Fifty patients sent to the Radiotherapy Service of the Mount Sinai Medical Center of New York City were interviewed by a psychiatrist. The focus of the initial interview was what they were told when referred for radiation. Although 60% were told by their doctors they had cancer, all arrived at the treatment center unprepared for the frequency, number, and procedure of treatment and for the efficacy of treatment by radiation. Patients believed that requiring radiation was very bad news. Radiation was feared as inherently damaging and quite possibly carcinogenic. Few expected it to be curative. Interviews after completing treatment revealed an incidence of depression and anxiety even greater than in the pre-treatment interviews, indicating that radiation treatment is stressful in itself. Fewer than one-third judged themselves improved by radiation. More than one-third felt worse and judged treatment to have been ineffective, not realizing their new distress resulted from side effects of radiation. Patients suffer irrational fears of damage and death because of erroneous preconceptions of radiation which doctors fail to correct. Ironically, the lay and medical concepts of the dismal manifestations and futility of radiation treatment are entirely false. In this series, only one patient suffered damage due to radiation. Sixty percent were free of signs of cancer at follow-up 18-36 months later.
Dual antiplatelet therapy with aspirin and clopidogrel is commonly used to prevent recurrent ischemic events in patients with cardiovascular disease. Whilst their effects on platelet reactivity are well documented, it is unclear, however, whether antiplatelet therapy inhibits platelet extracellular vesicle (EV) release. The aim of this study was to investigate the effects of antiplatelet therapy on platelet EV formation and procoagulant activity. Blood samples from 10 healthy controls not receiving antiplatelet therapy were incubated in vitro with aspirin or a P2Y12 inhibitor (MeSAMP). Blood samples from 50 patients receiving long-term dual antiplatelet therapy and undergoing coronary angiography were also studied. Platelet reactivity was assessed by Multiplate™ impedance aggregometry. Platelet EV formation and procoagulant activity of pretreated and untreated blood samples in response to arachidonic acid (AA), adenosine diphosphate (ADP), ADP+PGE1, and thrombin receptor-activating peptide (TRAP) stimulation were assessed by flow cytometry and Procoag-PL assays, respectively. Incubation of normal platelets with aspirin significantly inhibited AA-induced platelet reactivity, EV formation, and procoagulant activity, whilst MeSAMP significantly inhibited platelet reactivity and EV formation in response to AA, ADP, and TRAP, but had minimal effect on procoagulant activity. Most patients receiving dual antiplatelet therapy showed an appropriate reduction in platelet reactivity in response to their treatment; however there was not complete inhibition of increased platelet and EV procoagulant activity in response to ADP, AA, or TRAP. In addition, we could not find any correlation between platelet reactivity and procoagulant activity in patients receiving dual antiplatelet therapy.
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