Search Results (311)

Background: Low admission low-density lipoprotein cholesterol (LDL-C) is paradoxically associated with worse outcomes after acute coronary syndrome, but this may reflect confounding rather than causation. We examined the paradox in statin-naïve patients. Methods: We studied 388 statin-naïve patients with a first ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI) and followed for up to five years. Admission LDL-C was analyzed continuously and as three categories (<100, 100–130, >130 mg/dL), with all-cause mortality assessed using Kaplan–Meier, Cox regression, restricted cubic splines, and landmark sensitivity analyses. Results: Crude mortality was highest in the lowest LDL-C group (20.0% vs. 8.3% vs. 10.7%; p = 0.014), and LDL-C < 100 mg/dL predicted higher mortality (hazard ratio 2.03, 95% CI 1.02–4.03). After adjustment, this remained non-significant across the parsimonious and fully adjusted models (adjusted HR 1.27–1.43, all 95% CIs including 1); older age, lower ejection fraction, and diabetes were independent predictors of death. The lowest stratum also had lower albumin and higher CONUT scores, consistent with a frailty phenotype. Conclusions: In statin-naïve STEMI patients undergoing primary PCI, the lipid paradox reflected age- and frailty-related confounding rather than protection; low admission LDL-C marks a higher-risk phenotype and should not discourage guideline-directed lipid-lowering therapy. Full article

Background: Patients with type 2 diabetes mellitus (T2DM) who present with ST-segment elevation myocardial infarction (STEMI) remain at high risk of adverse remodeling after reperfusion. This observational study examined whether pre-admission glucose-lowering therapy class was associated with six-month left ventricular (LV) reverse remodeling and myocardial work recovery. Methods: We analyzed 253 patients with STEMI, baseline LV ejection fraction ≤ 50%, successful primary PCI, and complete baseline and six-month echocardiography. The primary inferential analyses focused on 75 patients with T2DM, grouped according to pre-admission therapy with SGLT-2 inhibitors, GLP-1 receptor agonists, DPP-4 inhibitors, or conventional therapy; non-diabetic patients were retained as a descriptive reference group. Clinical outcome, propensity-score, subgroup, and mediation analyses were considered exploratory because of small subgroup and event counts. Results: SGLT-2 inhibitor and GLP-1 receptor agonist exposure was associated with larger improvements in LVEF, LV volumes, and global work efficiency than DPP-4 inhibitors or conventional therapy. Crude MACE rates were highest in the conventional-therapy group, but event estimates were imprecise and confounded by baseline risk, revascularization status, and discharge therapy. Conclusions: In patients with T2DM recovering from STEMI, pre-admission exposure to SGLT-2 inhibitors and, to a lesser extent, GLP-1 receptor agonists was associated with more favorable structural and myocardial work recovery. These hypothesis-generating findings should be interpreted as associations and require confirmation in adequately powered prospective studies. Full article

Background/Objectives: Inflammation plays a central role in the pathophysiology and prognosis of non-ST-segment elevation myocardial infarction (NSTEMI). This study aimed to investigate the clinical and prognostic significance of the Cumulative Inflammatory Index (IIC) in patients with NSTEMI. Methods: This single-center, retrospective study included 2274 individuals, comprising 1172 patients with NSTEMI and 1102 angiographic controls without acute coronary syndrome or obstructive coronary artery disease. IIC was calculated using mean corpuscular volume, red cell distribution width, neutrophil count, and lymphocyte count. The primary outcome was 360-day all-cause mortality in the NSTEMI cohort. Logistic regression, receiver operating characteristic curve analysis, and DeLong testing were performed. Results: Patients with NSTEMI had significantly higher IIC values than controls [9.08 (4.05–15.03) vs. 1.90 (1.45–2.89), p < 0.001]. Among NSTEMI patients, non-survivors had significantly higher IIC levels than survivors [14.25 (8.56–26.59) vs. 8.57 (3.73–14.06), p < 0.001]. In multivariable logistic regression analysis, IIC remained independently associated with 360-day all-cause mortality after adjustment for age, diabetes mellitus, estimated glomerular filtration rate, hemoglobin, albumin, and C-reactive protein (OR: 1.045, 95% CI: 1.029–1.060; p < 0.001). IIC showed a modestly higher area under the curve among the evaluated indices (AUC: 0.704). Conclusions: IIC was significantly elevated in patients with NSTEMI and was independently associated with 360-day all-cause mortality. IIC may serve as a simple adjunctive marker for risk stratification in patients with NSTEMI. Full article

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. Full article

Background: The triglyceride–glucose (TyG) index has emerged as a simple surrogate marker of insulin resistance and metabolic disruption. In the context of ST-elevation myocardial infarction (STEMI), such disturbances have been associated with adverse cardiovascular outcomes, more complex angiographic profiles, and microvascular complications. However, data on the association between TyG and intracoronary thrombus burden (TB) in STEMI remain limited. Methods: In this prospective observational study, we included consecutive STEMI patients treated with primary percutaneous coronary intervention (pPCI). The TyG index was calculated using the following formula: ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2]. TB was graded according to the modified thrombolysis in myocardial infarction (mTIMI) thrombus classification score after restoration of antegrade flow with a wire or small balloon when the culprit vessel was initially totally occluded. Patients were categorized as low-TB (LTB; mTIMI grades 1–3) and high-TB (HTB; mTIMI grade 4). The primary outcome was HTB; secondary outcomes were distal embolization and no-reflow. Associations between TyG and outcomes were assessed using univariable and multivariable logistic regression, restricted cubic spline analysis, and receiver operating characteristic (ROC) curves to evaluate incremental predictive value. Results: A total of 309 patients were analyzed. The TyG index was significantly higher in the HTB group compared with the LTB group (9.12 ± 0.62 vs. 8.92 ± 0.64, p = 0.004). In a stepwise multivariable model, TyG remained independently associated with HTB (adjusted odds ratio = 1.61; 95% confidence interval: 1.11–2.37; p = 0.014). Adding TyG to a baseline clinical model only numerically improved discrimination for HTB, as reflected by a small increase in ROC area under the curve. Restricted cubic spline analysis demonstrated a monotonic rise in the probability of HTB with higher TyG values. Higher TyG also showed non-significant trends toward increased odds of distal embolization and no-reflow. Conclusions: The TyG index was independently associated with HTB in STEMI patients undergoing pPCI and may serve as an accessible adjunctive marker for incremental risk stratification beyond conventional clinical and angiographic factors. Full article

Non-ST-segment elevation myocardial infarction (NSTEMI) has become the predominant form of acute coronary syndrome (ACS) and is frequently associated with multivessel coronary artery disease (MVD). Patients presenting with NSTEMI and MVD represent a particularly high-risk population characterized by advanced age, comorbidities, and an increased atherosclerotic burden. Although advances in pharmacological therapy and early invasive management have improved prognosis, the optimal revascularization strategy in this setting remains uncertain. In contrast to ST-segment elevation myocardial infarction (STEMI), where randomized controlled trials consistently support complete revascularization, evidence in NSTEMI with MVD is limited and is largely derived from observational studies and registry data. This has generated ongoing debate regarding whether complete revascularization offers superior outcomes compared with culprit-only percutaneous coronary intervention (PCI), and whether non-culprit lesions should be treated during the index procedure (immediate strategy) or in a staged manner. Current data suggest that complete PCI is generally associated with reduced recurrent ischemia, reinfarction, and repeat revascularization, with potential long-term survival benefits. However, patient comorbidities, lesion complexity, and procedural risk continue to influence outcomes, highlighting the importance of individualized decision-making. This narrative review synthesizes contemporary evidence on PCI-based revascularization strategies in NSTEMI with MVD, focusing on two central aspects: the extent of revascularization (complete versus incomplete) and the timing of intervention (single-stage versus staged). By integrating findings from registries, randomized trials and guideline recommendations, the review identifies areas of consensus, persisting uncertainties, and key evidence gaps. Ultimately, it underscores the need for large, dedicated trials to guide practice and optimize outcomes for NSTEMI patients with multivessel coronary disease. Full article

Multivessel coronary artery disease is observed in a substantial proportion of patients presenting with ST-segment elevation myocardial infarction (STEMI) and identifies a higher-risk phenotype characterized by larger atherosclerotic burden, recurrent ischemic events, and greater need for subsequent revascularization. Over the past decade, randomized evidence has progressively shifted the interventional paradigm from culprit-lesion-only primary percutaneous coronary intervention (PCI) toward complete revascularization in hemodynamically stable STEMI patients with suitable non-culprit lesions. Nevertheless, several clinically relevant questions remain unresolved, including the optimal criteria for selecting non-culprit lesions, the relative value of angiography, coronary physiology, and intracoronary imaging, the timing of complete revascularization, and the management of patients presenting with cardiogenic shock. Angiography-guided complete revascularization has the strongest evidence base, while physiology-guided approaches may reduce unnecessary PCI but have not demonstrated superiority over angiography-guided strategies in direct randomized comparisons. Intracoronary imaging offers unique information on plaque vulnerability and PCI optimization, although dedicated outcome trials in STEMI remain limited. The timing of complete revascularization has also evolved, with contemporary trials supporting early treatment in selected stable patients but not establishing a universal immediate strategy. This review summarizes current evidence, unresolved controversies, and emerging directions regarding strategies and timing of complete revascularization in STEMI patients with multivessel disease. Full article

Background/Objectives: People with non-ST-segment elevation myocardial infarction (NSTEMI) with an occluded culprit vessel represent a unique subset of patients; however, their long-term outcomes remain unclear. This study aimed to compare 5-year mortality between NSTEMI patients treated with percutaneous coronary intervention (PCI) based on TIMI flow states in the culprit vessel on presentation (TIMI 0-1 compared to TIMI 2-3). Methods: A retrospective analysis of prospectively collected data of all NSTEMI patients who underwent PCI from 2012 to 2019 at a tertiary cardiac center (The Freeman Hospital, Newcastle-Upon-Tyne, UK) with follow up for 5 years until January 2024. Patients were identified from the database and categorized based on pre-procedural TIMI flow in the culprit vessel. A propensity score was used to pair TIMI 0-1 patients with a matched cohort of TIMI 2-3 patients. The primary outcome was 5-year all-cause mortality. Results: A total of 775 patients with TIMI 0-1 flow were matched with 750 patients who had TIMI 2-3 flow. Patients with TIMI 0-1 flow were more likely to have transient ST elevation (24% vs. 18%, p < 0.001) or Q waves (4% vs. 1%, p < 0.001) compared with patients who had TIMI 2-3 flow. They were also more likely to have moderately to severely impaired left ventricular systolic function compared with patients with TIMI 2-3 flow (21% vs. 16%, p = 0.01). In-hospital mortality (1.2% vs. 1.2%, p = NS), 1-year mortality (5% vs. 6.9%, p = NS), and 5-year mortality (16% vs. 18%, p = 0.34) were not significantly different between the two groups. The use of glycoprotein IIb/IIIa antagonists was associated with lower mortality, HR 0.64 (0.46 to 0.87). Conclusions: NSTEMI patients with occluded culprit vessels who underwent PCI had similar in-hospital and long-term outcomes to patients with patent culprit vessels. The use of glycoprotein IIb/IIIa inhibitors appears to be associated with lower mortality. Full article

Background: Hematological parameters derived from complete blood count (CBC) are inexpensive and widely available markers with potential utility in risk stratification of acute coronary syndrome (ACS). However, their incremental prognostic value when used alongside contemporary risk stratification tools such as the Troponin-only Manchester Acute Coronary Syndrome (T-MACS) score remains unclear. Methods: In this prospective, single-center cohort study, 521 patients presenting with non-ST-segment elevation myocardial infarction (NSTEMI) or unstable angina were enrolled. Admission CBC parameters (white blood cell count, neutrophils, monocytes, red cell distribution width, mean platelet volume) and derived inflammatory indices (neutrophil-to-lymphocyte ratio, white blood cell-to-mean platelet volume ratio, lymphocyte-to-monocyte ratio, mean platelet volume-to-platelet ratio, and red cell distribution width-to-platelet ratio) were recorded. T-MACS risk scores were calculated, and patients were followed for 30-day major adverse cardiac events (MACE), mortality, and coronary interventions. Associations were assessed using univariate and multivariate logistic regression analyses. Results: Patients experiencing 30-day MACE or mortality had significantly higher white blood cell counts, neutrophil counts, and WMR values (all p < 0.05). Several hematological indices showed significant associations with T-MACS risk categories. In multivariate analysis, intermediate- and high-risk T-MACS classifications independently predicted 30-day MACE (OR 4.49, 95% CI:1.46–13.77, p = 0.009; OR 9.34, 95% CI:3.00–29.03, p < 0.001, respectively), whereas white blood cell count, neutrophil count, and WMR did not demonstrate independent prognostic value beyond T-MACS classification. Conclusions: Admission white blood cell count, neutrophil count, and WMR are associated with short-term adverse outcomes and T-MACS risk severity in patients with NSTE-ACS. However, these markers do not provide additional prognostic value beyond T-MACS classification. These findings suggest that CBC-derived inflammatory markers primarily reflect disease severity rather than incremental prognostic information in the contemporary high-sensitivity troponin era. Full article

Background: Early assessment of myocardial injury severity at presentation remains challenging in acute myocardial infarction (AMI). Complete blood count (CBC)-derived inflammatory indices may provide accessible adjunctive biomarkers reflecting early systemic inflammatory activation associated with myocardial injury. This study evaluated the association and discriminative performance of CBC-derived inflammatory indices for presentation-time myocardial injury severity. Methods: This retrospective study included 252 patients with AMI. CBC-derived inflammatory indices, including the neutrophil-to-lymphocyte ratio (NLR) and neutrophil-to-lymphocyte × platelet ratio (NLPR), were calculated from blood samples obtained at presentation (0 h). Correlation analysis, multivariable linear regression, logistic regression, incremental model analysis, and receiver operating characteristic (ROC) analysis were performed to assess associations with high-sensitivity Troponin T (hs-Troponin T) levels and high myocardial injury, defined as the highest hs-Troponin T tertile. Results: Both log NLR and log NLPR showed significant positive correlations with log hs-Troponin T (ρ = 0.422 and 0.396, respectively; p < 0.001). In multivariable linear regression adjusted for clinical variables and AMI subtype, log NLR (B = 0.88, p < 0.001) and log NLPR (B =0.77, p < 0.001) remained independently associated with log hs-Troponin T. Incremental model analysis demonstrated significant increases in explanatory performance after addition of log NLR (ΔR² = 0.137) and log NLPR (ΔR² = 0.121, p < 0.001). In logistic regression, log NLR (adjusted OR 2.77, 95% CI 1.65–4.66) and log NLPR (adjusted OR 2.46, 95% CI 1.53–3.95) were independently associated with high myocardial injury. ROC analysis demonstrated modest improvement in discrimination after incorporation of inflammatory indices, with AUC increasing from 0.709 for the baseline clinical model to 0.778 with log NLR and 0.770 with log NLPR. Supplementary reclassification analyses demonstrated improved classification performance. Conclusions: CBC-derived inflammatory indices, particularly NLR and NLPR, were independently associated with presentation-time myocardial injury severity in patients with AMI, even after adjustment for AMI subtype. Although improvements in ROC-based discrimination were modest, supplementary reclassification analyses suggested incremental value beyond conventional clinical variables and AMI subtype. These findings support the potential utility of CBC-derived inflammatory indices for early assessment of myocardial injury during AMI presentation. Full article

Background: Chronic hepatitis C virus (HCV) infection is increasingly recognized as a systemic inflammatory condition associated with accelerated atherosclerosis and adverse cardiovascular outcomes. However, its relationship with coronary anatomical complexity in patients presenting with ST-segment elevation myocardial infarction (STEMI) remains insufficiently defined. Aims: This study aimed to evaluate the association between chronic HCV infection and coronary artery disease complexity assessed by the SYNTAX score in STEMI patients undergoing primary percutaneous coronary intervention (pPCI) and to investigate its relationship with in-hospital mortality. Methods: In this retrospective single-center cohort study, 1647 STEMI patients treated with pPCI between January 2021 and December 2025 were analyzed; 106 (6.4%) were HCV-positive. Propensity score matching based on baseline demographic and cardiovascular risk factors yielded 105 matched pairs. The primary endpoint was the SYNTAX score, while the secondary endpoint was in-hospital all-cause mortality. Results: HCV-positive patients demonstrated significantly higher SYNTAX scores than HCV-negative patients before (19.5 ± 8.5 vs. 15.8 ± 9.6; p < 0.001) and after propensity score matching (19.4 ± 8.5 vs. 15.6 ± 9.2; p = 0.002). Coronary artery bypass grafting referral was more frequent among HCV-positive patients both before (11.3% vs. 5.3%; p = 0.010) and after matching (11.4% vs. 2.9%; p = 0.016). Notably, HCV-positive patients exhibited higher coronary anatomical complexity despite lower total and LDL cholesterol levels. In multivariable analyses, HCV positivity remained independently associated with higher SYNTAX scores in both unmatched and matched cohorts. In-hospital mortality rates were comparable between groups, and HCV positivity was not independently associated with mortality. Conclusions: Chronic HCV infection was independently associated with increased coronary anatomical complexity in STEMI patients undergoing pPCI, suggesting a relationship with a more diffuse and structurally complex atherosclerotic phenotype rather than short-term in-hospital outcomes. These findings support the concept of HCV infection as a non-traditional cardiovascular risk factor associated with adverse coronary vascular remodeling. Full article

Background: Myocardial fibrosis plays a key role in adverse remodeling after ST-segment-elevated myocardial infarction (STEMI). The effect of sodium–glucose cotransporter 2 inhibitors (SGLT2is) on myocardial fibrosis deposition among patients with STEMI undergoing primary percutaneous coronary intervention (pPCI) is unclear. Objectives: To assess the effects of SGLT2is on myocardial fibrosis among patients with STEMI undergoing pPCI. Methods: Patients with STEMI undergoing pPCI with left ventricular ejection fraction ≤ 50% were randomized to dapagliflozin 10 mg or placebo. The primary endpoint was cardiac magnetic resonance (CMR)-derived 6-month changes in remote myocardium extracellular volume (ECV) fraction from baseline. Secondary endpoints included changes in CMR-derived myocardial volumes, change in serum fibrosis biomarker levels, and adverse events. Multivariable adjustment for infarction location and diabetes status was performed as sensitivity. The study was halted prematurely due to slow recruitment. Results: Fifty-two patients underwent randomization between May 2021 and April 2024 and completed follow-up. At 6 months, dapagliflozin resulted in a non-significant reduction in ECV change compared to placebo (−0.39 [4.7] vs. 1.43 [5.7]; difference: −1.82 [−4.86; 1.23]; p-value = 0.235) while also leding to a higher degree of reduction in N-terminal pro-peptide of type III collagen (−177.0 pg/mL [416.1] vs. 3.6 pg/mL [553.8]; p-value = 0.208). No significant differences in other biomarkers or adverse events were noted in the main analysis. After adjustment, dapagliflozin was associated with increased reduction in left ventricular end-systolic volume (−4.02 mL [7.4] vs. 0.10 mL [10.1]; difference: −4.92 [−9.8; −0.1]; p-value = 0.047). Conclusions: In STEMI patients undergoing pPCI, dapagliflozin did not result in a significant reduction in ECV or biomarkers of fibrosis at 6 months. Full article

Colchicine has emerged as a prominent anti-inflammatory candidate in cardiovascular medicine, supported by a hierarchy of evidence spanning chronic and acute coronary syndromes, post-myocardial infarction care, revascularization, atrial fibrillation, pericardial disease, heart failure, peripheral arterial disease, and mechanistic translational models. Across this literature, the most mature study architecture and the strongest clinical support are derived from completed randomized trials in chronic coronary disease and secondary prevention, where colchicine has been shown to prevent major cardiovascular events (MACEs) when added to standard of care. The clearest clinical benefits are the reduction in non-fatal ischemic events in atherosclerotic disease, prevention of recurrent pericarditis and postoperative atrial fibrillation, and attenuation of inflammatory and plaque-related markers. By contrast, mixed or lower-tier evidence renders its application less consistent in acute coronary syndromes, ST-elevation MI (STEMI), percutaneous coronary intervention (PCI)-related hard outcomes, and heart failure, while a definitive mortality benefit has not been demonstrated. Overall, colchicine is best understood as a targeted clinical adjunct whose value depends heavily on precise indication, timing, dose, gastrointestinal tolerability, and the maturity of the supporting evidence. Full article

Background and Objectives: The electrocardiogram (ECG)–based STEMI/NSTEMI classification determines the urgency of invasive management in acute myocardial infarction. However, it often underestimates the presence of acute coronary occlusion (ACO) in patients presenting with non-ST-elevation myocardial infarction (NSTEMI). Artificial intelligence (AI)-assisted ECG interpretation has emerged as a potential tool to improve early recognition of ACO. This study aimed to determine the prevalence of ACO among NSTEMI patients, to compare clinical characteristics between patients with and without ACO and to explore the potential role of AI in earlier recognition of ACO. Materials and Methods: All consecutive NSTEMI patients undergoing coronary angiography between September 2022 and December 2024 were included. Contrary to other studies that included TIMI flow grades 0–1, 0–2, or 0–3, ACO in our study was defined strictly as a culprit lesion with TIMI flow grade 0 at index coronary angiography. Clinical characteristics were compared between ACO and non-ACO patients. Admission 12-lead ECGs from ACO patients were retrospectively analysed using a clinically validated AI-based ECG interpretation model and classified according to the urgency of invasive management. Results: Among 520 NSTEMI patients, 49 (9.4%) had angiographically confirmed ACO. Within the non-ACO group, 7.0% of patients had TIMI flow grade 1 on index coronary angiography (6.3% of the total population). Therefore, 15.7% of the study population had TIMI flow grade 0/1. ACO patients were younger (60.9 ± 12.8 vs. 66.3 ± 12.0 years, p = 0.0065). Clinical characteristics did not differ between the groups, except for dyslipidemia, which was more prevalent in non-ACO patients (38.8% vs. 53.9%, p = 0.043). Revascularisation rates were higher in the ACO group (93.9% vs. 82.2%, p = 0.037). Culprit vessel distribution differed markedly between the groups (p < 0.0001). In multivariable logistic regression analysis, age was independently associated with ACO (OR 0.96, 95% CI 0.93–0.99, p = 0.007). AI-assisted ECG analysis was performed in 42 ACO patients; 57.1% were classified as requiring immediate invasive management. Conclusions: A significant proportion of NSTEMI patients have ACO. AI-assisted ECG interpretation may support earlier identification of ACO, although its clinical impact requires further validation. Future studies are warranted to confirm these findings. Full article

Background and Objectives: Residual coronary anatomical complexity following culprit-lesion-only percutaneous coronary intervention (PCI) remains a major determinant of clinical outcomes in patients with multivessel coronary artery disease (CAD). Platelet distribution width (PDW), a marker of platelet heterogeneity and activation, has been associated with adverse cardiovascular outcomes; however, its relationship with post-procedural residual disease burden remains unclear. This study aimed to evaluate the association between PDW and residual SYNTAX (Synergy between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) score and to determine its incremental predictive value beyond established clinical variables. Materials and Methods: In this retrospective, single-center study, 140 patients with multivessel CAD undergoing culprit-lesion-only PCI followed by planned staged revascularization were included. Clinical presentation was categorized as chronic coronary syndrome (CCS), non-ST-elevation myocardial infarction (NSTEMI), or ST-elevation myocardial infarction (STEMI). Residual SYNTAX score was calculated after the index procedure, and patients were stratified into low (≤22) and high (≥23) groups. Associations between PDW and residual SYNTAX score were assessed using correlation and regression analyses. Model discrimination and incremental predictive value were evaluated using ROC analysis, hierarchical logistic regression, and reclassification metrics. Nonlinear relationships were explored using restricted cubic spline analysis, and clinical utility was assessed by decision curve analysis. Results: PDW was significantly correlated with residual SYNTAX score (Spearman ρ = 0.503, p < 0.001) and increased progressively across SYNTAX severity strata and clinical presentation groups. In multivariable analysis, PDW remained independently associated with high residual SYNTAX score (OR 1.38, 95% CI 1.07–1.82, p = 0.016). The addition of PDW to a hierarchical clinical model significantly improved model performance (ΔR² = 0.049, p = 0.012). Although the improvement in area under the curve (AUC) was modest, reclassification analyses demonstrated significant net reclassification and discrimination improvements. Spline analysis revealed a nonlinear relationship, with a marked increase in risk beyond PDW levels of approximately 13 fL. Decision curve analysis confirmed the clinical utility of PDW across a range of threshold probabilities. Conclusions: PDW is independently associated with post-procedural coronary anatomical complexity and provides incremental predictive value beyond established clinical variables. However, PDW should be interpreted as a biomarker reflecting platelet heterogeneity within a thromboinflammatory context, without the ability to distinguish between acute and chronic components. Full article