Otuz dört yaşında erkek hasta, atipik göğüs ağrısı, elektrokardiyografi (EKG) değişiklikleri ve yüksek duyarlılıklı kardiyak troponin yüksekliği nedeniyle ST yükselmesiz miyokard enfarktüsü (NSTEMI) ön tanısıyla değerlendirildi. Koroner anjiyografide sol ön inen arterin orta segmentinde çoklu ince kanallara ayrılıp distal segmentte yeniden birleşen, woven koroner arter anomalisi ile uyumlu görünüm izlendi. Distal Thrombolysis in Myocardial Infarction (TIMI) 3 akımın korunması, hastanın hemodinamik olarak stabil seyretmesi ve devam eden iskemi bulgusunun izlenmemesi nedeniyle konservatif medikal tedavi tercih edildi. Bu olgu, woven koroner arter anomalisi ile spontan koroner arter diseksiyonu, rekanalize trombüs ve kompleks aterosklerotik lezyon ayrımının klinik yönetim açısından önemini vurgulamaktadır. A 34-year-old male patient was evaluated with a preliminary diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) because of atypical chest pain, electrocardiographic changes, and elevated high-sensitivity cardiac troponin. Coronary angiography revealed a characteristic appearance compatible with a woven coronary artery anomaly in the mid segment of the left anterior descending artery, consisting of multiple thin channels that separated and then rejoined distally. Because distal Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow was preserved, the patient remained hemodynamically stable, and there was no evidence of ongoing ischemia, conservative medical treatment was preferred. This case highlights the clinical importance of distinguishing woven coronary artery anomaly from spontaneous coronary artery dissection, recanalized thrombus, and complex atherosclerotic lesions, as this distinction may directly affect management.

Purpose: This study aimed to investigate the association between the Aggregate Index of Systemic Inflammation (AISI) and non-dipper blood pressure (BP) pattern in hypertensive (HT) patients with type 2 diabetes mellitus (DM). Given the well-established role of systemic inflammation in circadian BP regulation, we hypothesized that elevated AISI levels would be associated with impaired nocturnal BP decline. Patients and Methods: A total of 356 newly diagnosed HT patients with type 2 DM and 170 normotensive control subjects were included in this observational study. HT patients were further classified as dipper (n=186) or non-dipper (n=170) based on 24-hour ambulatory blood pressure monitoring (ABPM). AISI was calculated using neutrophil, lymphocyte, platelet, and monocyte counts. Correlation analyses were performed to evaluate the relationship between AISI and ambulatory BP parameters. Multivariate logistic regression analysis with a backward stepwise method was conducted to determine independent predictors of non-dipper status. Receiver operating characteristic (ROC) curve analysis was used to assess the discriminative performance of AISI and other inflammatory indices. Results: AISI and ln(AISI) levels were significantly higher in non-dipper HT patients than in dipper HT patients and normotensive controls (p< 0.001 for all). Ln(AISI) was positively correlated with nighttime systolic and diastolic BP (p< 0.05). In multivariate logistic regression analysis, ln(AISI) emerged as the strongest independent predictor of non-dipper blood pressure pattern (OR: 14.13, 95% CI: 3.68– 54.32, p< 0.001). In ROC analysis, ln(AISI) showed the highest discriminative performance for identifying non-dipper status, with a sensitivity of 71.0% and specificity of 74.1% at a cutoff value of 5.80 (AUC: 0.757, p< 0.001), outperforming NLR, PLR, SII, and SIRI. Conclusion: Elevated AISI levels were independently associated with non-dipper blood pressure pattern in hypertensive patients with type 2 diabetes mellitus. These findings suggest that AISI may serve as a practical and integrative biomarker for identifying high-risk patients with impaired circadian blood pressure regulation.

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 and Objectives: Angiographic no-reflow (NRF) after percutaneous coronary intervention (PCI) reflects impaired microvascular reperfusion despite successful treatment of the epicardial culprit lesion. Brain-derived neurotrophic factor (BDNF) is a neurotrophin involved in endothelial signaling, platelet biology, inflammation, and angiogenesis. Its relationship with NRF in non-ST-segment elevation myocardial infarction (NSTEMI) remains insufficiently characterized. Materials and Methods: This single-center prospective observational cohort study included 700 consecutive NSTEMI patients undergoing culprit-lesion PCI. Admission serum total BDNF was measured before PCI using a standardized enzyme-linked immunosorbent assay protocol. Angiographic NRF was defined as final thrombolysis in myocardial infarction (TIMI) flow <3 and/or TIMI 3 flow with myocardial blush grade (MBG) 0–1 in the absence of residual stenosis, dissection, severe spasm, or other mechanical obstruction. Four sequential logistic regression models were used to evaluate the stability of the association between BDNF and NRF: Model 1 adjusted for clinical variables; Model 2 further adjusted for laboratory and inflammatory variables; Model 3 further adjusted for cardiac injury and functional variables; and Model 4 further adjusted for angiographic and procedural variables. Discrimination, calibration, reclassification, decision-curve analysis, and internal validation were assessed. Results: NRF occurred in 114 of 700 patients (16.3%). Serum total BDNF was higher in the NRF group than in the reflow group [555 (465–688) vs. 386 (292–496) pg/mL, p < 0.001]. BDNF remained independently associated with NRF across sequential models: Model 1 OR 1.67 per 100 pg/mL (95% CI 1.43–1.96), Model 2 OR 1.49 (95% CI 1.24–1.79), Model 3 OR 1.41 (95% CI 1.16–1.72), and Model 4 OR 1.31 (95% CI 1.07–1.60). The BDNF-only AUC was 0.787, while the final BDNF-enriched Model 4 reached an AUC of 0.866. The optimism-corrected bootstrap AUC was 0.852 and the 10-fold cross-validated AUC was 0.845. Conclusions: Higher admission serum total BDNF was independently associated with angiographic NRF in NSTEMI patients undergoing PCI and improved risk discrimination when added to clinical, biochemical, cardiac, and angiographic predictors. These findings suggest that serum total BDNF may reflect a context-dependent biomarker signal related to acute thrombo-inflammatory, platelet-associated, and microvascular injury pathways; however, the observed incremental value was modest and requires external validation.