2. Central sleep apnea after acute coronary syndrome and association with ticagrelor use
Ph Meurin, A Ben Driss, C Defrance, R Dumaine, H Weber, N Renaud, L Bonnevie, S Mouram, J Y Tabet Sleep Med. 2021 Apr;80:39-45. doi: 10.1016/j.sleep.2021.01.026. Epub 2021 Jan 20.
Study objectives: By modifying the apneic threshold, the antiplatelet agent ticagrelor could promote central sleep apnea hypopnea syndrome (CSAHS). We aimed to assess the association between CSAHS and ticagrelor administration. Methods: Patients were prospectively included within 1 year after acute coronary syndrome (ACS), if they had no heart failure (and left ventricular ejection fraction ≥ 45%) and no history of sleep apnea. After an overnight sleep study, patients were classified as "normal" with apnea hypopnea index (AHI) < 15, "CSAHS patients" with AHI ≥ 15 mostly with central sleep apneas, and "obstructive sleep apnea hypopnea syndrome (OSAHS) patients" with AHI ≥ 15 mostly with obstructive sleep apneas. Results: We included 121 consecutive patients (mean age 56.8 ± 10.8, 88% men, mean body mass index 28.3 ± 4.4 kg/m2, left ventricular ejection fraction 56 ± 5%, at a mean of 67 ± 60 days (median 40 days, interquartile range: 30-80 days) after ACS. In total, 49 (45.3%) patients had AHI ≥ 15 (27 [22.3%] CSAHS %, 22 [18.2%] OSAHS). For 80 patients receiving ticagrelor, 24 (30%) had CSAHS with AHI ≥ 15, and for 41 patients not taking ticagrelor, only 3 (7.3%) had CSAHS with AHI ≥ 15 (chi-square = 8, p = 0.004). On multivariable analysis only age and ticagrelor administration were associated with the occurrence of CSAHS, (p = 0.0007 and p = 0.0006).
3. Accuracy of a portable international normalized ratio monitor for patients receiving a low molecular weight heparin as a bridge pending full oral anticoagulant efficacy
Ph Meurin, J Y Tabet, M Monchi, H Weber, C Fabre, B Gibier, N Renaud, A Ben Driss Thromb Res. 2010 Feb;125(2):192-5. doi: 10.1016/j.thromres.2009.09.004. Epub 2009 Nov 25.
Background: Point of care (POC) devices measuring the international normalized ratio (INR) are accurate for patients with stable disease, but their efficiency has not been prospectively assessed during the "bridging period" when patients are receiving a low molecular weight heparin (LMWH) on top of a vitamin K antagonist (VKA) until the target INR is reached. Methods: 188 dual INR measurement using the POC (INR(POC)) and the laboratory (INR(lab)) at the same time were consecutively determined : 69 in patients receiving LMWH+VKA (bridging group) and 119 in patients receiving only a VKA (control group). INRpoc was compared to INR(lab). Results: Test strip failure rate was higher in the bridging group than in the control group (29% vs 4%; p<0,001). In successful tests, POC accuracy was not modified by LMWH administration: the correlation coefficients between POC and lab INR values for the bridging group and the control group were 0,81 and 0,87 respectively, and the relative measure of divergence (RMD=INR(lab) - INR(poc)/INR(lab)) was lower in the bridging group than in the control group (4+/-7% vs 10+/-14%; p=0,02). Finally, clinically relevant agreement between POC and laboratory was of 90% in the bridging group and 92.1% in the control group (p=0.6). Conclusion: With the POC used (INRatio), in patients receiving LMWH when the POC gives a result, it is as accurate as in patients not receiving a LMWH.
