Atherothrombotic events are influenced by systemic hypercoagulability and fibrinolytic activity. The present study evaluated thrombogenicity indices and their prognostic implications according to disease acuity. From the consecutive patients undergoing percutaneous coronary intervention (PCI), those with thrombogenicity indices (n = 2705) were grouped according to disease acuity [acute myocardial infarction (AMI) vs. non-AMI]. Thrombogenicity indices were measured by thromboelastography (TEG). Blood samples for TEG were obtained immediately after insertion of the PCI sheath, and TEG tracing was performed within 4 h post-sampling. Major adverse cardiovascular events (MACE, a composite of cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke) were evaluated for up to 4 years. Compared with non-AMI patients, AMI patients had higher platelet-fibrin clot strength [maximal amplitude (MA): 66.5 ± 7.8 vs. 65.3 ± 7.2 mm, P < 0.001] and lower fibrinolytic activity [clot lysis at 30 min (LY₃₀): 0.9 ± 1.8% vs. 1.1 ± 1.9%, P < 0.001]. Index AMI presentation was associated with MA [per one-mm increase: odds ratio (OR): 1.024; 95% confidence interval (CI): 1.013–1.036; P < 0.001] and LY₃₀ (per one% increase: OR: 0.934; 95% CI: 0.893–0.978; P = 0.004). The presence of high platelet-fibrin clot strength (MA ≥68 mm) and low fibrinolytic activity (LY₃₀ < 0.2%) was synergistically associated with MACE occurrence. In the multivariable analysis, the combined phenotype of ‘MA ≥ 68 mm’ and ‘LY₃₀ < 0.2%’ was a major predictor of post-PCI MACE in the AMI group [adjusted hazard ratio (HR): 1.744; 95% CI: 1.135–2.679; P = 0.011], but not in the non-AMI group (adjusted HR: 1.031; 95% CI: 0.499–2.129; P = 0.935). AMI occurrence is significantly associated with hypercoagulability and impaired fibrinolysis. Their combined phenotype increases the risk of post-PCI atherothrombotic event only in AMI patients. These observations may support individualized therapy that targets thrombogenicity for better outcomes in patients with AMI. Gyeongsang National University Hospital (G-NUH) Registry, NCT04650529. The association between thrombogenicity and AMI occurrence, and their prognostic implications for long-term cardiovascular outcomes were investigated. Abbreviations: AMI, acute myocardial infarction; HR, hazard ratio; LY30, percentage of the clot that has lysed 30 minutes after the time of maximum amplitude; MA, maximum amplitude; MACE, major adverse cardiovascular events; OR, odds ratio; PCI, percutaneous coronary intervention; TEG, thromboelastography.

Objectives: To evaluate the effect of clopidogrel vs. aspirin monotherapy on vascular function and hemostatic measurement. Background: Monotherapy with P2Y₁₂ receptor inhibitor vs. aspirin can be a useful alterative to optimize clinical efficacy and safety in high-risk patients with coronary artery disease (CAD). Methods: We performed a randomized, open-label, two-period crossover study in stented patients receiving at least 6-month of dual antiplatelet therapy (DAPT). Thirty CAD patients with moderate-to-high ischemic risk were randomly assigned to receive either 75 mg of clopidogrel or 100 mg of aspirin daily for 4 weeks, and were crossed over to the other strategy for 4 weeks. Vascular function was evaluated with reactive hyperemia-peripheral arterial tonometry (RH-PAT) and brachial-ankle pulse wave velocity (baPWV). Hemostatic profiles were measured with VerifyNow and thromboelastography (TEG). The primary endpoint was the reactive hyperemia index (RHI) during clopidogrel or aspirin monotherapy. Results: Clopidogrel vs. aspirin monotherapy was associated with better endothelial function (RHI: 2.11 ± 0.77% vs. 1.87 ± 0.72%, p = 0.045), lower platelet reactivity (130 ± 64 vs. 214 ± 50 P2Y12 reaction unit [PRU], p < 0.001) and prolonged reaction time (TEG R: 5.5 ± 1.2 vs. 5.1 ± 1.1 min, p = 0.037). In multivariate analysis, normal endothelial function (RHI ≥ 2.1) was significantly associated with clot kinetics (TEG angle ≤ 68 degree) and ‘PRU ≤ 132’. ‘PRU ≤ 132’ was achieved in 46.2% vs. 3.8% during clopidogrel administration vs. aspirin monotherapy (odds ratio 21.4, 95% confidence interval 2.7 to 170.1, p < 0.001). Conclusions: In CAD patients, clopidogrel vs. aspirin monotherapy was associated with better endothelial function, greater platelet inhibition and lower coagulation activity, suggesting pleiotropic effects of clopidogrel on endothelial function and hemostatic profiles.

Background and Aims: Limited data exist on optimal antiplatelet strategies for high-risk patients undergoing complex percutaneous coronary intervention (PCI). This study aimed to investigate the efficacy and safety of tailored antiplatelet treatment with temporal modulation of the intensity of platelet inhibition in patients undergoing complex high-risk PCI. Methods: We randomly assigned 2018 patients with high-risk anatomical or clinical characteristics undergoing complex PCI to a tailored antiplatelet strategy with early escalation (low-dose ticagrelor at 60 mg twice daily plus aspirin 6 months) or dual antiplatelet therapy (clopidogrel plus aspirin for 12 months). The primary outcome was a composite of death from any cause, myocardial infarction, stroke, stent thrombosis, unplanned urgent revascularization, and clinically relevant bleeding (Bleeding Academic Research Consortium Type 2, 3, or 5) at 12 months. Results: The mean age was 64.0 years, 22.6% had left main PCI, 19.5% had complex bifurcation PCI, 84.1% had diffuse long lesions, 93.7% had multivessel PCI, and 36.7% had medically treated diabetes. At 12 months, a primary outcome event occurred in 105 patients (10.5%) assigned to tailored antiplatelet therapy and in 89 patients (8.8%) assigned to dual antiplatelet therapy [hazard ratio, 1.19; 95% confidence interval (CI), 0.90–1.58; P = .21]. The incidence of major ischaemic events appeared to be similar in both groups. The incidence of clinically relevant bleeding at 12 months was 7.2% in the tailored-therapy group and 4.8% in the dual-therapy group (difference, 2.45% points; 95% CI, 0.37–4.53). Conclusions: Among high-risk patients undergoing complex PCI, tailored antiplatelet strategy with early escalation and late de-escalation, as compared with dual antiplatelet therapy, did not decrease the incidence of primary net adverse events at 12 months. Clinical Trial Registration: ClinicalTrials.gov number, NCT03465644.

Amlodipine has a potential to reduce clopidogrel bioactivation through the cytochrome P450 3A4 enzyme in vivo, but the clinical impact of this interaction remains controversial. This randomized, open-label, two-period, crossover study was performed to evaluate the influence of amlodipine on the haemostatic profiles of high-risk patients during clopidogrel treatment. We recruited 40 Asian patients (Male/Female: n = 36/4) receiving clopidogrel (75 mg/day), aspirin (100 mg/day) and rosuvastatin for at least 6 months following percutaneous coronary intervention. Patients were randomly assigned to receive either 5 mg daily amlodipine or not for 2 weeks, and then were crossed over to the other treatment for 2 weeks. Haemostatic measurements were conducted with the VerifyNow assay and thromboelastography (TEG). Primary endpoint was P2Y12 Reaction Units (PRU) during on- versus off-amlodipine treatment. The on-amlodipine strategy showed higher level of PRU compared with the off-amlodipine strategy (176.8 ± 75.4 vs. 150.7 ± 65.5 PRU; ∆mean: 26.1 PRU; ∆95% confidence interval [CI]: 4.5–47.7 PRU; p = 0.019). Platelet-fibrin clot strength measured by TEG was lower during on- versus off-amlodipine treatment (7,712 ± 1,889 vs. 8,559 ± 2,174 dyne/cm²; ∆mean: –847 dyne/cm²; ∆95% CI: –1,632 to –62 dyne/cm²; p = 0.035). After amlodipine discontinuation, 27 patients (67.5%) showed a decrease in PRU, which was associated with ‘PRU ≥ 160 on-amlodipine’ in multivariate analysis (odds ratio: 62.014; 95% CI: 2.302–1670.328; p = 0.014). In conclusion, amlodipine increases platelet reactivity and decreases platelet-fibrin clot strength during clopidogrel treatment. In addition, the effect of amlodipine discontinuation on clopidogrel responsiveness is associated with on-amlodipine platelet reactivity. The authors are solely responsible for the design and conduct of this study, all study analyses, the drafting and editing of the manuscript and its final contents.

Perioperative myocardial infarction (MI) and myocardial injury after noncardiac surgery (MINS) remain major causes of postoperative morbidity and mortality, yet optimal perioperative cardiovascular risk stratification remains challenging. This narrative review examines how cardiovascular imaging and circulating biomarkers may be integrated to improve perioperative risk assessment and to support more individualized preventive strategies in patients undergoing noncardiac surgery. We reviewed major clinical guidelines, landmark perioperative cohort studies, and key investigations addressing coronary computed tomography angiography, coronary calcium burden, natriuretic peptides, and cardiac troponin in the perioperative setting. Available evidence suggests that imaging and biomarkers provide complementary information, with imaging primarily reflecting structural coronary disease burden and biomarkers reflecting myocardial stress, biological vulnerability, and perioperative injury. Such multimodal assessment may refine risk estimation beyond conventional clinical indices alone, particularly in selected intermediate-risk patients or those with uncertain functional capacity. However, important limitations remain. Current evidence is heterogeneous across study populations, testing strategies, and endpoints, and standardized pathways for integrating imaging and biomarkers into routine clinical decision-making are not yet established. In addition, cost-effectiveness, accessibility, and the extent to which improved risk discrimination translates into better perioperative outcomes remain uncertain. Overall, the integration of imaging and biomarkers offers a clinically relevant framework for moving from perioperative risk stratification toward prevention, but its practical implementation and outcome benefit require further prospective validation.

Kim BS, et al. Clin Hypertens. 2026 ;32:e15. https://doi.org/10.5646/ch.2026.32.e15