Abstract Background Rhythm and conduction disturbances are critical determinants of ST-elevation myocardial infarction (STEMI) outcomes. While potassium and calcium imbalances are well-established contributors to arrhythmogenesis, the role of serum sodium, a key electrolyte modulating myocardial excitability, remains underexplored in acute STEMI. Purpose To evaluate whether serum sodium concentration independently predicts in-hospital arrhythmias (ventricular tachycardia (VT), ventricular fibrillation (VF), and atrial fibrillation (AF)) in STEMI patients treated with primary percutaneous coronary intervention (pPCI), after adjusting for key covariates. Methods This retrospective cohort study investigated the impact of serum sodium concentration on arrhythmias in 398 adults with acute STEMI who underwent pPCI. We excluded hypo-/hyperkalemia and abnormal glomerular filtration rate (GFR). Patients were stratified into two groups: Group 1 with plasma sodium level ≤140 mmol/L (n = 279), and Group 2 with plasma sodium level >140 mmol/L (n = 119). Baseline characteristics, including GFR, diabetes mellitus (DM), plasma potassium level, and left ventricular ejection fraction (LVEF), were comparable between the groups. Backward stepwise logistic regression (Wald method) assessed predictors of arrhythmia, adjusting for LVEF, potassium, DM, and sodium groups. Results The analysis showed no statistically significant differences in baseline characteristics between Group 1 and Group 2. Specifically, GFR was 106.1 ± 18.1 vs. 109.8 ± 24.2 mL/min/1.73m² (p = 0.84), potassium 4.16 ± 0.40 vs. 4.15 ± 0.40 mmol/L (p = 0.74), DM prevalence 23.3% vs. 19.3% (p = 0.75), and LVEF was 37.99% ± 7.31 vs. 39.64% ± 7.36 (p = 0.067). The mean serum sodium level was 136.7 ± 3.3 mmol/L in Group 1 and 141± 2.3 mmol/L in Group 2 (p = 0.83). Among the study cohort, 25 cases of arrhythmia (including VT, VF, AF) were identified, representing 6.3% of the total population. However, serum sodium levels were not found to be predictive of in-hospital arrhythmias (OR:1.02, 95% CI: 0.94–1.11, p = 0.62). In contrast, reduced LVEF (OR: 0.95, 95% CI: 0.92–0.98, p = 0.001) and potassium levels (OR: 1.89, 95% CI: 1.12–3.20, p = 0.017) emerged as significant predictors of arrhythmic events. Conclusion In this cohort of STEMI patients treated with primary PCI, serum sodium concentration did not independently influence the incidence of in-hospital arrhythmias. These findings suggest that serum sodium concentration (≤140 vs. >140 mmol/L) may not have a clinically significant impact on arrhythmogenesis in acute STEMI.
Abstract Background Coronary artery disease is the leading cause of mortality in Armenia. To address the lack of national real-world data on reperfusion practices and outcomes, the Armenian National Registry of Myocardial Infarction (ARMI) was established in December 2023 as the first nationwide prospective STEMI registry. Objectives The primary endpoint of the study was to determine in-hospital mortality rates in patients admitted with STEMI across all participating national centers. The secondary endpoints included assessing 30-day and 12-month cardiovascular mortality, all-cause mortality, and rehospitalization rates. Methods ARMI prospectively enrolled consecutive adults aged 18-93 years presenting with STEMI within 48 hours of symptom onset across 13 specialized hospitals nationwide. Trained investigators collected standardized clinical, procedural, and outcome data using a secure national REDCap electronic database. All patients were followed prospectively for 12 months, with structured assessments at 30 days and 12 months. Enrollment ran from 1 December 2023 to 1 July 2025. Results A total of 2,222 patients were enrolled across all 13 centers. The present analysis includes 1,392 patients with complete follow-up data. The cohort was predominantly male (81.1%; n=1,129), with 18.9% women (n=263). Percutaneous coronary intervention (PCI) was performed in 96.8% of patients (n=2,098), of whom 99.6% underwent primary PCI (n=2,090). Medical therapy alone was used in 2.7% (n=58), and 0.6% (n=12) required coronary artery bypass grafting. In-hospital reinfarction and recurrent ischemia occurred in 3.4% and 4.2% of patients, respectively. Overall in-hospital mortality was 3.1%. Cardiovascular causes accounted for 91.0% of all in-hospital deaths. Reduced systolic function was a major contributor, with 62.5% of deceased patients having LVEF ≤40%. Acute HF with Killip class 3-4 at presentation was identified in 8.0% of patients. In-hospital mortality in patients with Killip class 3-4 was substantially higher at 9.0% versus 3.1% for the overall cohort. At one year, all-cause mortality was 8% in the overall population and 32% in patients presenting with Killip class 3-4, confirming the powerful adverse prognostic impact of early HF severity. HF-related rehospitalization occurred in 13% of Killip class 3-4 patients versus 36% in the overall cohort, reflecting ongoing morbidity burden. Conclusions ARMI establishes the first national benchmark for STEMI care in Armenia, demonstrating near-universal primary PCI use and low in-hospital mortality (3.1%), comparable to that reported in European registries. Acute HF at presentation identified a high-risk subgroup with markedly higher in-hospital and 1-year mortality. Left ventricular ejection fraction ≤40% emerged as a key prognostic marker. The ARMI registry provides a foundation for future translational research and nationwide quality improvement initiatives.
Abstract Background Statins are foundational therapy for cardiovascular prevention; however, up to 50% of patients discontinue treatment within one year. Randomized trials show similar adverse event rates in statin and placebo groups, suggesting that nocebo effects contribute substantially to perceived intolerance and non-adherence. Objectives To evaluate the impact of statin-related nocebo effects on medication adherence, cardiovascular outcomes, and the effectiveness of mitigation strategies. Methods A scoping review was conducted across PubMed, Cochrane CENTRAL, Google Scholar, and ClinicalTrials.gov. Eligible studies included randomized controlled trials (RCTs), observational cohorts, qualitative studies, and systematic reviews of adults prescribed statins for primary or secondary prevention. Study quality was assessed using validated tools (Cochrane Risk of Bias, Newcastle–Ottawa Scale, AMSTAR-2). Evidence was synthesized according to PRISMA-ScR methodology using thematic analysis. Results Twenty-five studies (5 RCTs, 13 observational, 4 qualitative, 3 systematic reviews) comprising >3.2 million participants were included. N-of-1 trials demonstrated that ~90% of symptom burden during statin therapy was attributable to nocebo effects, with comparable symptoms during placebo phases. Among 37,668 placebo-treated participants, 42.6% reported statin-typical adverse effects without active drug exposure. Discontinuation patterns were frequently early and inconsistent with pharmacologic toxicity. High-intensity regimens showed reduced persistence despite non-proportional biological risk, supporting an expectation–dose relationship. Discontinuation within six months following myocardial infarction independently predicted increased all-cause mortality. Qualitative evidence highlighted clinician communication as a key determinant of expectations. Behavioral and cognitive interventions reduced nocebo responses and improved persistence. Conclusions A substantial proportion of statin-associated symptoms are mediated by nocebo mechanisms. Expectation-driven discontinuation is associated with increased cardiovascular risk. Targeted communication strategies and structured rechallenge approaches may improve adherence and reduce preventable cardiovascular events.
Abstract Background Atrial fibrillation (AF) frequently complicates arterial hypertension (AH), yet the mechanistic transition from pressure overload to arrhythmia remains incompletely understood. Chronic diastolic burden and vascular stiffening may induce inflammatory–fibrotic atrial remodeling, giving rise to a structural and mechanical substrate of atrial cardiomyopathy (ACM) that precedes clinically overt AF. Aim To determine whether ACM represents the mechanistic substrate underlying incident AF in patients with AH and to assess the role of left atrial (LA) mechanical dysfunction in arrhythmic transition. Methods This multicenter cohort included 307 patients with AH and no prior AF. Baseline assessment comprised inflammatory–fibrotic biomarkers: high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6), transforming growth factor beta 1 (TGF-β1) and comprehensive transthoracic echocardiography including peak atrial longitudinal strain (PALS), indexed minimal and maximal LA volumes (LAVImin, LAVImax), average E/e′ and left ventricular global longitudinal strain (LV GLS). Arterial stiffness was quantified using the cardio-ankle vascular index (CAVI). Patients were followed for 3 years for incident AF. Independent predictors were identified using age- and sex-adjusted multivariable logistic regression (two-sided p<0.05). Results Incident AF occurred in 99/307 patients (32%). Compared with those remaining in sinus rhythm, patients who developed AF had lower PALS (20.3±3.4% vs 28.6±4.9%, p<0.001), higher E/e′ (16.2±3.4 vs 11.8±2.9, p<0.001) and larger LAVImin (14.2±5.0 vs 10.4±4.2 ml/m², p<0.001). LAVImax was within normal limits and did not differ between groups (28.4±5.6 vs 27.1±6.1 ml/m², p=0.31), suggesting that LA mechanical dysfunction precedes overt dilatation. Inflammatory–fibrotic markers were higher in the AF group: hsCRP (7.9±1.4 vs 4.2±1.3 mg/L, p<0.002), IL-6 (6.4±0.8 vs 3.6±1.2 pg/ml, p=0.03) and TGF-β1 (1240±75 vs 900±43 pg/ml, p=0.02). CAVI was increased (9.5±0.21 vs 8.3±0.76, p=0.01), whereas LV GLS showed a non-significant trend (−18.1±1.9% vs −20.2±1.8%, p=0.07). A PALS <25% identified a high-risk arrhythmogenic phenotype. In multivariable analysis adjusted for age and sex, impaired PALS (OR 3.78, p<0.001) was the strongest independent determinant of incident AF, followed by TGF-β1 (OR 3.54, p=0.02), CAVI (OR 3.25, p=0.01), hsCRP (OR 1.83, p<0.002) and E/e′ (OR 1.76, p<0.001). Addition of LA mechanical parameters significantly improved model discrimination beyond clinical and hemodynamic variables. Conclusions Incident AF in AH is driven by a pre-existing arrhythmogenic substrate of ACM characterized by LA mechanical dysfunction, inflammatory–fibrotic activation and vascular stiffening. PALS emerges as a central integrator of this process and a pivotal imaging biomarker for early identification of patients at risk of arrhythmic transition.Table
