Evaluation of the algorithm of Anticlot Assistant: an anticoagulant management system based on mobile health technology.

The purpose is to evaluate the algorithm of Anticlot Assistant, a novel anticoagulant management system based on mobile health technology which was developed to facilitate patient self-management. The eligible patients managed warfarin therapy with usual care, following the prescriptions of the doctors. The actual prescriptions of doctors and the virtual recommendations by Anticlot Assistant were compared and analyzed. There were no significant differences between the next test dates recommended by Anticlot Assistant and those prescribed by doctors. The mean warfarin dosage prescribed by doctors was lower than that recommended by Anticlot Assistant (2.74 ±â€Š1.17 vs. 2.79 ±â€Š1.21 mg, 95% confidence interval for the difference: -0.01--0.09, P = 0.019, n = 139), resulting in the international normalized ratio a high time below the therapeutic range (TTR) (29.9 ±â€Š17.9%), and a low time above TTR [0.0% (0.0-18.7%)]. A mixed linear model revealed that 'the variations of the dosages prescribed by doctors from those recommended by Anticlot Assistant' were positively correlated with 'variations of next international normalized ratios from TTR' after controlling for other factors (estimate of the effect = 0.231, 95% confidence interval: 0.034-0.428, P = 0.022). Anticlot Assistant can mimic the doctors' prescriptions for the next test date and the warfarin dosages recommended by Anticlot Assistant might be more reasonable than those prescribed by doctors, which indicated that the algorithm was reliable and it was possible for the patients to manage warfarin therapy themselves with the aid of Anticlot Assistant.

Patient compliance with an anticoagulation management system based on a smartphone application.

We developed a novel anticoagulation management system (Anticlot Assistant) based on a smartphone application (App). This study was performed to evaluate patient compliance with Anticlot Assistant. This prospective case series study involved patients receiving warfarin therapy. The eligible patients were managed via Anticlot Assistant, and outcome data were analyzed. Thirty patients were recruited. The mean time within the therapeutic range (TTR) was 56.5% ± 26.2% and the mean patient compliance with Anticlot Assistant was 52.7% ± 40.4%. The patients in good compliance group had higher TTR (65.6 ± 25.0% vs. 40.0 ± 21.0%, P = 0.009), lower time in the extremely low range (9.4 ± 10.6% vs. 27.4 ± 13.2%, P = 0.000) and in the extremely high range (1.3 ± 2.8% vs. 14.1 ± 22.3%, P = 0.004) than those in poor compliance group. Logistic regression analysis revealed that receiving an education of > 6 years was the only independent predictor of good compliance (odds ratio 8.400, 95% confidence interval 1.274-55.394, P = 0.027). Patient compliance is critical important for good outcomes and it might increase with improvements in education and more widespread use of information technology. Although further improvement is needed, Anticlot Assistant is promising and this study offered valuable experiences for further research.

Protein kinase C enhances the swelling-induced chloride current in human atrial myocytes.

Swelling-activated chloride currents (ICl.swell) are thought to play a role in several physiologic and pathophysiologic processes and thus represent a target for therapeutic approaches. However, the mechanism of ICl.swell regulation remains unclear. In this study, we used the whole-cell patch-clamp technique to examine the role of protein kinase C (PKC) in the regulation of ICl.swell in human atrial myocytes. Atrial myocytes were isolated from the right atrial appendages of patients undergoing coronary artery bypass and enzymatically dissociated. ICl.swell was evoked in hypotonic solution and recorded using the whole-cell patch-clamp technique. The PKC agonist phorbol dibutyrate (PDBu) enhanced ICl.swell in a concentration-dependent manner, which was reversed in isotonic solution and by a chloride current inhibitor, 9-anthracenecarboxylicacid. Furthermore, the PKC inhibitor bis-indolylmaleimide attenuated the effect and 4α-PDBu, an inactive PDBu analog, had no effect on ICl.swell. These results, obtained using the whole-cell patch-clamp technique, demonstrate the ability of PKC to activate ICl,swell in human atrial myocytes. This observation was consistent with a previous study using a single-channel patch-clamp technique, but differed from some findings in other species.

Antibiotic therapy did not prevent the rupture of mycotic aneurysm of the superior mesenteric artery.

Mycotic aneurysm of the superior mesenteric artery (SMA) is a rare complication of infective endocarditis. We report a case with infective endocarditis involving the aortic valve complicated by multiple septic embolisms. The patient was treated with antibiotics for 6 weeks. During preparation for surgical treatment, the patient developed acute abdominal pain and was diagnosed with a ruptured SMA aneurysm, which was successfully treated with an emergency operation of aneurysm ligation. The aortic valve was replaced 17 days later and the patient recovered uneventfully. In conclusion, we present a rare case with infective endocarditis (IE) complicated by SMA aneurysm. Antibiotic treatment did not prevent the rupture of SMA aneurysm. Abdominal pain in a patient with a recent history of IE should be excluded with ruptured aneurysm.

Effects of α1-adrenoceptor agonist phenylephrine on swelling-activated chloride currents in human atrial myocytes.

Swelling-activated chloride currents (ICl.swell) play an important role in cardiac electrophysiology and arrhythmogenesis. However, the regulation of these currents has not been clarified to date. In this research, we focused on the function of phenylephrine, an α1-adrenoceptor agonist, in the regulation of I(Cl.swell) in human atrial myocytes. We recorded I(Cl.swell) evoked by a hypotonic bath solution with the whole-cell patch-clamp technique. We found that I(Cl.swell) increased over time, and it was difficult to achieve absolute steady state. Phenylephrine potentiated I(Cl.swell) from -1.00 ± 0.51 pA/pF at -90 mV and 2.58 ± 1.17 pA/pF at +40 mV to -1.46 ± 0.70 and 3.84 ± 1.67 pA/pF, respectively (P < 0.05, n = 6), and the upward trend in ICl.swell was slowed after washout. This effect was concentration-dependent, and the α1-adrenoceptor antagonist prazosin shifted the dose-effect curve rightward. Addition of prazosin or the protein kinase C (PKC) inhibitor bisindolylmaleimide (BIM) attenuated the effect of phenylephrine. The PKC activator phorbol 12,13-dibutyrate (PDBu) activated I(Cl.swell) from -1.69 ± 1.67 pA/pF at -90 mV and 5.58 ± 6.36 pA/pF at +40 mV to -2.41 ± 1.95 pA/pF and 7.05 ± 6.99 pA/pF, respectively (P < 0.01 at -90 mV and P < 0.05 at +40 mV; n = 6). In conclusion, the α1-adrenoceptor agonist phenylephrine augmented I(Cl.swell), a result that differs from previous reports in other animal species. The effect was attenuated by BIM and mimicked by PDBu, which indicates that phenylephrine might modulate I(Cl,swell) in a PKC-dependent manner.