Prasugrel 60 mg given at the start of a 2-h infusion of cangrelor can provide a sufficient platelet inhibition post-cangrelor. This approach prevents the transient gap in platelet inhibition seen with oral loading after discontinuation of cangrelor. (Impact of Extent of Clopidogrel-Induced Platelet Inhibition during Elective Stent Implantation on Clinical Event Rate - Advanced Loading Strategies [ExcelsiorLOAD2]; DRKS00009739).

Reticulated platelets are associated with impaired antiplatelet response to thienopyridines. It is uncertain whether this interaction is caused by a decreased drug exposure due to high platelet turnover reflected by elevated levels of reticulated platelets or by intrinsic properties of reticulated platelets. This study sought to investigate if the impact of reticulated platelets on early antiplatelet response to thienopyridines is mainly caused by platelet turnover as previously suggested. Elective patients undergoing coronary intervention were randomised to loading with clopidogrel 600 mg or prasugrel 60 mg (n=200). Adenosine diphosphate (ADP)-induced platelet reactivity was determined by impedance aggregometry before, at 30, 60, 90, and 120 minutes and at day 1 after loading. Immature platelet count was assessed as marker of reticulated platelets by flow cytometry. Platelet reactivity increased with rising levels of immature platelet count in both groups. This effect was more distinctive in patients on clopidogrel as compared to patients on prasugrel. Overall, immature platelet count correlated well with on-treatment platelet reactivity at all time-points (p < 0.001). These correlations did not change over time in the entire cohort as well as in patients treated with clopidogrel or prasugrel indicating an effect independent of platelet turnover (comparison of correlations 120 minutes/day 1: p = 0.64). In conclusion, the association of immature platelet count with impaired antiplatelet response to thienopyridines is similar early and late after loading. This finding suggests as main underlying mechanism another effect of reticulated platelets on thienopyridines than platelet turnover.

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Lipid lowering therapy in primary cardiovascular prevention / Drug treatment of acute coronary syndrome patients 645hyperlipidaemia had a lower incidence of subsequent breast cancer compared to those without it (0.5% vs 0.8%). Logistic regression demonstrated a significantly lower risk of breast cancer in hyperlipidaemia patients . Patients with hyperlipidaemia at baseline also had lower mortality rates compared to those without it (13.8% vs 23.7%). Mortality in hyperlipidaemia patients was significantly reduced compared to non-hyperlipidaemia patients after cox regression adjusting for age, ethnic frequency and the top contributors to mortality in the UK (OR 0.603 95% CI 0.571-0.637 p<0.001). The KM survival plot is shown in Figure 1. Conclusion: We demonstrate using a large, longitudinal database that a diagnosis of hyperlipidaemia has a highly protective effect on the subsequent development of breast cancer. The underlying reasons are yet to be elucidated but treatment with statins or a healthier lifestyle may contribute. The potentially beneficial effect of lipid-lowering medications amongst cancer patients should be further investigated. Background: Low-dose aspirin protects against ischaemic cardiovascular events and colorectal cancer, yet may be associated with a small increased risk of intracranial bleeds (ICB). Purpose: To explore the effect of low-dose aspirin on risk of ICB subtypes by sex, case-fatality and trauma-status, using The Health Improvement Network electronic medical record database in the UK . Methods: From a population aged 40-84 years and free of previous low-dose aspirin use, a cohort of new users of low-dose aspirin (75-300 mg; N=199,079) was identified. Each member was matched to a person still free of low-dose aspirin on that day by age, sex, time since study entry and primary care practitioner visits in the previous year. Cohorts (mean age at entry, 63.9 years) were followed (max. 14 years) to identify incident cases of ICB, with validation by manual review of patient records and/or linkage to hospitalization data. Fatalities were deaths ≤30 days after ICB. Nested case-control analysis was conducted using cases from both cohorts. To account for changes in aspirin exposure over time, an "as-treated" analysis was used. Controls (n=10,000) were frequency-matched to cases by age, sex and calendar year. Adjusted odds ratios (ORs) with 95% confidence intervals (CIs) were calculated for current use of low-dose aspirin (0-7 days before the index date [ICB date for cases, random date for controls]) by logistic regression; reference group was never use. Results: There were 1611 cases of ICB (n=743 for intracerebral haemorrhage [ICH], n=483 for subdural haematoma [SDH] and n=385 for subarachnoid haemorrhage [SAH]). ORs (95% CI) among men and women were 0.84 (0.63-1.12) vs. 1.16 (0.86-1.56) for ICH, 1.18 (0.86-1.64) vs. 1.29 (0.85-1.95) for SDH, 1.13 (0.73-1.74) vs. 0.57 (0.39-0.82) for SAH. Current use of low-dose aspirin was not associated with a statistically significant change in risk of a...