Background and Objectives: Psychological distress is common in acute coronary syndrome (ACS), yet its relationship with objective coronary anatomical complexity is incompletely understood. The Kessler Psychological Distress Scale-10 (K10) is a brief self-report instrument that measures non-specific psychological distress over the preceding four weeks. We investigated whether the K10 score is associated with the anatomical SYNTAX I score and the clinical–anatomical SYNTAX II PCI score in patients hospitalized with ACS. Materials and Methods: This prospective, single tertiary-center observational study assessed 865 adult patients with suspected or confirmed ACS between 6 January 2026 and 5 June 2026. After applying predefined inclusion and exclusion criteria, 750 consecutive eligible patients with complete K10, SYNTAX I, and SYNTAX II PCI data were included in the final analytic cohort. The cohort consisted of STEMI in 337 patients (44.9%), NSTEMI in 310 (41.3%), and unstable angina pectoris in 103 (13.7%). The validated Turkish version of the K10 scale was administered after pain control and hemodynamic stabilization, within 24–48 h of admission, by trained study personnel blinded to the final SYNTAX analysis. SYNTAX I and SYNTAX II PCI scores were calculated by two blinded interventional cardiologists. The primary endpoint was SYNTAX I score ≥ 23; the key secondary endpoint was SYNTAX II PCI score ≥ 36, interpreted as a cohort-based high clinical–anatomical risk threshold. Results: Mean age was 61.3 ± 11.6 years, and 543 patients (72.4%) were men. Mean K10, SYNTAX I, and SYNTAX II PCI scores were 23.7 ± 6.7, 22.4 ± 9.5, and 31.2 ± 9.6, respectively. K10 score correlated with SYNTAX I (Spearman rho = 0.417, p < 0.001) and SYNTAX II PCI (rho = 0.348, p < 0.001). Each 5-point increase in K10 was independently associated with SYNTAX I ≥ 23 (extended model-adjusted odds ratio [OR] 1.84, 95% confidence interval [CI] 1.59–2.12; p < 0.001) and SYNTAX II PCI ≥ 36 (extended model-adjusted OR 2.26, 95% CI 1.85–2.75; p < 0.001). K10 predicted SYNTAX I ≥ 23 with an area under the curve (AUC) of 0.706 (95% CI 0.674–0.744; cutoff ≥ 24) and SYNTAX II PCI ≥ 36 with an AUC of 0.693 (95% CI 0.654–0.736; cutoff ≥ 26). Adding K10 to the extended clinical model improved cross-validated AUC for SYNTAX I ≥ 23 from 0.708 to 0.774 and for SYNTAX II PCI ≥ 36 from 0.871 to 0.905; bootstrap optimism-corrected AUCs were 0.754 and 0.899, respectively. The findings remained consistent in sensitivity analyses excluding prior CABG patients, adjusting for psychiatric history/medication use, and evaluating patients whose K10 was completed before angiography. Conclusions: In this prospective ACS cohort, early in-hospital assessment of K10-defined recent psychological distress was independently associated with both anatomical and clinical–anatomical coronary complexity. K10 should not replace angiographic risk scoring, but it may help identify a psychocardiological phenotype characterized by higher coronary disease burden and greater clinical vulnerability.

Background: Intermediate-risk acute pulmonary embolism (PE) is clinically heterogeneous, and early deterioration may occur despite initial normotension. The Endothelial Activation and Stress Index (EASIX) is a readily available laboratory index reflecting endothelial activation, cellular injury, renal-perfusion stress, and platelet-related thromboinflammatory burden. We investigated whether admission EASIX and echocardiographic right ventricular-pulmonary arterial (RV-PA) coupling assessed by the TAPSE/PASP ratio identify intermediate-risk PE patients at increased risk for an early adverse clinical outcome (EACO). Methods: This retrospective cohort study included 900 consecutive intermediate-risk acute PE patients admitted between 1 January 2020 and 10 June 2025. EASIX was calculated as LDH (U/L) × creatinine (mg/dL)/platelet count (10⁹/L). The primary endpoint was EACO within the first seven days after PE diagnosis during the index hospitalization, including hemodynamic decompensation, vasopressor/inotrope requirement, intensive care unit transfer, rescue reperfusion therapy, ventilatory support, cardiac arrest, or PE-related death. Hierarchical logistic regression, ROC analysis, calibration assessment, bootstrap internal validation, and 10-fold cross-validation were performed. Results: EACO occurred in 110 patients (12.2%). Patients with EACO had higher EASIX (2.28 [1.52–3.27] vs. 1.27 [0.86–2.00], p < 0.001) and lower TAPSE/PASP ratio (0.29 [0.23–0.36] vs. 0.42 [0.33–0.57], p < 0.001). log2-EASIX correlated inversely with TAPSE/PASP (Spearman rho = −0.30, p < 0.001). In the final combined model, log2-EASIX (OR 1.55 per doubling, 95% CI 1.14–2.10, p = 0.005) and TAPSE/PASP per 0.1-unit decrease (OR 1.36, 95% CI 1.10–1.68, p = 0.004) remained independently associated with EACO after adjustment for clinical variables, troponin, lactate, D-dimer, and C-reactive protein-to-albumin ratio. The final model showed higher discrimination than the clinical-laboratory model, although the absolute AUC increment was modest (AUC 0.920 vs. 0.904). Bootstrap optimism-corrected AUC was 0.910 and 10-fold cross-validated AUC was 0.904. Conclusions: Admission EASIX and impaired RV-PA coupling may provide complementary prognostic information for early risk stratification in intermediate-risk acute PE. Because this was a retrospective single-center study without external validation, these findings should be considered hypothesis-generating and should not be used as definitive treatment-escalation triggers before independent external validation.