冠心病患者住院期间痛风急性发作及危险因素分析
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摘要
目的:分析冠心病患者住院期间痛风急性发作情况及其危险因素。方法:选取2014年1月1日至2016年12月31日在我院心血管内科病房住院的4 620例冠心病患者,观察其住院期间有无痛风急性发作。根据有、无痛风急性发作分为痛风急性发作组(n=54)和无痛风急性发作组(n=4 566)。按住院期间干预方式分为接受冠状动脉造影(CAG)组(CAG组,n=1 431)、接受经皮冠状动脉介入治疗(PCI)组(PCI组,n=1545)及对照组(没有接受上述干预的冠心病患者,n=1 644)。应用Logistic回归方程对痛风急性发作及基本资料进行危险因素关联分析。结果:住院期间冠心病患者痛风急性发作发生率为1.17%(54/4 620),其中CAG组、PCI组、对照组痛风急性发作发生率依次为1.12%(16/1 431)、2.01%(31/1 545)、0.43%(7/1 644),组间比较差异有统计学意义(P<0.05)。痛风急性发作组中男性占96.30%,高于无痛风急性发作组(70.52%,P=0.00)。痛风急性发作组患者的尿酸水平高于无痛风急性发作组[(463.36±84.55)mmol/L vs(383.28±105.72)mmol/L,P<0.05];两组在年龄、糖尿病、高血压、肾功能不全、高脂血症方面的差异无统计学意义。二分类Logistics回归分析结果显示,男性(OR=9.215,95%CI:2.237～37.959,P=0.002)、血尿酸水平(OR=1.005,95%CI:1.003～1.007,P=0.000)、CAG(OR=3.706,95%CI:1.460～9.409,P=0.006)和PCI(OR=6.507,95%CI:2.719～15.573,P=0.000)是痛风急性发作的独立危险因素。结论:住院冠心病患者接受CAG、PCI后痛风发生率较无上述干预的患者更高;CAG/PCI干预、男性、高血尿酸水平患者更容易发生痛风急性发作。
Objectives: To observe the incidence of acute gout attacks(AGA) and investigate the risk factors in hospitalized patients with coronary heart disease.Methods: Hospitalized patients with coronary heart disease of cardiovascular ward in the first affiliated hospital of Xiamen University during January 1, 2014 to December 31, 2016 were survey in this study. Patients were divided into AGA(n=54) and non-AGA(n=4 566) group. The patients were further divided into three groups: Group CAG: patients received coronary angiography(n=1431); Group PCI: patients received PCI treatment(n=1 545); Control Group: patients received neither CAG nor PCI treatment(n=1 644). The occurrence of acute gout attacks in each group were recorded. Risk factors of acute gout attacks were evaluated with logistic regression analysis. Results: The incidence of acute gout attacks in hospitalized CHD patients was 1.17%(54/4620), and the incidence was significantly higher in PCI group(2.01%, 31/1 545) and CAG group(1.12%,16/1 431) than in in control group(0.43%, 7/1644, P<0.05). Prevalence of male gender(96.30% vs 70.52%, P=0.000) and serum uric acid level([463.36±84.55] mmol/L vs [383.28±105.72] mmol/L, P<0.05) were significantly higher in AGA group than in non-AGA group, while age, prevalence of diabetes mellitus, hypertension, hyperlipidemia and renal insufficiency were similar between AGA and non-AGA groups(all P>0.05). Binary logistic regression analysis showed that male(OR=9.215, 95%CI: 2.237-37.959, P=0.002), higher level of serum uric acid( OR=1.005, 95%CI:1.003-1.007, P=0.000), CAG(OR=3.706, 95%CI: 1.460-9.409, P=0.006) and PCI(OR=6.507, 95%CI: 2.719-15.573, P=0.000) were significantly associated with acute gout attacks in hospitalized CHD patients. Conclusions: The incidence of acute gout attacks is higher in hospitalized patients with coronary heart disease after CAG and PCI than those without the CAG and PCI. CAG, PCI intervention, male and hyperuricemia are independent risk factors for acute gout attacks in hospitalized CHD patients.
Objectives: To observe the incidence of acute gout attacks(AGA) and investigate the risk factors in hospitalized patients with coronary heart disease.Methods: Hospitalized patients with coronary heart disease of cardiovascular ward in the first affiliated hospital of Xiamen University during January 1, 2014 to December 31, 2016 were survey in this study. Patients were divided into AGA(n=54) and non-AGA(n=4 566) group. The patients were further divided into three groups: Group CAG: patients received coronary angiography(n=1431); Group PCI: patients received PCI treatment(n=1 545); Control Group: patients received neither CAG nor PCI treatment(n=1 644). The occurrence of acute gout attacks in each group were recorded. Risk factors of acute gout attacks were evaluated with logistic regression analysis. Results: The incidence of acute gout attacks in hospitalized CHD patients was 1.17%(54/4620), and the incidence was significantly higher in PCI group(2.01%, 31/1 545) and CAG group(1.12%,16/1 431) than in in control group(0.43%, 7/1644, P<0.05). Prevalence of male gender(96.30% vs 70.52%, P=0.000) and serum uric acid level([463.36±84.55] mmol/L vs [383.28±105.72] mmol/L, P<0.05) were significantly higher in AGA group than in non-AGA group, while age, prevalence of diabetes mellitus, hypertension, hyperlipidemia and renal insufficiency were similar between AGA and non-AGA groups(all P>0.05). Binary logistic regression analysis showed that male(OR=9.215, 95%CI: 2.237-37.959, P=0.002), higher level of serum uric acid( OR=1.005, 95%CI:1.003-1.007, P=0.000), CAG(OR=3.706, 95%CI: 1.460-9.409, P=0.006) and PCI(OR=6.507, 95%CI: 2.719-15.573, P=0.000) were significantly associated with acute gout attacks in hospitalized CHD patients. Conclusions: The incidence of acute gout attacks is higher in hospitalized patients with coronary heart disease after CAG and PCI than those without the CAG and PCI. CAG, PCI intervention, male and hyperuricemia are independent risk factors for acute gout attacks in hospitalized CHD patients.
引文
[1] Kleber ME, Delgado G, Grammer TB, et al. Uric acid and cardiovascular events:a mendelian randomization study[J]. J Am Soc Nephrol, 2015, 26(11):2831-2838. DOI:10. 1681/ASN.2014070660.
[2]中华医学会内分泌分会.高尿酸血症和痛风治疗的中国专家共识[J].中华内分泌代谢杂志,2013, 29(11):913-920. DOI:10. 3760/cma. j. issn. 1000-6699. 2013. 11. 001.
[3] Krishnan E. Gout and coronary artery disease:epidemiologic clues[J]. Curn Rheumatol Rep, 2008, 10(3):249-255. DOI:10. 1186/ar3684.
[4] Khanna D, Fitzgerald JD, Khanna PP. 2012 American College of Rheumatology guidelines for management of gout. PartⅠ:systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia[J]. Arthritis Care Res(Hoboken), 2012, 64(10):1431-1446. DOI:10. 1002/acr. 21772.
[5] Khanna D, Khanna PP, Fitzgerald JD. 2012 American College of Rheumatology guidelines for management of gout. PartⅡ:Therapy and antiinflammatory prophylaxis of acute gout arthritis[J]. ArthritisCare Res(Hoboken), 2012, 64(10):1447-1461. DOI:10. 1002/acr.21773.
[6]葛均波,徐永健.内科学[M].第八版.北京:人民卫生出版社,2013:220-256.
[7]邵苗,张学武.2015年欧洲抗风湿病联盟/美国风湿病学会痛风分类新标准[J].中华风湿病学杂志,2015, 19(12):854-855. DOI:10. 3760/cma. j. issn. 1007-7480. 2015. 12. 012.
[8] Dincer HE, Dincer AP. Levinson. Asymptomatic hyperuricemia:to treat or not to treat[J]. Cleve Clinic J Med, 2002, 69(8):594-608.
[9]高立建,陈纪林.急性冠状动脉综合征介入治疗最新进展[J].中国循环杂志,2013, 28(1):3-5. DOI:10. 3969/j. issn. 1000-3614.2013.01.002.
[10] Nozue T,Michishita I,Iwaki T,et al. Contrast medium volume to estimated glomerular filtration rate ratio as a predictor of contrastinduced nephropathy developing after elective percutaneous coronary intervention[J]. J Cardiol, 2009, 54(2):214-220. DOI:10. 1016/j.jjcc. 2009. 05. 008.
[11] Xu JZ, Zhang ML, Ni YH. Impact of low hemoglobin on the development of contrast-induced nephropathy:a retrospective cohort study[J]. Exp Ther Med, 2016, 12(2):603-610. DOI:10. 3892/etm.2016. 3416.
[12] Klein LW, Sheldon MW, Brinker J, et al. The use of radiographic contrast media during PCI:a focused review:a position statement of the Society of Cardiovascular Angiography and Interventions[J].Catheter Cardiovasc Interv, 2009, 74(5):728-746. DOI:10. 1002/ccd. 22113.
[13]钱懿轶,张峻.PCI后造影剂肾病并痛风急性发作1例及用药分析[J].临床合理用药杂志,2011,4(34):93-94. DOI:10. 3969/j. issn.1674-3296. 2011.34.081.
[14] Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout[J]. Ann Rheum Dis,2017, 76(1):1-14. DOI:10. 1136/annrheumdis-2016-209707.
[15] Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II[J]. Arthritis Rheum, 2008, 58(1):26-35. DOI:10.1002/art. 23176.
[16] Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk[J]. N Eng J Med, 2008, 359(17):1811-1821. DOI:10. 1056/NEJMra0800885.
[17] Chuang SY, Lee SC, Hsieh YT, et al. Trends in hyperuricemia and gout prevalence:nutrition and health survey in Taiwan from 1993-1996 to 2005-2008[J]. Asia Pac J Clin Nutr, 2011, 20(2):301-308.
[18] Krishnan E,Baker JF,Furst DE,et al. Gout and the risk of acute myocardial infarction[J]. Arthritis Rheum, 2006, 54(8):2688-2696.DOI:10. 1002/art. 22014.
[19] DeVera MA, Rahman MM, Bhole V, et al. Independent impact of gout on the risk of acute myocardial infarction among elderly women:a population-based study[J]. Ann Rheum Dis, 2010, 69(6):1162-1164. DOI:10. 1136/ard. 2009. 122770.
[20]曾玮,苏清芳,吴广明.冠心病并发急性痛风40例临床分析[J].实用医学杂志,2010, 26(3):430-431. DOI:10.3969/j.issn.1006-5725.2010.03.039.
[2]中华医学会内分泌分会.高尿酸血症和痛风治疗的中国专家共识[J].中华内分泌代谢杂志,2013, 29(11):913-920. DOI:10. 3760/cma. j. issn. 1000-6699. 2013. 11. 001.
[3] Krishnan E. Gout and coronary artery disease:epidemiologic clues[J]. Curn Rheumatol Rep, 2008, 10(3):249-255. DOI:10. 1186/ar3684.
[4] Khanna D, Fitzgerald JD, Khanna PP. 2012 American College of Rheumatology guidelines for management of gout. PartⅠ:systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia[J]. Arthritis Care Res(Hoboken), 2012, 64(10):1431-1446. DOI:10. 1002/acr. 21772.
[5] Khanna D, Khanna PP, Fitzgerald JD. 2012 American College of Rheumatology guidelines for management of gout. PartⅡ:Therapy and antiinflammatory prophylaxis of acute gout arthritis[J]. ArthritisCare Res(Hoboken), 2012, 64(10):1447-1461. DOI:10. 1002/acr.21773.
[6]葛均波,徐永健.内科学[M].第八版.北京:人民卫生出版社,2013:220-256.
[7]邵苗,张学武.2015年欧洲抗风湿病联盟/美国风湿病学会痛风分类新标准[J].中华风湿病学杂志,2015, 19(12):854-855. DOI:10. 3760/cma. j. issn. 1007-7480. 2015. 12. 012.
[8] Dincer HE, Dincer AP. Levinson. Asymptomatic hyperuricemia:to treat or not to treat[J]. Cleve Clinic J Med, 2002, 69(8):594-608.
[9]高立建,陈纪林.急性冠状动脉综合征介入治疗最新进展[J].中国循环杂志,2013, 28(1):3-5. DOI:10. 3969/j. issn. 1000-3614.2013.01.002.
[10] Nozue T,Michishita I,Iwaki T,et al. Contrast medium volume to estimated glomerular filtration rate ratio as a predictor of contrastinduced nephropathy developing after elective percutaneous coronary intervention[J]. J Cardiol, 2009, 54(2):214-220. DOI:10. 1016/j.jjcc. 2009. 05. 008.
[11] Xu JZ, Zhang ML, Ni YH. Impact of low hemoglobin on the development of contrast-induced nephropathy:a retrospective cohort study[J]. Exp Ther Med, 2016, 12(2):603-610. DOI:10. 3892/etm.2016. 3416.
[12] Klein LW, Sheldon MW, Brinker J, et al. The use of radiographic contrast media during PCI:a focused review:a position statement of the Society of Cardiovascular Angiography and Interventions[J].Catheter Cardiovasc Interv, 2009, 74(5):728-746. DOI:10. 1002/ccd. 22113.
[13]钱懿轶,张峻.PCI后造影剂肾病并痛风急性发作1例及用药分析[J].临床合理用药杂志,2011,4(34):93-94. DOI:10. 3969/j. issn.1674-3296. 2011.34.081.
[14] Richette P, Doherty M, Pascual E, et al. 2016 updated EULAR evidence-based recommendations for the management of gout[J]. Ann Rheum Dis,2017, 76(1):1-14. DOI:10. 1136/annrheumdis-2016-209707.
[15] Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic conditions in the United States. Part II[J]. Arthritis Rheum, 2008, 58(1):26-35. DOI:10.1002/art. 23176.
[16] Feig DI, Kang DH, Johnson RJ. Uric acid and cardiovascular risk[J]. N Eng J Med, 2008, 359(17):1811-1821. DOI:10. 1056/NEJMra0800885.
[17] Chuang SY, Lee SC, Hsieh YT, et al. Trends in hyperuricemia and gout prevalence:nutrition and health survey in Taiwan from 1993-1996 to 2005-2008[J]. Asia Pac J Clin Nutr, 2011, 20(2):301-308.
[18] Krishnan E,Baker JF,Furst DE,et al. Gout and the risk of acute myocardial infarction[J]. Arthritis Rheum, 2006, 54(8):2688-2696.DOI:10. 1002/art. 22014.
[19] DeVera MA, Rahman MM, Bhole V, et al. Independent impact of gout on the risk of acute myocardial infarction among elderly women:a population-based study[J]. Ann Rheum Dis, 2010, 69(6):1162-1164. DOI:10. 1136/ard. 2009. 122770.
[20]曾玮,苏清芳,吴广明.冠心病并发急性痛风40例临床分析[J].实用医学杂志,2010, 26(3):430-431. DOI:10.3969/j.issn.1006-5725.2010.03.039.