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Objective To investigate the prevalence and the risk factors of gastroduodenal damages induced by nonsteroidal anti-inflammatory drugs (NSAIDs). Methods One hundred and eighty-four patients who were prescribed NSA1Ds for long time in rheumatology and cardiovascular clinics were enrolled. Clinical data such as age, sex, medication history and body mass index were recorded. The lesions were estimated by endoscopy and the specimens were tested for Helicobacter pylori (H. pylori) infection. Results Peptic ulcer was found in 63 (34. 24%) patients including gastric ulcer in 22, duodenal ulcer in 34 and compound ulcer in 7. The endoscopic examination showed that 57 out of 121 patients without peptic ulcer had ≥3 erosive lesions. Logistic regression analysis revealed that H. pylori infection was important risk factor that induced the peptic ulcer in those who were taking NSAIDs for long time (OR = 13. 86, 95% CI: 6. 53 ～ 29. 43). The incidence of gastroduodenal damage was similar in patients taking NSAIDs and low dose aspirin (OR =0.45,95CI:0.16～ 1.28). Conclusions NSAIDs may cause gastroduodenal damages in long-term users and H. pylori infection was an important risk factor. The effect of low dose aspirin on gastroduodenal damages is as same as NSAIDs.
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Objective To evaluate the value of the TIMI risk index in predicting 30-day and one-yosr mortality and incidence of heart failure in patients with ST-elevation myocardial infarction (STEMI).Method Data of 229 patients with STEM1 from August 1999 to March 2006 in the First Affiliated Hospital,Sun Yat-sen University,were retrospeclively collected,analyzed and scored with TIMI risk index.When categorized into quintiles(≤12.5,12.5～17.5,17.5～22.5,22.5～30,>30) and modeled as a continuous variable,difference of prediction of 30day and one-year mortality and 30-day incidence of heart failure of patients were compared respectively.Results When categorized into quintilos and modeled as a continuous variable,30-day and one-year mortality and 30-day incidence of heart failure were increasing with increasing score of risk index (P<0.05).The area under the recewer operating characteristic curve were 0.65,0.68,0.67 and 0.70,0.72,0.70,respectively.Conclusions The TIM1 risk index can be used as a simple,rapid and practical tool to risk-stratify patients with STEMI.
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Objective To study the levels of soluble thrombomodulin (sTM)in patients with acute coronary syndrome (ACS) and evaluate its clinical significance. Method Measured the sTM levels with enzyme linked immunosorbent assay, and described the characteristics of coronary arteriography, risk factors of coronary heart disease, and adverse events in a case-control study of 48 ACS patients (ACS group)and 10 normal people (control group). Results The level of sTM in ACS group was (3.67±1.71) μg/L, and (2.34±0.43)μg/L in control group (P<0.05). The level of sTM in the patients of risk factors or impaired vessels number more than 2 increased significantly than those in the patients of risk factors or impaired vessols number inferior or equal to 2, (4.93±2.76) μg/Lvs (3.13±0.81) μg/L, P<0.05, (4.60± 2.83) μg/L vs (2.91±0.23) μg/L, P < 0.05 respectively. The incidence of cardiac events in the patients of sTM more than 3.2 μg/L (70.0%)was higher significantly than that in the patients of sTM inferior or equal to 3.2 μg/L(35.7%), P< 0.05. Conclusions The levels of sTM are valuable markers to evaluate the impaired degree and scope of endothelial cells in ACS. They are also associated with the number of risk factors, and useful in predicting the extent and prognosis of the disease.
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Objective To investigate the diagnostic value of postexercise systolic blood pressure(SBP) response in detecting coronary artery disease(CAD) in patients with electrocardiographic left ventricular(LV) hypertrophy.Methods Acording to their results of selective coronary angiography,58 patients with electrocardiographic LV hypertrophy were divided into group 1(27 patients without significant coronary lesions) and group 2(31 patients with significant coronary lesions).Symptom-limited treadmill exercise testing was conducted in those patients.Results The SBP ratio(SBP at 3 minutes of recovery divided by SBP at peak exercise) was significantly higher in group 2 than in group 1(0 98?0 11 vs 0 84?0 11,P
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Objective To investigate the effects of angiotensin-(1-7) on angiotensin Ⅱ and its receptor in pressure-overloaded rats. Methods Rat models of pressure-overloaded heart was induced by constriction of abdominal aorta. Forty-five male Sprague Dawley rats were randomized into sham-operated group,model control group and angiotensin-(1-7) treatment group. They were treated with intravenous infusion of 25?g/kg/h angiotensin-(1-7) or same volume of saline after operation. After the treatment for 4 weeks, the ratio of left ventricular weight to body weight(LVW/BW)was determined, angiotensin Ⅱ concentrations in plasma and myocardium were measured by radioimmunoassay, and the expression levels of type 1(AT_1) and type 2(AT_2) angiotension Ⅱ receptor mRNA in left ventricular myocardium were assessed by RT-PCR. Results Compared with sham-operated group, myocardial angiotensin II concentration and AT_1 receptor mRNA level in model control group obviously increased 4 weeks after operation. Compared with model control group, angiotensin II concentrations in plasma and myocardium in angiotensin-(1-7) treatment group had not obvious change, the expression level of myocardial AT_1 receptor mRNA decreased, and the ratio of LVW/BW obviously decreased. There was no significant difference in myocardial AT_2 receptor mRNA level among the three groups. Conclusion Exogenous angiotensin-(1-7) can attenuate cardiac hypertrophy possibly by inhibiting myocardial AT_1 receptor mRNA expression in pressure-overloaded rats.
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【Objective】 To explore the significance of electrocard iogram monitoring during the effective application of radiofrequency energy to s low atrioventricular (AV) nodal pathway ablation. 【Methods】 Slow AV nodal pathway ablation was performed in 58 patients with slownfast AV nodal ree-trant tachyca rdi a (AVNRT). The changes of electrocardiogram were monitored during the effective application of low radiofrequency RF energy (15～25 W). A faster rate of junctio nal ectopy (>150 min-1), ventriculoatrial (VA) block in association with j unctional ectopy, and l ong P-R interval during sinus beat were considered as harbingers of atrioventri cular (AV) block. RF energy deliveries were discontinued as soon as the harbinge rs of AV block occurred. Otherwise, RF energy continued until junctional ectopie s were decreased or vanished. If junctionnal ectopies were not decreased, RF ene rgy continued lasted for 90～120 s. 【Results】 Slow AV nodal pathway ablation w as successful in all patients who had junctional ectopy during the effective del ivery of RF energy. The effective ablation time was (128±26) s. 54 patients exp erienced one time successful ablation, and 4 patients experienced two times abla tion. Unsustained AV block occurred in 6 patinets after RF energy deliveries whi ch were immediately terminated because of VA block in association with junctiona l ectopy in 4 patinets and long P-R interval during sinus beats in 2 patients. No patients developed permanent AV block. Recurrent AVNRT requiring second ablat ion occurred in 2 of 58 successfully ablated slow pathway during (18±16) months of follow-up. 【Conclusion】 RF energy deliveries could be instructed b y intracardiac electrocardiogram monitoring during AVNRT ablation, which could e nhance the successful rate of slow pathway ablation, reduce recurrence and avoide permanent AV block.
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AIM: To investigate the effects and mechanisms of angiotensin-(1-7) on cardiac hypertrophy in pressure-overloaded rats. METHODS: Ar at model of pressure-overloaded heart was induced by constriction of abdominal aorta. Seventy-five male Sprague Dawley rats were randomized to sham-operated group, model control group and angiotensin-(1-7) treatment group. They were treated with intravenous infusion of angiotensin-(1-7) (25 microgram/kg per hour) or saline by minipump. RESULTS: Abdominal aortic banding resulted in a significant increases in LVW/BW, myocardial angiotensinⅡlevels, and p-ERK1/2 expression. Angiotensin-(1-7) had no effect on aortic banding-induced increases in myocardial angiotensinⅡlevels, but it significantly attenuated aortic banding-induced increases in LVW/BW and p-ERK1/2 expression. CONCLUSION: Angiotensin-(1-7) attenuates the development of cardiac hypertrophy in pressure-overloaded rats. It may be associated with the inhibition of p-ERK1/2 expression in cardiac tissue.
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AIM:To evaluate complement activation in patients with all forms of acute coronary syndromes(ACS)and to examine the relationship between the degree of complement activation and myocardial injury.METHODS:The subjects were divided into 2 groups:110 ACS patients(group ACS)and 18 healthy persons(group control).One hundred and ten patients with ACS were divided into 3 sub-group:51 patients with ST-segment elevated myocardial infarction(STEMI),28 patients with non-ST-segment elevated myocardial infarction(NSTEMI)and 31 patients with unstable angina(UA).Complement 3(C3),complement 4(C4),troponin T(TnT)as well as creatine kinase MB(CK-MB)were evaluated.RESULTS:Plasma C3 and C4 peak levels were significantly higher in patients with STEMI [(1 525?302)mg/L and(423?123)mg/L] and NSTEMI [(1 516?289)mg/L and(396?68)mg/L] than those in patients with UA [(1 275?172)mg/L and(356?91)mg/L] and the control subjects [(1 072?196)mg/L and(182?73)mg/L](P