Data suggest that our developed algorithm is more accurate than the IWPC algorithm when the application is focused on patients from the Brazilian population. Population-specific derivation and/or calibration of warfarin dosing algorithms may lead to improved performance compared with general use dosing algorithms currently available. Original submitted 26 November 2014; Revision submitted 9 April 2015.
Introdution: COVID-19 is associated with an increased risk of thrombotic events. However, the contribution of platelet reactivity (PR) to the aetiology of the increased thrombotic risk associated with COVID-19 remains unclear. Our aim was to evaluate PR in stable patients diagnosed with COVID-19 and hospitalized with respiratory symptoms (mainly dyspnoea and dry cough), in comparison with a control group comprised of non-hospitalized healthy controls. Methods: Observational, case control study that included patients with confirmed COVID-19 (COVID-19 group, n = 60) and healthy individuals matched by age and sex (control group, n = 60). Multiplate electrode aggregometry (MEA) tests were used to assess PR with adenosine diphosphate (MEA-ADP, low PR defined as\53 AUC), arachidonic acid (MEA-ASPI, low PR\86 AUC) and thrombin receptoractivating peptide 6 (MEA-TRAP, low PR\97 AUC) in both groups. Results: The rates of low PR with MEA-ADP were 27.5% in the COVID-19 group and 21.7% in the control group (OR = 1.60, p = 0.20); with MEA-ASPI, the rates were, respectively, 37.5% and 22.5% (OR = 3.67, p\0.001); and with MEA-TRAP, the incidences were 48.5% and 18.8%, respectively (OR = 9.58, p\0.001). Levels of D-dimer, fibrinogen, and plasminogen activator inhibitor 1 (PAI-1) were higher in the COVID-19 group in comparison with the control group (all p\0.05). Thromboelastometry was utilized in a subgroup of patients and showed a hypercoagulable state in the COVID-19 group.
Compared with cardiac magnetic resonance, CK-MB was more accurate than cTnI for diagnosing MI. These data suggest a higher troponin cutoff for the diagnosis of procedure-related MI.
Thromboembolic events are associated with high mortality and morbidity indexes. In this context, warfarin is the most widely prescribed oral anticoagulant agent for preventing and treating these events. This medication has a narrow therapeutic range and, consequently, patients usually have difficulty in achieving and maintaining stable target therapeutics. Some studies on the literature about oral anticoagulant management showed that pharmacists could improve the efficiency of anticoagulant therapy. However, the majority of these studies included general patients retrospectively. The aim of this study was to prospectively evaluate a pharmacist’s warfarin management in patients with poor quality of anticoagulation therapy (Time in the Therapeutic Range- TTR < 50%). We included 268 patients with atrial fibrillation (AF) and without stable dose of warfarin (TTR < 50%, based on the last three values of International Normalized Ratio-INR). We followed them up for 12 weeks, INR values were evaluated and, when necessary, the dose adjustments were performed. During the first four visits, patient’s INR was measured every 7 days. Then, if INR was within the target therapeutic range (INR: 2–3), the patient was asked to return in 30 days. However, if INR was out the therapeutic target, the patient was asked to return in 7 days. Adherence evaluation was measured through questionnaires and by counting the pills taken. Comparison between basal TTR (which was calculated based on the three last INR values before prospective phase) and TTR of 4 weeks (calculated by considering the INR tests from visits 0 to 4, in the prospective phase of the study) and basal TTR and TTR of 12 weeks (calculated based on the INR tests from visits 0 to 12, in the prospective phase of the study) revealed significant statistical differences (0.144 ± 0.010 vs. 0.382 ± 0.016; and 0.144 ± 0.010 vs. 0.543 ± 0.014, p < 0.001, respectively). We also observed that the mean TTR of 1 year before (retrospective phase) was lower than TTR value after 12 weeks of pharmacist-driven treatment (prospective phase) (0.320 ± 0.015; 0.540 ± 0.015, p < 0.001). In conclusion, pharmaceutical care was able to improve TTR values in patients with AF and poor quality of anticoagulation with warfarin.
High renin hypertension is usually accompanied by impairment of the baroreceptor reflexes. This feature has been mostly ascribed to overactivity of the renin-angiotensin system. However, renal nerves could also modulate the baroreceptor reflexes. In the present experiments, the effect of renal denervation on the depressed baroreceptor reflexes was studied in rats subjected to aortic ligation between the renal arteries. Renal denervation of the ischemic kidney was performed at the same time as aortic ligation. The resulting effects on arterial pressure, heart rate, plasma renin activity, and baroreceptor reflex control of heart rate were studied 10-12 days after ligation and denervation. Aortic ligation induced high levels of mean arterial pressure (166 +/- 6 versus 110 +/- 3 mm Hg in controls), heart rate (380 +/- 9 versus 352 +/- 8 beats per minute in controls), and plasma renin activity (44 +/- 5 versus 6 +/- 1.2 ng angiotensin I/ml/hr). The baroreceptor reflex sensitivity for bradycardia and tachycardia was significantly reduced (-0.18 +/- 0.04 and -0.18 +/- 0.05, respectively, versus -2.3 +/- 0.01 and -2.4 +2- 0.1 beats per minute per mm Hg in controls). Denervation of the ischemic kidney attenuated the development of hypertension in aortic-ligated rats (122 +/- 3 mm Hg), lowering heart rate (319 +/- 8 beats per minute) and normalizing baroreceptor reflex sensitivity to bradycardia (-2.0 +/- 0.2 beats per minute per mm Hg) and to tachycardia (-4.0 +/- 0.1 beats per minute per mm Hg). Plasma renin activity was also normalized (4.3 +/- 2.4 ng angiotensin I/ml/hr).(ABSTRACT TRUNCATED AT 250 WORDS)
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