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OBJECTIVE:To evaluate the pharmacoeconomics characteristic of olmesartan medoxomil in ARB anti-hypertension drugs,and to provide reference for clinical drug use. METHODS:The literatures on the pharmacoeconomics study of olmesartan medoxomil published from Jan. 2002 to Dec. 2013 were searched with assigned search strategy from domestic and international data-bases like CNKI,PubMed,etc.,and comprehensive comparison and consistency analysis were conducted. RESULTS:4 literatures about pharmacoeconomics study of olmesartan medoxomil in different countries were screened,with essential hypertension patients as target population cost-minimization analysis or cost-effectiveness analysis as method,and 9 months-5 years as study course. The results consistency was well and showed the treatment cost of olmesartan medoxomil was usually less or better cost-effectiveness. CONCLUSIONS:Olmesartan medoxomil shows pharmacoeconomics advantage among ARBs drugs based on existed literature re-view.
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ObjectiveTo study the effect of pre-arrest and post-arrest mild hypothermia after restoration of spontaneous circulation (ROSC) on myocardial function, ultrastructure, apoptosis of myocardial cells in rabbits with ventricular fibrillation.Methods Sixty-two male New Zealand rabbits were randomly allocated into five groups: namely normothermic control group (NTC group,n = 10), hypothermia control group (HTC group,n = 10), normothermic resuscitation group (NTR group,n = 14), hypothermia pre-arrest group (HPRA group,n = 14), and hypothermia post-arrest group (HPOA group,n = 14). The normal temperature was controlled at (39.0±0.5)℃, and the hypothermia (33.5±0.5)℃. Ventricular fibrillation cardiac arrest (CA) was reproduced in rabbits by transcutaneous epicardium electrical stimulation. The parameters of hemodynamics were monitored dynamically for 4 hours in all the groups, including heart rate (HR), left ventricular end diastolic and systolic pressure (LVEDP/LVESP), maximal rate of increase/decrease in left ventricular pressure (±dp/dt max), and mean arterial pressure (MAP). The body temperature of rabbits in hypothermia groups was maintained by surface cooling for 4 hours followed by rewarming. The survived rabbits were sacrificed at 48 hours after resuscitation, and myocardial apical tissue was harvested for observation of ultrastructure with electronic microscope, and to observe apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.Results① Resuscitation investigation: there was no significant difference in rate of ROSC, time of CPR and energy of defibrillation among HPRA, HPOA, and NTR groups [rate of ROSC: 85.71%, 71.43%, 71.43%; time of CPR (seconds): 45.3±30.2, 61.2±41.3, 82.3±63.8;energy of defibrillation (J): 14.3±8.9, 22.0±15.5, 25.0±15.8, allP> 0.05].② Hemodynamics: compared with normal temperature groups, animals in hypothermia groups exhibited lower levels of HR (allP< 0.05). Compared with NTR group, HPRA group exhibited higher levels of LVESP (mmHg, 1 mmHg = 0.133 kPa) at 0.5, 1, 2 and 3 hours post ROSC (0.5 hour: 103.8±14.3 vs. 91.6±13.3, 1 hour: 107.2±14.1 vs. 82.7±8.5, 2 hours: 109.0±16.9 vs. 88.8±12.9, 3 hours: 109.1±14.6 vs. 89.3±14.3, allP< 0.05). Compared with NTR group and HPOA group, HPRA group exhibited lower levels of LVEDP (mmHg) at 0.5 hour post ROSC (3.70±0.85 vs. 7.61±2.73, 7.02±3.12, both P< 0.05). Compared with NTR group, HPRA group exhibited lower levels of LVEDP at 1 hour post ROSC (4.34±1.44 vs. 6.99±1.96,P< 0.05). In HPRA group, the level of+dp/dt max (mmHg/s) was higher than that of NTR group and HPOA group at 1 hour and 2 hours post ROSC (1 hour: 2 759.5±321.6 vs. 2 123.0±304.5, 2 283.7±234.2, 2 hours:2 730.6±425.1 vs. 2 221.5±392.9, 2 252.6±476.0, allP< 0.05). There were no significant differences in -dp/dt max and MAP levels among three CPR groups.③ The survival rate at 48 hours post ROSC of NTR, HPRA and HPOA groups was 60%, 75%, and 100%, respectively. Compared with NTR group, higher survival rate was found in HPOA group at 48 hour post ROSC (P< 0.05).④ Compared with NTR group, less damage to myocardial ultrastructure was found in HPRA and HPOA groups. Apoptosis index (AI) was lower in HPRA and HPOA groups than that in NTR group [(28.05±9.82) %, (26.39±8.98) % vs. (42.02±13.36) %, bothP< 0.05].Conclusions Our study shows that mild hypothermia has no effect on ROSC rate. Pre-arrest hypothermia can ameliorate myocardial systolic function of rabbit in early stage after ROSC, and it has no negative influence on diastolic function. Post-arrest mild hypothermia produces no negative influence on myocardial function of rabbit, but it improves 48 hours survival rate in ROSC rabbits. Both pre-arrest and post-arrest mild hypothermia therapy can attenuate myocardial injury in CA model of rabbits by ameliorating mitochondrial injuries and suppressing apoptosis of myocardial cells.
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Objective To investigate the impact of prior cerebral infarction (PCI) on in-hospital mortality in patients with Acute Myocardial Infarction (AMI).MethodsA retrospective analysis of documents of a total of 3572 consecutive patients with AMI admitted to Xuanwu Hospital of Capital Medical University from 2002 Jan.1 to 2009 Dec.31 were performed.Results There were 564 patients ( 15.8% )with PCI.Compared with the group of without PC1,the group with PCI were substantially older[(69.4 ±9.9) vs (64.2 ± 12.9)years,P =0.000],and had a higher prevalence of hypertensive disease,diabetes mellitus,prior myocardial infarction (MI) and non-ST-segment elevation myocardial infarction(NSTEMI)( respectively,71.0% vs 57.3%; 41.0% vs 25.7%,12.9% vs 9.5%; 14.9% vs 10.7%,P ＜ 0.01 ),and a higher in-hospital mortality ( 16.5% vs 10.0%,P= 0.000).Univariate analysis demonstrated that in-hospital mortality associated with age,gender,extensive anterior MI,anterior MI,diabetes mellitus,prior cerebral infarction,prior myocardial infarction,coronary angiography and percutaneous coronary intervention.Logistic regression analysis found that risk factors were age,extensive anterior MI,anterior MI,diabetes mellitus and prior cerebral infarction,and protective factors were coronary angiography and percutanous coronary intervention.PCI was independently associated with in-hospital mortality,OR 1.368,95% CI 1.047-1.787,P = 0.022.Conclusion In patients with acute myocardial infarction,the presence of PCI increases the risk of worse in-hospital outcome.