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.

Her AY, et al. Yonsei Med J. 2022 May;63(5):413-421. https://doi.org/10.3349/ymj.2022.63.5.413

Background and Aims: Platelet-fibrin clot strength (PFCS) is linked to major adverse cardiovascular event (MACE) risk. However, the association between PFCS and platelet reactivity and their prognostic implication remains uncertain in patients undergoing percutaneous coronary intervention (PCI). Methods: In PCI-treated patients (n = 2512) from registry data from January 2010 to November 2018 in South Korea, PFCS using thromboelastography and platelet reactivity using VerifyNow were measured. High PFCS (PFCSHigh) was defined as thromboelastography maximal amplitude ≥ 68 mm, and high platelet reactivity (HPR) was defined as >208 P2Y12 reaction units. Patients were stratified into four groups according to maximal amplitude and P2Y12 reaction unit levels: (i) normal platelet reactivity (NPR)-PFCSNormal (31.8%), (ii) HPR-PFCSNormal (29.0%), (iii) NPR-PFCSHigh (18.1%), and (iv) HPR-PFCSHigh (21.1%). Major adverse cardiovascular event (all-cause death, myocardial infarction, or stroke) and major bleeding were followed up to 4 years. Results: High platelet reactivity and PFCSHigh showed an additive effect for clinical outcomes (log-rank test, P < .001). Individuals with NPR-PFCSNormal, NPR-PFCSHigh, HPR-PFCSNormal, and HPR-PFCSHigh demonstrated MACE incidences of 7.5%, 12.6%, 13.4%, and 19.3%, respectively. The HPR-PFCSHigh group showed significantly higher risks of MACE compared with the NPR-PFCSNormal group [adjusted hazard ratio (HRadj) 1.89; 95% confidence interval (CI) 1.23–2.91; P = .004] and the HPR-PFCSNormal group (HRadj 1.60; 95% CI 1.12–2.27; P = .009). Similar results were observed for all-cause death. Compared with HPR-PFCSNormal phenotype, NPR-PFCSNormal phenotype was associated with a higher risk of major bleeding (HRadj 3.12; 95% CI 1.30–7.69; P = .010). Conclusions: In PCI patients, PFCS and platelet reactivity demonstrated important relationships in predicting clinical prognosis. Their combined assessment may enhance post-PCI risk stratification for personalized antithrombotic therapy.

Purpose: Non-adherence to medications can be classified as unintentional and intentional. The aim of this study was to establish the major determinants of each non-adherence in myocardial infarction (MI). We also evaluated the effects of non-adherences on healthy behaviors. Materials and Methods: We enrolled 510 patients >1 year after MI. Nonadherences classified as unintentional or intentional were measured by a self-reported questionnaire. Polynomial and multiple regression analysis were performed to evaluate the determinant of each type of nonadherences. Results: Among patients with nonadherence, 263 (70.7%) patients were unintentionally non-adherent while 109 (29.3%) patients were intentionally non-adherent. Psychological belief and attitude were important in unintentional non-adherence (Exp(β) = 0.917, p = 0.050 for anxiety; Exp(β) = 1.191, p = 0.001 for concerns). Beliefs about medications were the strongest determinant of intentional non-adherence (Exp(β) = 0.812, p < 0.001 for necessity; Exp(β) = 1.421, p < 0.001 for concerns). Anxiety was important determinant of intentional non-adherence (Exp(β) = 0.889, p = 0.015). Conclusion: Psychological factors and beliefs about medication were important determinants of both types of non-adherence. Combined approaches targeting the beliefs about medications and psychological distress are needed to improve drug adherence in patients with MI.

A 48-year-old female patient underwent a heart transplantation for acute fulminant myocarditis, following heterologous vaccination with the ChAdOx1 nCoV-19 and Pfizer-BioNTech COVID-19. She had no history of severe acute respiratory syndrome coronavirus-2 infection. She did not exhibit clinical signs or have laboratory findings of concomitant infection before or after vaccination. Heart transplantation was performed because her heart failed to recover with venoarterial extracorporeal oxygenation support. Organ autopsy revealed giant cell myocarditis, possibly related to the vaccines. Clinicians may have to consider the possibility of the development of giant cell myocarditis, especially in patients with rapidly deteriorating cardiac function and myocarditis symptoms after COVID-19 vaccination.

Her AY, et al. Yonsei Med J. 2023 Jun;64(6):359-365. https://doi.org/10.3349/ymj.2022.0633