cardiovascular disease. Epidemiologic studies have demonstrated that pediatric hypertension may increase the risk of premature heart disease. Pediatric hypertension affects about 4% of children and clusters with other risk factors and social disparities in health. In addition to observed target organ damage, there is evidence for tracking blood pressure from childhood to adulthood. Ambulatory blood pressure monitoring is the recommended method for diagnosis, and echocardiography is used to assess target organ damage. A diagnostic workup in children depends on the age at presentation, severity of hypertension, diurnal pattern, evidence of target organ damage, and response to treatment. Treatment follows a similar framework to adult hypertension and studies demonstrate improvement in intermediate outcomes with treatment. However, further studies are needed to establish benefit in hard outcomes. This review focuses on studies evaluating the epidemiology of pediatric hypertension and its association with cardiovascular outcomes. Relevant domains included prevalence, blood pressure tracking, and cardiovascular sequelae. To compile data for this narrative review, a PubMed/MEDLINE database search was performed for studies published between 1997 and April 2026. Full article

Background: The impact of overweight and obesity on blood pressure and cardiac remodelling in pediatric congenital heart disease (CHD) remains incompletely defined, particularly across different ventricular physiologies and cardiac anatomies. Aim: To assess the association of overweight and obesity with arterial blood pressure and cardiac remodelling in pediatric and young adult patients with CHD, according to ventricular physiology and cardiac anatomy. Methods: In this observational study, pediatric CHD patients undergoing clinical and echocardiographic evaluation were classified by weight status and ventricular physiology, with additional stratification by cardiac anatomy. Associations between body mass index (BMI), arterial hypertension, and echocardiographic parameters were analyzed. Results: A total of 451 patients were included (mean age 13.1 ± 3.9 years; 74 univentricular, 377 biventricular). Overall, 16% were overweight and 7% obese. Hypertension was present in 16% and increased across BMI categories (14%, 26%, and 50%). BMI was associated with blood pressure category (p < 0.001), higher systolic blood pressure (p < 0.001), and increased left ventricular (LV) mass (p = 0.007), interventricular septal thickness (p < 0.001), and posterior wall thickness (p < 0.001), without evidence of systolic dysfunction. In adjusted models, overweight/obesity remained associated with worse blood pressure classification, both as a three-category outcome (OR 2.1, 95% CI 1.4–3.2; p < 0.001) and as a binary outcome (OR 2.3, 95% CI 1.5–3.7; p < 0.001), as well as with higher systolic blood pressure (β = 5.1 mmHg, 95% CI 2.4–7.8; p < 0.001), left ventricular mass index (LVMI) (β = 10.0, 95% CI 4.3–15.8; p < 0.001), interventricular septal thickness at end-diastole (IVSd) (p < 0.001), and left ventricular posterior wall in diastole (LVPWd) (p < 0.001), but not with diastolic blood pressure or systolic function. No significant associations were observed in univentricular patients, whereas in biventricular circulation higher BMI was consistently associated with worse blood pressure and remodeling, without systolic dysfunction. Conclusions: Excess body weight is independently associated with adverse blood pressure status and early LV structural remodelling in pediatric and young adult patients with CHD, despite preserved systolic function. These findings support early cardiovascular risk surveillance and preventive strategies targeting overweight and obesity in CHD care. Full article

Background: Penetrating keratoplasty (PK) is a technically demanding corneal transplant procedure frequently performed in elderly patients with substantial systemic comorbidities. In this population, an anesthetic strategy that ensures hemodynamic stability, cooperative sedation, adequate analgesia, and preserved spontaneous ventilation is highly desirable. Dexmedetomidine, a highly selective alpha2-adrenergic agonist, provides “cooperative” sedation with minimal risk of respiratory depression and additional sympatholytic benefits. Methods: This single-center retrospective observational case series included 50 consecutive patients (American Society of Anesthesiologists [ASA] II–III, age 50–90 years) undergoing PK under sub-Tenon block combined with continuous dexmedetomidine infusion. Dexmedetomidine was administered without a loading bolus at 0.7 mcg/kg/h for 10–15 min, then reduced to 0.5 mcg/kg/h, targeting a Ramsay Sedation Scale (RSS) score of 2–3. The sub-Tenon block was performed using a mixture of levobupivacaine 0.5% and lidocaine 2% (3–5 mL). Heart rate (HR), mean arterial pressure (MAP), oxygen saturation (SpO₂) and RSS were recorded in nine predefined perioperative phases. Data were analyzed descriptively. Results: The mean age was 72 ± 9 years; 52% of patients were ASA III. Hypertension was present in all patients; 30% had cardiovascular disease, 28% diabetes mellitus type II, and 30% chronic obstructive pulmonary disease. Progressive, controlled bradycardia was observed (mean HR decreased from 76 to 57 beats/min during graft transplantation), while MAP gradually decreased from hypertensive baseline values (150–160 mmHg) to an optimal intraoperative range of 115–130 mmHg, without episodes of clinically significant hypotension. SpO₂ remained stable at 98–99% throughout all phases, with no episodes of desaturation or need for airway intervention or supplemental oxygen. Target sedation (RSS 2–3) was achieved in all patients (median RSS 3), with preserved spontaneous breathing and cooperation. Sub-Tenon block-related bulging occurred in 6% of cases. No episodes of clinically significant bradycardia, malignant arrhythmia, respiratory compromise, or need to discontinue dexmedetomidine were recorded. No opioids or non-steroidal analgesics were required intraoperatively or in the early postoperative period. Conclusions: The combination of sub-Tenon block and continuous dexmedetomidine sedation without a loading bolus represents a hemodynamically stable and respiratory-safe anesthetic strategy for PK in elderly, high-risk patients. These preliminary, hypothesis-generating findings suggest that the protocol provides stable surgical conditions and a favorable safety profile, justifying future prospective randomized controlled trials to establish its comparative efficacy against general anesthesia or standard sedative regimens. Full article