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With the rapid development of imaging and percutaneous coronary intervention, the application of contrast media has become more and more widespread, and contrast-associated AKI has become one of the most common causes of acute kidney injury. Contrast-associated AKI seriously threatens patients' health and brings greater economic burden to patients, so it is particularly important to prevent the contrast-associated AKI. Nicorandil is a common vasodilator drug in clinical practice, widely used in the treatment of angina pectoris, with the effects of anti-oxidative stress, anti-apoptosis, anti-inflammatory and vasodilation, and is considered to be effective in preventing contrast - associated AKI. However, there is still a lack of further research on the efficacy of nicorandil in preventing contrast-associated AKI.
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Objective Little research has been done on how Cx37 changes the current density of mononuclear macrophage in atherosclerosis.The purpose of this study was to detect the effects of Cx37 on the current density of mononuclear macrophage in atherosclerosis.Methods A total of 30 Wistar mice were randomly divided into Cx37+ group and Cx37-group equally.The atherosclerosis model was constructed by a high-fat diet.According to different parts of sample collection, these two groups were subdivided into Cx37+ plaque group, Cx37-plaque group, Cx37+blood group and Cx37-blood group.RT-PCR was applied to detect the expression of Cx37 in different body parts.The mononuclear macrophages were cultured after being separated from blood and plague in both groups.The current density of mononuclear macrophage was detected by the whole cell recording.Results The relative expression of Cx37 in Cx37 + plaque group was higher than that in plaque group ([1.10±0.02] vs [0.60±0.03]).Energy Spectrum CT was used to detect the carotid artery plaque in both Cx37 + and Cx37-groups, which verified the successful model construction.At 80,120 and 160ms, the current density in Cx37 + plaque group([0.61± 0.06], [0.67±0.07], [0.91±0.03]A/cm2) was significantly higher than those in Cx37 + blood group([0.49±0.02], [0.61±0.03], [0.67±0.02]A/cm2) , Cx37-plaque group([0.48±0.02], [0.60±0.02], [0.64±0.02]A/cm2) and Cx37-blood group([0.49±0.02], [0.59±0.02], [0.64±0.02]A/cm2).The same goes for those at 200, 240, 320ms(P<0.05).Conclusion Cx37 has more significant impact on the current density in the plaque of mononuclear macrophage than in the peripheral blood in promoting macrophages activation and atherosclerosis progress.
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<p><b>OBJECTIVE</b>To explore the characteristics and therapies of patients with acute myocardial infarction (AMI) in Wuxi city, China.</p><p><b>METHODS</b>A network was established to obtain information of patients with AMI who were admitted to 9 designated hospitals between 2011 and 2012. A total of 1 714 patients were enrolled (1 334 males, 754 smokers, 1 076 hypertension, 270 hyperlipidemia and 398 diabetes) including 1 410 patients with acute ST-segment elevation myocardial infarction (STEMI) and 304 patients with acute non ST-segment elevation myocardial infarction (NSTEMI). Patients' characteristics, therapies, the incidence of major adverse cardiovascular events (MACEs) and all-cause mortality were analyzed.</p><p><b>RESULTS</b>(1) Medication therapy was as follows: antiplatelet therapy 98.3% (1 685 cases) , beta-blockers 59.1% (1 013 cases) , ACEI or ARB 67.6% (1 159 cases) , statins 98.1% (1 682 cases) , and nitrates 71.1% (1 218 cases) . Of the patients, 7.1% (132 cases) received temporary pacemakers, 34.0% (480 cases) with acute STEMI underwent reperfusion [direct PCI 18.4% (260 cases) and thrombolysis 15.6% (220 cases)]. (2) According to the hospital admission data, patients were divided into three groups: group A, transported to the hospital by ambulance (n = 361); group B, transported to the hospital by private vehicles (n = 1 318); and group C, AMI occurred in the hospital (n = 35). The median time of AMI onset to physician contact of the 3 groups was 178 min, 368 min, and 9 min, respectively. The median time from AMI onset to the first ECG was 181 min, 379 min, and 10 min, respectively. The median time from AMI onset to cardiology specialist consultation was 187 min, 431 min, and 69 min, respectively. AMI onset-to-physician contact, AMI onset-to-first ECG, and AMI onset-to-specialized treatment time was the shortest in group C, followed by group A and group B. For patients with STEMI underwent reperfusion therapy, the median AMI onset-to-reperfusion therapy time was significantly shorter in group A patients than group B patients [thrombolysis group: 224(171, 514) min vs. 378 (158, 785) min, PCI group: 318 (154, 674) min vs. 489 (143, 816) min, all P < 0.05]. (3) The total incidence of MACEs was 16.3% (279/1 714), the all-cause in-hospital mortality rate was 13.1% (224/1 714). According to the AMI onset-to-physician contact, patients were divided into 4 groups: <3 h, 3-6 h, 6-12 h, and >12 h. The incidence of MACEs [4.4% (23/517), 13.3% (60/451), 19.1% (77/404) and 34.8% (119/342),χ(2) = 114.36, P < 0.01] and all-cause in-hospital mortality rate [4.1% (21/517) , 10.4% (47/451), 18.6% (75/404), 23.7% (81/342), χ(2) = 84.36, P < 0.01] increased in proportion to the time of AMI onset-to-physician contact. Among STEMI patients, the incidence of MACEs [5.8% (15/260) , 12.3% (27/220) , 20.9% (194/930) ,χ(2) = 39.93, P < 0.01] and all-cause in-hospital mortality [1.5% (4/260) , 10.0% (22/220) , 18.2% (170/930) ,χ(2) = 50.90, P < 0.01] was the lowest in the primary PCI group, followed by thrombolysis group and was the highest in the early conservative treatment group.</p><p><b>CONCLUSIONS</b>Guideline is well followed in terms of drug treatments of AMI in this cohort, but only a small proportion of AMI patients in Wuxi received reperfusion therapy. There is a considerable out-of-hospital time delay for AMI patients in this cohort which is shorter in group A than in group B. All-cause in-hospital mortality and MACEs is the lowest in AMI patients underwent primary PCI.</p>
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Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , China , Cross-Sectional Studies , Myocardial Infarction , TherapeuticsABSTRACT
Objective To investigate the effect of different loading doses of atorvastatin in patients with stable plaques.Methods Consecutive 174 patients with stable plaque who underwent coronary arteriongraphy (CAG) and intravascular unltrasound(IVUS) were randomly assigned to receive 10 mg atorvastatin treatment (group 10 mg,n =47),20 mg atorvastatin treatment(group 20 mag,n =45),40 mg atorvastatin treatment (group 40 mg,n =43) and 80 mg atorvastatin treatment (group 80 mg,n =39).The endpoints including low density lipoprotein-cholesterol(LDL-C),high density lipoprotein-cholesterol (HDL-C),high-sensitivity C-reactive protein (hs-CRP) levels,necrotic and plaque volumes,were assessed after 3-6 months' follow-up.Results Mean LDL-C,HDL-C,hs-CRP,the percentage of necrotic,plaques volumes were similar at baseline (P ＞ 0.05).During 3-6 months of follow up:(1)LDL-C levels in group 10 mg,20 mg,40 mg,80 mg were lower than at baseline (t =3.12,4.23,3.26 and 5.21 respectively,P ＜ 0.01).There was significant difference between the 20 mg group and the 40 mg group(P ＜ 0.05) ; (2) There was no significant difference of HDL-C levels in 10 mg,20 mg and 40 mg groups after atorvastatin treatment.However,its level was significantly higher in the 80 mg group after atorvastatin treatment than other dose groups(P ＜ 0.05) and were higher than at baseline(t =2.35,P ＜ 0.01) ;(3)the 80 mg group's hs-CRP levels decreased significantly after treatment than at baseline((3.59 + 1.07)mg/L vs (6.10 + 2.12) mg/L,t =2.37,P ＜ 0.01);(4)According to the VH of IVUS,the percentage of necrotic in 10 mg group became higher than at baseline ((16.54 + 1.76) ％ vs.(7.83 + 1.03) ％,t =2.38,P ＜0.01) and conformed to unstable plaques diagnostic criteria(＞ 10％).There was no significant difference in group 20 mg,40 mg and 80 mg with at baseline (t =1.24,0.21,0.69 respectively,P =0.069,0.846,0.643respectively) ; (5)Plaques volumes in group 10 mg,20 mg were not larger than at baseline.However,in group 40mg and 80 mg.Plaques volumes were smaller than at baseline ((30.69 ± 8.12) mm3 vs (37.09 + 12.01)mm3,t=l.29,P=0.019;(24.99±l.01) mm3 vs (36.47+14.68) mm3,t =2.62,P＜0.01).Conclusion The effects of atorvastatin on stable plaques vary with doses.(1) For LDL-C,the use of atorvastation 20 mg/d can make LDL-C reaching standard,and atorvastation 40 mg/d was superior to 20 mg/d and similar to 80 mg/d.(2)For HDL-C,atorvastation 80 mg/d can make it higher.(3)Atorvastation 80 mg/d can make hs-CRP lower.(4)Atorvastation≥20 mg/d can make plaques stable and atorvastation 80 mg/d was superior to 20 mg/d and 40mg/d.Atorvastation 40-80 mg/d can make plaques dwindled.