Dual antiplatelet therapy up to the time of non-elective coronary artery bypass grafting with prophylactic platelet transfusion: is it safe?

BACKGROUND: Guidelines suggest that patients discontinue Clopidogrel at least 5 days prior to coronary artery bypass grafting (CABG). Those with acute coronary syndrome (ACS) are at high risk for myocardial infarction (MI) if not treated with dual antiplatelet therapy (DAPT). We sought to assess pre and post-operative outcomes of patients maintained on Clopidogrel and aspirin up to the time of surgery and compare them with those on aspirin alone. METHODS: From the cardiac surgery database, 240 patients were retrospectively registered between January and May 2017. There were 126 patients with ACS who underwent CABG on DAPT (Clopidogrel group [CG]) and 114 patients who underwent elective CABG on aspirin alone (control). The CG received intraoperative prophylactic platelet transfusion (PPT). Demographics, comorbidities, and laboratory data were prospectively entered at the time of surgery and were subsequently retrieved for analysis. Per and postoperative findings were identified and compared between both groups. RESULTS: The cohort consisted of 240 patients (mean age 61 years, 81.3% were male, SD ± 9.58). Patients in the CG were younger (Median 57 vs. 63, P-value 0.001), and with male predominance (86% versus 75%, P-value 0.028). In addition, they had less prevalence for diabetes and renal failure as compared to control (P-values 0.003, and 0.005, respectively). There were no significant differences between both groups in number of vessels grafts, duration of on-pump and aortic clamp. Hematologic laboratory data had also similar baseline values. The CG had similar bleeding rate, redo surgery and in-hospital death (P-values non-significant), however more infection and total hospital stay as compared to control (p-values 0.048 and 0.001). CONCLUSION: Patients who are at increased risk for MI can be maintained on DAPT up to the time of CABG because surgery is safe when patients are offered PPT.

Thyroxine transfer from cerebrospinal fluid into choroid plexus and brain is affected by brefeldin A, low sodium, BCH, and phloretin, in ventriculo-cisternal perfused rabbits.

BACKGROUND: Thyroxine (T4) hormone is synthesized by the thyroid gland and then released into the systemic circulation where it binds to a number of proteins. Dysfunction in T4 transport mechanisms has been demonstrated in multiple central nervous system (CNS) diseases including Alzheimer's disease. In the presence of different compounds that inhibit potential T4 transport mechanisms, this study investigated the transfer of T4 from cerebrospinal fluid (CSF) into Choroid Plexus (CP) and other brain tissues. The compounds used were brefeldin A, low sodium artificial CSF (aCSF), BCH, phloretin, and taurocholate (TA). METHODS: Radiolabeled T4 ((125)I-T4) was perfused continuously into the CSF and was assessed in several brain compartments with reference molecule (14)C-mannitol and blue dextran, using the in vivo ventriculo-cisternal perfusion (V-C) technique in the rabbit. The aCSF containing the drug of interest was infused after 1 h of perfusion. Drugs were applied independently to the aCSF after 1 h of control perfusion. RESULTS: Of interest, in presence of low sodium or BCH, the percentage recovery of (125)I-T4, was increased compared to controls, with concomitant increase in T4 clearance. Conversely, brefeldin A, phloretin, and TA did not exert any significant effect on the recovery and clearance of (125)I-T4 assessed in aCSF. On the other hand, the uptake of (125)I-T4 into CP was raised by 18 fold compared to controls in the presence of brefeldin A. In addition, low sodium, BCH, or phloretin alone, enhanced the uptake of (125)I-T4 by almost 3-fold, whereas TA did not show any significant effect. Finally, the uptake and distribution of (125)I-T4 into other brain regions including ependymal region (ER) and caudate putamen (CAP) were significantly higher than in controls. CONCLUSION: Our study suggests the involvement of different mechanisms for the transfer of (125)I-T4 from CSF into CP and other brain regions. This transfer may implicate sodium-dependent mechanisms, amino acid "L" system, or organic anion transporting polypeptide (OATP).