Robertsstorm0114

For long-term therapy (after one year post-PCI), recent studies have found oral anticoagulation alone without any antiplatelet therapy has a favorable benefit risk ratio. Thus, while dropping aspirin at varying times post-PCI has become an attractive strategy in many patient groups, careful patient selection and individualized assessment of the riskbenefit balance is warranted.Dual antiplatelet therapy (DAPT), the combination of aspirin (ASA), and a P2Y12 inhibitor, protects against stent thrombosis and new atherothrombotic events after a stent implantation or an acute coronary syndrome, but exposes patients to an increased risk of bleeding. In most current practices, the P2Y12 inhibitor is stopped at 6 to 12 months and ASA is continued indefinitely. The advent of safer stents, with less risk of stent thrombosis, has challenged this standard of care, however. A number of alternative strategies involving earlier de-escalation of the antiplatelet therapy have therefore been proposed. In these approaches, standard DAPT is switched to a less potent antithrombotic combination at an earlier time-point than recommended by guidelines. Three different de-escalation variations have been tested to date. The first one maintains DAPT but switches from the potent P2Y12 inhibitors ticagrelor or prasugrel to either a lower dose or to clopidogrel, while maintaining ASA. The 2 other approaches involve changing DAPT to a single antiplatelet at some earlier time-point after the percutaneous coronary intervention procedure, by stopping either the P2Y12 inhibitor or ASA. These strategies have all demonstrated some benefit in clinical trials so far, but especially the contribution of ASA in secondary prevention is clearly evolving as its role in increasing bleeding complications while not providing increased ischemic benefit is becoming more and more clear. In contemporary practice, the type and duration of DAPT should now be based on an individualized decision, and the de-escalation strategies, if used wisely, can be added to the existing options.Aspirin (ASA) has historically been one of the most important drugs in cardiology and has long been the cornerstone of antiplatelet therapy. Although its role in acute coronary syndrome remains undisputed, emerging data suggest that reappraisal of the efficacy of long-term ASA in some primary and secondary prevention may be warranted. The aim of this review is to place these new results in the context of previous evidence on aspirin by appraising the current body of evidence on its use of for cardiovascular diseases. This overview first summarizes the history of the discovery of aspirin, as well as its pharmacology and the concept of ASA resistance. We subsequently recapitulate the evidence of ASA on primary prevention and secondary prevention starting from the classical studies in order to serve as an introductory background to the examination of the most recent clinical trials that will be performed in the rest of the articles of this Supplement. Although the benefit of ASA in acute coronary syndrome remains incontrovertible, emerging evidence challenge the universal need for primary prevention, or for lifelong treatment in secondary prevention or all adults with stable coronary disease who are at highest risk for ASA-induced bleeding. The role of aspirin is quickly changing in recent times and this review provides a review for the clinician about the current role of this drug in cardiovascular care.Aspirin (ASA) is the most commonly prescribed antiplatelet agent. Although the evidence for efficacy of aspirin for secondary prevention of ischemic events in patients with established cardiovascular disease is strong, its role in primary prevention has been subject of controversies over the past decades. In fact, historical trials have shown only modest benefit in terms of reduction of ischemic events, mostly myocardial infarction and to a lesser extent stroke, and only at the expense of an increased risk of bleeding. These observations have led to divergent recommendations from professional societies on the use of ASA for primary prevention of cardiovascular disease manifestations. However, recent results from three trials of primary prevention have shown either no benefit or modest benefit on combined ischemic end points, without any impact on hard cardiovascular events such as myocardial infarction or stroke, accompanied by an increased risk of bleeding. Overall, this translated into neutral net benefit or even harm with the use of aspirin in patients with no overt cardiovascular disease. These results have accordingly led to a downgrade in the current recommendations on the use of ASA for primary prevention. This article provides an overview on the current evidence on the use of aspirin for primary prevention of cardiovascular disease.Aspirin (ASA) is the original antiplatelet agent. Its routine use, long unquestioned for both primary and secondary prevention in cardiovascular disease, is under increasing scrutiny as the riskbenefit balance for ASA becomes less clear and other disease- and risk-modifying approaches are validated. It can be viewed as a significant advance in evidence-based medicine that the use of an inexpensive, readily available, long-validated therapy is being questioned in large, rigorous trials. In this overview we present the important questions surrounding a more informed approach to ASA therapy duration of therapy, assessment of net clinical benefit, and timing of start and stop strategies. We also consider potential explanations for "breakthrough" thrombosis when patients are on ASA therapy. Other manuscripts in this Supplement address the specifics of primary prevention, secondary prevention, triple oral antithrombotic therapy, and the future of ASA in cardiovascular medicine.Plants have evolved stress-sensing machineries that initiate rapid adaptive environmental stress responses. Cytosolic calcium ion (Ca2+) is the most prominent second messenger that couples extracellular signals with specific intracellular responses. Essential early events that generate a cytosolic Ca2+ spike in response to environmental stress are starting to emerge. We review sensory machineries, including ion channels and transporters, which perceive various stress stimuli and allow cytosolic Ca2+ influx. We highlight integrative roles of Ca2+ channels in plant responses to various environmental stresses, as well as possible interplay of Ca2+ with other early signaling components, which facilitates signal propagation for systemic spread and spatiotemporal variations in respect to external cues. https://www.selleckchem.com/products/ha15.html The early Ca2+ signaling schemes inspire the identification of additional stress sensors.

To describe the communication of polygenic risk scores (PRS) in the familial breast cancer setting.

Consultations between genetic healthcare providers (GHP) and female patients who received their PRS for breast cancer risk were recorded (n = 65). GHPs included genetic counselors (n = 8) and medical practitioners (n = 5) (i.e. clinical geneticists and oncologists). A content analysis was conducted and logistic regression was used to assess differences in communication behaviors between genetic counselors (n = 8) and medical practitioners (n = 5).

Of the 65 patients, 31 (47.7 %) had a personal history of breast cancer, 18 of whom received an increased PRS (relative risk >1.2). 25/34 unaffected patients received an increased PRS. Consultations were primarily clinician-driven and focused on biomedical information. There was little difference between the biomedical information provided by genetic counselors and medical practitioners. However, genetic counselors were significantly more likely to utilize strategies to build patient rapport and counseling techniques.

Our findings provide one of the earliest reports on how breast cancer PRSs are communicated to women.

Key messages for communicating PRSs were identified, namely discussing differences between polygenic and monogenic testing, the multifactorial nature of breast cancer risk, polygenic inheritance and current limitation of PRSs.

Key messages for communicating PRSs were identified, namely discussing differences between polygenic and monogenic testing, the multifactorial nature of breast cancer risk, polygenic inheritance and current limitation of PRSs.

Growth-differentiation factor-15 (GDF-15) has recently been described as a potential biomarker for predicting risk of mortality and cardiovascular events in patients with atrial fibrillation (AF) but requires validation in clinical practice.

The study population consisted of 362 patients (mean age 71 years, 37% women) with non-valvular AF included in a prospective cohort study. Relationship of GDF-15 with all-cause mortality and major adverse cardiac events (MACE) was analyzed using Cox regression. Survival analysis stratified by GDF-15 was based on national death records, while MACE was recorded at personal follow-up. Further, we evaluated the recently developed GDF-15 based prognostic score towards prediction of all-cause mortality (ABC-death score).

Over a median observation period of 4.3 years, 81 (23.3%) patients died, and over a median personal follow-up of 316 days 47 MACE occurred. GDF-15 was independently associated with all-cause mortality (adjusted HR per double increase 2.33, 95%CI 1.74-3.13) and MACE (adjusted HR per double increase 2.33, 95%CI 1.60-3.39). GDF-15 levels, measured at follow-up, were similarly associated with mortality, and longitudinal measurements of GDF-15 did not significantly differ. Six-year survival probability of patients above vs. below the median GDF-15 level was 44% (95%CI 34-57) and 84% (95%CI 76-93), respectively. The ABC-death score revealed a C-statistic of 0.80.

GDF-15 predicts risk of all-cause mortality and MACE in patients with non-valvular AF. Further, the ABC-death score showed good predictive accuracy in a "real-world" cohort. Therefore, introduction of GDF-15 into clinical practice would enhance risk prediction of morbidity and mortality in AF patients.

GDF-15 predicts risk of all-cause mortality and MACE in patients with non-valvular AF. Further, the ABC-death score showed good predictive accuracy in a "real-world" cohort. Therefore, introduction of GDF-15 into clinical practice would enhance risk prediction of morbidity and mortality in AF patients.Every state in the United States has established laws that allow an unharmed newborn to be relinquished to personnel in a safe haven, such as hospital emergency departments, without legal penalty to the parents. These Safe Haven, Baby Moses, or Safe Surrender laws are in place so that mothers in crisis can safely and legally relinquish their babies at a designated location where they can be protected and given medical care until a permanent home can be found. It is important for health care professionals to know about and understand their state's law and how to respond should an infant be surrendered at their facility. No articles were found in the peer-reviewed literature that describe a method to evaluate nurse competency during infant relinquishment at a Safe Haven location. This article will describe commonalities and differences among these Safe Haven Laws, responsibilities of the hospital and staff receiving a relinquished infant, and 1 hospital's experience when running an infant relinquishment drill in their emergency department.