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Results from multiple electrode aggregometry (MEA) may vary according to pre-analytic factors. This study aimed to analyze the association of time from blood draw to MEA in patients undergoing percutaneous coronary intervention (PCI). In this observational single-center cohort study, platelet aggregation (aggregation units, U) was quantified by MEA (Multiplate Analyzer) after stimulation with adenosine diphosphate (ADP; final concentration [Fc] 6.4 μM), thrombin receptor activating peptide (TRAP; Fc 32 μM), or arachidonic acid (AA; Fc 0.5 mM) in patients treated with ASA and clopidogrel following PCI. High on-clopidogrel platelet reactivity (HPR) was defined as ADP-induced platelet aggregation ≥ 46 U. The manufacturer recommends performing the analysis within 30–180 min after blood draw. Patients were grouped according to the time from blood draw to MEA: 30–180 min, 180 min. Platelet function of 273 patients with coronary artery disease undergoing PCI with dual antiplatelet therapy was analyzed. The median age was 72 years (interquartile range, IQR 62–79) and 179 (66%) were male. Median ADP-, TRAP-, and AA-induced aggregation was 25 (IQR 18–36) U, 79 (IQR 63–96) U, and 12 (IQR 7–18) U, respectively. For those analyzed within 30–180 min from blood draw, no significant correlation of time from blood draw to MEA was observed 1) ADP (r = − 0.04, p = 0.51); 2) TRAP (r = − 0.06, p = 0.32); 3) AA (r = − 0.03, p = 0.67). In patients undergoing percutaneous coronary intervention and treated with dual antiplatelet therapy, the time from blood draw to multiple electrode aggregometry does not correlate with ADP- induced aggregation when the measurement occurred within the recommended time interval of 30–180 min after blood draw.

Introduction Patients with atrial fibrillation (AF) after percutaneous coronary intervention (PCI) receive clopidogrel and direct oral anticoagulation. Platelet inhibition by clopidogrel varies according to CYP2C19 genotype. This study aimed to investigate the association of CYP2C19 genotype with antiplatelet effect of clopidogrel and ischemic and bleeding risk. Methods In this prospective observational study, patients with AF after PCI were grouped according to CYP2C19*2 and *17 diplotypes: *2/non-17* or *2/*2 as reduced metabolizers (RM), non-*2/*17 or *17/*17 as increased metabolizers (IM), and the remaining as normal metabolizers (NM). Platelet aggregation [U] was quantified by multiple electrode aggregometry. The primary outcome was time to death, myocardial infarction, or stroke (MACE) at 6 months. The secondary outcome was time to non-major clinically relevant (NMCR) or major bleedings. Results 156 patients were enrolled between May 2020 and May 2021. The median age was 78 years (interquartile range, IQR 71–82) and 109 (70%) were male. 31 patients (20%) were RM, 74 patients (47%) NM and 51 patients (33%) IM. The median ADP-induced platelet aggregation was not significantly different across these groups (RM: 12.8 [U]; NM: vs. 12.8 [U]; IM: 11.7 [U]; P = 0.39).The primary outcome occurred in 11 (7%) patients (RM: 1 [3%]; NM: 7 [9%]; IM 3[6%]). The secondary outcome occured in 3 RM (10%) and in 20 (16%) with NM + IM subtypes (HR 0.65 [95% CI 0.19–2.18], P = 0.485). Conclusion In this analysis reduced metabolizers were not at excessively increased risk of MACE. A trend for less bleeding was observed in carriers of loss-of-function allele CYP2C19*2.

Background: High on-clopidogrel platelet reactivity (HPR) following percutaneous coronary intervention (PCI) is associated with increased ischemic risk. It is unclear whether conventional definitions of HPR apply to patients with concomitant oral anticoagulation (OAC). This study aimed to compare the performance of multiple platelet aggregometry (MEA) and thrombelastography (TEG) to detect HPR in patients with atrial fibrillation (AF) and indication for an OAC. Methods: In this observational single-center cohort study, MEA and TEG were performed in patients with AF with an indication for OAC on day 1 to 3 after PCI. The primary outcome was HPR as assessed by MEA (ADP area under the curve ≥ 46 units [U]) or TEG (MAADP ≥ 47 mm), respectively. The secondary exploratory outcomes were a composite of all-cause death, myocardial infarction (MI) or stroke and bleeding, as defined by the International Society on Thrombosis and Hemostasis, at 6 months. Results: Platelet function of 39 patients was analyzed. The median age was 78 (interquartile range [IQR] was 72–82) years. 25 (64%) patients were male, and 19 (49%) presented with acute coronary syndrome. All patients received acetylsalicylic acid and clopidogrel prior to PCI. Median (IQR) ADP-induced aggregation, MAADP, TRAP-induced aggregation, and MAthrombin were 9 (6–15) U, 50 (43–60) mm, 54 (35–77) U and 65 (60–67) mm, respectively. The rate of HPR was significantly higher if assessed by TEG compared with MEA (25 [64%] vs. 1 [3%]; p < 0.001). Within 6 months, four (10%) deaths, one (3%) MI and nine (23%) bleeding events occurred. Conclusion: In patients with AF undergoing PCI, the rates of HPR detected by TEG were significantly higher compared with MEA. Conventional cut-off values for HPR as proposed by consensus documents may need to be re-evaluated for this population at high ischemic and bleeding risk. Further studies are needed to assess the association with outcomes.

COVID-19 is a viral prothrombotic respiratory infection. Heparins exert antithrombotic and anti-inflammatory effects, and might have antiviral properties. We aimed to investigate whether thromboprophylaxis with enoxaparin would prevent untoward hospitalisation and death in symptomatic, but clinically stable outpatients with COVID-19.OVID was a randomised, open-label, parallel-group, investigator-initiated, phase 3 trial and was done at eight centres in Switzerland and Germany. Outpatients aged 50 years or older with acute COVID-19 were eligible if they presented with respiratory symptoms or body temperature higher than 37·5°C. Eligible participants underwent block-stratified randomisation (by age group 50-70 vs70 years and by study centre) in a 1:1 ratio to receive either subcutaneous enoxaparin 40 mg once daily for 14 days versus standard of care (no thromboprophylaxis). The primary outcome was a composite of any untoward hospitalisation and all-cause death within 30 days of randomisation. Analysis of the efficacy outcomes was done in the intention-to-treat population. The primary safety outcome was major bleeding. The study was registered in ClinicalTrials.gov (NCT04400799) and has been completed.At the predefined formal interim analysis for efficacy (50% of total study population), the independent Data Safety Monitoring Board recommended early termination of the trial on the basis of predefined statistical criteria having considered the very low probability of showing superiority of thromboprophylaxis with enoxaparin for the primary outcome under the initial study design assumptions. Between Aug 15, 2020, and Jan 14, 2022, from 3319 participants prescreened, 472 were included in the intention-to-treat population and randomly assigned to receive enoxaparin (n=234) or standard of care (n=238). The median age was 57 years (IQR 53-62) and 217 (46%) were women. The 30-day risk of the primary outcome was similar in participants allocated to receive enoxaparin and in controls (8 [3%] of 234 vs 8 [3%] of 238; adjusted relative risk 0·98; 95% CI 0·37-2·56; p=0·96). All hospitalisations were related to COVID-19. No deaths were reported during the study. No major bleeding events were recorded. Eight serious adverse events were recorded in the enoxaparin group versus nine in the control group.These findings suggest thromboprophylaxis with enoxaparin does not reduce early hospitalisations and deaths among outpatients with symptomatic COVID-19. Futility of the treatment under the initial study design assumptions could not be conclusively assessed owing to under-representation of older patients and consequent low event rates.SNSF (National Research Programme COVID-19 NRP78: 198352), University Hospital Zurich, University of Zurich, Dr-Ing Georg Pollert (Berlin), Johanna Dürmüller-Bol Foundation.

Background: Guidelines consider platelet function testing to guide dual antiplatelet therapy (DAPT) de-escalation in selected patients. On-clopidogrel platelet reactivity as measured by multiple electrode aggregometry (MEA) varies according to patients′ characteristics but may also depend on pre-analytic factors. Purpose: This study aimed to analyze the association of time from blood draw to MEA results in patients undergoing percutaneous coronary intervention (PCI). Methods: In this observational single center cohort study, in patients undergoing PCI, all patients received DAPT with ASA and clopidogrel. Platelet aggregation (aggregation units, U) was quantified by MEA (Multiplate Analyzer) after stimulation with adenosine diphosphate (ADP; 6.4 μM in patients treated with ASA and clopidogrel following PCI. High on-clopidogrel platelet aggregation (HPR) was defined as ≥46 U. The manufacturer recommends performing the analysis within 30-180 min after blood draw. Thus, patients were grouped according to the time from blood draw to MEA: 1) 30-180 min 2) 180 min. Results: Platelet function of 273 patients with coronary artery disease undergoing PCI with DAPT were analyzed. The median age was 72 years (interquartile range, IQR 62-79) and 179 (66%) were male. Median ADP-induced aggregation was 25 (IQR 18-36) U. HPR was observed in 34 patients (12%). Median time to MEA was 65 (IQR 45-113) min and 245 measurements (90%) were performed within 30-180 min as recommend by the manufacturer of the aggregometer. Compared with measurements performed within the manufacturers′ recommendations (25 [IQR 18-36] U, median ADP-induced aggregation was not significantly different if performed outside these recommendations (180min: 25 [IQR 21-40] U, p=0.31). For those analyzed within 30-180 min from blood draw, no relevant correlation of time from blood draw to MEA with ADP-induced platelet aggregation was observed (r= - 0.04; p=0.51). Conclusion: In patients undergoing percutaneous coronary intervention and treated with dual antiplatelet therapy, the time from blood draw to multiple electrode aggregometry does not correlate with ADP-induced aggregation.

Introduction: Dronedarone was introduced as a promising Amiodarone-analogue with a good safety profile and comparing efficacy. Because of a two-fold increase in all-cause death, stroke, myocardial infarction, and hospitalization in permanent AF, recommendations regarding the use of dronedarone therapy are limited. We aimed to evaluate the risk of periprocedural thromboembolic events (TE) in a group of patients who underwent catheter ablation for AF under on-going dronedarone therapy. Methods: We retrospectively studied 2254 AF cases who underwent catheter ablation between Jan 2011 and May 2017. A group of 145 cases out of the above cohort (mean age 65 yrs; male 54%; CHADSVASc >2 on 51% of the cases; Persistent AF 21%) was under dronedarone at the time of catheter ablation. We compared the dronedarone (DG) vs non-dronedarone group (nDG) in terms of periprocedural TE, specifically transient ischemic attack and stroke. To assess the impact of other possible explanatory variables we performed a multivariate regression analysis with interaction terms. All patients were under optimal oral anticoagulation at the time of catheter ablation. Results: DG showed a significantly higher frequency of 2,06 % periprocedural TE compared to 0.5% in nDG (p=0,024). Significant predictors of TE in DG were found to be age (OR 2,7 p=0,036), persistent AF (OR 3,6 p=0,036), NYHA class at the time of catheter ablation (OR 2,35 p=0,006) and left ventricular systolic function (OR 1,37 p= 0,05).Intraprocedural median ACT (OR 1,04 p=0,024) and electrical cardioversion (OR 10,3 p= 0,003) were the two significant intraprocedural predictors for stroke among patients on Dronedarone at the time of pulmonary vein isolation. Not predictive for periprocedural stroke were the type of catheter ablation technique, gender, HASBLEED score and spontaneous echo contras in left atrium. There was a significantly higher risk of stroke in DG patients under Phenprocoumon vs the ones on NOACs (OR 6, p= 0,047). CHADSVasc > 2 showed a trend in increasing the risk for stroke among DG patients (OR 3,1 p=0,07). Conclusions: Dronedarone therapy is associated with an increased risk for stroke in patients undergoing catheter ablation, with higher risk among the elderly, persistent AF, and heart failure patients.

Introduction: On-clopidogrel platelet reactivity (PR) is associated with thrombotic and bleeding risk in patients undergoing percutaneous coronary intervention (PCI). Patient-related factors affect the level of PR. Patients with atrial fibrillation (AF) undergoing PCI are treated concomitantly with oral anticoagulants (OAC) potentially interacting with platelet function. This study aimed to investigate the association of PR with demographic and clinical characteristics in these patients. Methods: In this single-centre prospective observational cohort study, patients with AF with an indication for OAC were enrolled during hospitalization after PCI with clopidogrel. TRAP- and ADP- induced PR (TRAP 32 μM, ADP 6.4 μM) were assessed by multiple electrode aggregometry. ADP-induced PR was normalized to TRAP-induced PR (r-ADP-agg). Results: 159 patients were enrolled between May 2020 and May 2021. The median age was 78 years (interquartile range, IQR 72-82), 112 (70%) were male and 39 (25%) presented with ACS. 68 (43%) presented with chronic kidney disease (CKD), defined as GFR Conclusions: In this patient cohort the association of on-clopidogrel PR as assessed by multiple electrode aggregometry with patient related factors was weak and most pronounced for chronic kidney disease.

In women a higher risk of instent restenosis is suggested due to an increased incidence of diabetes and smaller coronary arteries. Bioresorbable vascular scaffolds (BVS) may have the potential of both repair and healing of the diseased vessel wall, but due to its thick struts (157 μm) the anti