目的 观察卡托普利和美托洛尔对慢型克山病患者的治疗效果.方法 2007年在山东省莒县、五莲县、沂水县、平邑县、泗水县和邹城市6个克山病病区县(市),根据<克山病诊断标准>选择195例慢型克山病病例,按美国纽约心脏病学会心功能分级随机分为对照组、卡托普利组和美托洛尔组,3组患者均给予利尿剂、洋地黄、血管扩张剂等基础治疗,卡托普利组与美托洛尔组分别在此基础上加服卡托普利或美托洛尔,随访12个月,观察心脏原因死亡情况以及住院次数、住院天数、心脏大小、心电图、血压、心率变化情况.结果卡托普利组和美托洛尔组死亡率[4.76%(3/63)、5.00%(3/60)]均低于对照组[10.61%(7/66)],但差异无统计学意义(P>0.05).卡托普利组、美托洛尔组年住院时间[(19.12±20.35)、(18.86±21.52)d/年]均低于对照组[(21.45±21.74)d/年,q=3.17、3.38,P<0.05].治疗后卡托普利组与美托洛尔组患者心胸比率缩小的检出率分别为45.0%(27/60)和40.4%(23/57),均明显高于对照组[18.6%(11/59),χ2=9.51、6.59,P均<0.0125],而3组的心胸比率增大和不变的检出率组间比较差异均无统计学意义(χ2=2.50、4.75,P均>0.05).美托洛尔组异位心律消失率[56.5%(13/23)]高于对照组与卡托普利组[23.8%(5/21)、22.7%(5/22)],但差异无统计学意义(χ2=5.35、4.86,P均>0.0125).3组患者治疗前后收缩压、舒张压及心率差异均有统计学意义(F=47.51、44.23、80.66,P均<0.01),治疗时间与药物的交互作用对收缩压和心率有影响(F=3.19、37.44,P均<0.05),对舒张压无影响(F=2.21,P>0.05).治疗前3组收缩压、舒张压及心率组间差异均无统计学意义(F=0.28、0.57、1.80,P均>0.05).卡托普利组、美托洛尔组及对照组治疗后收缩压及舒张压[(109.0±10.9)、(112.2±12.8)、(114.7±13.2)mm Hg,(69.3±7.2)、(72.1±9.5)、(73.3±9.3)mm Hg]均低于治疗前[(117.1±13.4)、(119.0±14.4)、(117.6±14.1)mm Hg,(74.2±10.2)、(76.3±10.8)、(75.4±11.1)mm Hg,t=4.79、4.47、2.08,5.12、4.32、2.15,P均<0.05].美托洛尔组治疗后心率[(66.2±7.7)次/min]明显低于治疗前[(75.9±11.5)次/min,t=10.81,P<0.01],卡托普利组与对照组心率[(70.6±8.0)、(72.6±10.5)次/min]较治疗前[(71.9±10.4)、(73.8±12.2)次/min]均无明显变化(t=1.77、1.74,P均>0.05).治疗后,卡托普利组收缩压与舒张压明显低于对照组(q=3.52、3.56,P均<0.05);美托洛尔组心率显著低于对照组与卡托普利组(q=5.44、3.73,P均<0.01).结论卡托普利与美托洛尔治疗慢型克山病,有降低心脏原因死亡的趋势,并可逆转或延缓心肌重构,减少住院率,且安全可靠,医疗费用少,具有重要的临床推广价值.
目的 觀察卡託普利和美託洛爾對慢型剋山病患者的治療效果.方法 2007年在山東省莒縣、五蓮縣、沂水縣、平邑縣、泗水縣和鄒城市6箇剋山病病區縣(市),根據<剋山病診斷標準>選擇195例慢型剋山病病例,按美國紐約心髒病學會心功能分級隨機分為對照組、卡託普利組和美託洛爾組,3組患者均給予利尿劑、洋地黃、血管擴張劑等基礎治療,卡託普利組與美託洛爾組分彆在此基礎上加服卡託普利或美託洛爾,隨訪12箇月,觀察心髒原因死亡情況以及住院次數、住院天數、心髒大小、心電圖、血壓、心率變化情況.結果卡託普利組和美託洛爾組死亡率[4.76%(3/63)、5.00%(3/60)]均低于對照組[10.61%(7/66)],但差異無統計學意義(P>0.05).卡託普利組、美託洛爾組年住院時間[(19.12±20.35)、(18.86±21.52)d/年]均低于對照組[(21.45±21.74)d/年,q=3.17、3.38,P<0.05].治療後卡託普利組與美託洛爾組患者心胸比率縮小的檢齣率分彆為45.0%(27/60)和40.4%(23/57),均明顯高于對照組[18.6%(11/59),χ2=9.51、6.59,P均<0.0125],而3組的心胸比率增大和不變的檢齣率組間比較差異均無統計學意義(χ2=2.50、4.75,P均>0.05).美託洛爾組異位心律消失率[56.5%(13/23)]高于對照組與卡託普利組[23.8%(5/21)、22.7%(5/22)],但差異無統計學意義(χ2=5.35、4.86,P均>0.0125).3組患者治療前後收縮壓、舒張壓及心率差異均有統計學意義(F=47.51、44.23、80.66,P均<0.01),治療時間與藥物的交互作用對收縮壓和心率有影響(F=3.19、37.44,P均<0.05),對舒張壓無影響(F=2.21,P>0.05).治療前3組收縮壓、舒張壓及心率組間差異均無統計學意義(F=0.28、0.57、1.80,P均>0.05).卡託普利組、美託洛爾組及對照組治療後收縮壓及舒張壓[(109.0±10.9)、(112.2±12.8)、(114.7±13.2)mm Hg,(69.3±7.2)、(72.1±9.5)、(73.3±9.3)mm Hg]均低于治療前[(117.1±13.4)、(119.0±14.4)、(117.6±14.1)mm Hg,(74.2±10.2)、(76.3±10.8)、(75.4±11.1)mm Hg,t=4.79、4.47、2.08,5.12、4.32、2.15,P均<0.05].美託洛爾組治療後心率[(66.2±7.7)次/min]明顯低于治療前[(75.9±11.5)次/min,t=10.81,P<0.01],卡託普利組與對照組心率[(70.6±8.0)、(72.6±10.5)次/min]較治療前[(71.9±10.4)、(73.8±12.2)次/min]均無明顯變化(t=1.77、1.74,P均>0.05).治療後,卡託普利組收縮壓與舒張壓明顯低于對照組(q=3.52、3.56,P均<0.05);美託洛爾組心率顯著低于對照組與卡託普利組(q=5.44、3.73,P均<0.01).結論卡託普利與美託洛爾治療慢型剋山病,有降低心髒原因死亡的趨勢,併可逆轉或延緩心肌重構,減少住院率,且安全可靠,醫療費用少,具有重要的臨床推廣價值.
목적 관찰잡탁보리화미탁락이대만형극산병환자적치료효과.방법 2007년재산동성거현、오련현、기수현、평읍현、사수현화추성시6개극산병병구현(시),근거<극산병진단표준>선택195례만형극산병병례,안미국뉴약심장병학회심공능분급수궤분위대조조、잡탁보리조화미탁락이조,3조환자균급여이뇨제、양지황、혈관확장제등기출치료,잡탁보리조여미탁락이조분별재차기출상가복잡탁보리혹미탁락이,수방12개월,관찰심장원인사망정황이급주원차수、주원천수、심장대소、심전도、혈압、심솔변화정황.결과잡탁보리조화미탁락이조사망솔[4.76%(3/63)、5.00%(3/60)]균저우대조조[10.61%(7/66)],단차이무통계학의의(P>0.05).잡탁보리조、미탁락이조년주원시간[(19.12±20.35)、(18.86±21.52)d/년]균저우대조조[(21.45±21.74)d/년,q=3.17、3.38,P<0.05].치료후잡탁보리조여미탁락이조환자심흉비솔축소적검출솔분별위45.0%(27/60)화40.4%(23/57),균명현고우대조조[18.6%(11/59),χ2=9.51、6.59,P균<0.0125],이3조적심흉비솔증대화불변적검출솔조간비교차이균무통계학의의(χ2=2.50、4.75,P균>0.05).미탁락이조이위심률소실솔[56.5%(13/23)]고우대조조여잡탁보리조[23.8%(5/21)、22.7%(5/22)],단차이무통계학의의(χ2=5.35、4.86,P균>0.0125).3조환자치료전후수축압、서장압급심솔차이균유통계학의의(F=47.51、44.23、80.66,P균<0.01),치료시간여약물적교호작용대수축압화심솔유영향(F=3.19、37.44,P균<0.05),대서장압무영향(F=2.21,P>0.05).치료전3조수축압、서장압급심솔조간차이균무통계학의의(F=0.28、0.57、1.80,P균>0.05).잡탁보리조、미탁락이조급대조조치료후수축압급서장압[(109.0±10.9)、(112.2±12.8)、(114.7±13.2)mm Hg,(69.3±7.2)、(72.1±9.5)、(73.3±9.3)mm Hg]균저우치료전[(117.1±13.4)、(119.0±14.4)、(117.6±14.1)mm Hg,(74.2±10.2)、(76.3±10.8)、(75.4±11.1)mm Hg,t=4.79、4.47、2.08,5.12、4.32、2.15,P균<0.05].미탁락이조치료후심솔[(66.2±7.7)차/min]명현저우치료전[(75.9±11.5)차/min,t=10.81,P<0.01],잡탁보리조여대조조심솔[(70.6±8.0)、(72.6±10.5)차/min]교치료전[(71.9±10.4)、(73.8±12.2)차/min]균무명현변화(t=1.77、1.74,P균>0.05).치료후,잡탁보리조수축압여서장압명현저우대조조(q=3.52、3.56,P균<0.05);미탁락이조심솔현저저우대조조여잡탁보리조(q=5.44、3.73,P균<0.01).결론잡탁보리여미탁락이치료만형극산병,유강저심장원인사망적추세,병가역전혹연완심기중구,감소주원솔,차안전가고,의료비용소,구유중요적림상추엄개치.
Objective To observe the curative effect of captopril and metoprolol in the treatment of chronic Keshan disease (CKD). Methods One hundred and ninty-five patients with CKD chosen from Juxian, Wulian, Yishui, Pingyi, Sishui and Zoucheng in Shandong Province were randomly assigned to control group, captopril group and metoprolol group according to NYHA cardiac functional grading. All cases were given diuretics, digitalis and vasodilating agents as routine treatment. On this basis, captopril and metoprolol was administered in captopril group and metoprolol group respectively. After 12 months of follow-up visit, the causes of cardiac death, hospitalization status and the changes of heart size, electrocardiogram, blood pressure and heart rate were all observed. Results It was found that the mortality of captopril group and metoprolo] group was 4.76% (3/63), 5.00% (3/60) respectively, both lower than the control group 10.61%(7/66). But this difference had no statistically significance(P=0.39). Besides, the hospitalization days of each year in captopril group and metoprolol group was respectively (19.12± 20.35) and(18.86±21.52)days, much more reduced than in the control group[(21.45±21.74)days, q=3.17, 3.38, P<0.05]. The detection rate of cardiothoracic ratio decreased in captopril group and metoprolol group [45% (27/60) and 40.4% (23/57)] After treatment showed more pronounced amelioration than the control group [18.6% (11/59), χ2=9.51,6.59, all P<0.0125], still the detection rate of cardiomegaly and invariability had no significant difference among three groups (χ2=2.50,4.75, all P>0.05). The elimination coefficient of ectopic rhythm in metoprolol group [56.5% (13/23)] was pronounced higher than the control group and captopril group [23.8% (5/21), 22.7% (5/22)], but differences had no statistically significance(P=0.0358,0.0331, all P>0.0125). Significant differences were found in systolic blood pressure(SBP), diastolic blood pressure(DBP) and heart rate(HR) in three groups prior and post-treatment(F=47.51,44.23,80.66, all P<0.01). The interaction of therapy and treatment time had influence on SBP and HR (F=3.19,37.44, all P<0.05), but had no influence on DBP(F=2.21, P> 0.05). There was no difference in SBP, DBP or HR among three groups before treatment(F=0.28,0.57,1.80, all P>0.05). After treatment, SBP and DBP in captopril group, metoprolol group and the control group[(109.0±10.9), (112.2±12.8), (114.7±13.2)mm Hg, (69.3±7.2), (72.1±9.5), (73.3±9.3)mm Hg] were all lowered compared with pre-treatment[ (117.1±13.4), (119.0±14.4), (117.6±14.1)mm Hg and (74.2±10.2), (76.3±10.8), (75.4±11.1)mm Hg, t=4.79,4.47,2.08,5.12, 4.32,2.15, all P<0.05]. HR was reduced in metoprolol group, being [(66.2±7.7), (75.9±11.5)times/min] before and after treatment(t=10.81, P<0.01), while it remained unchanged in captopril group and control group[(70.6±8.0), (72.6±10.5) times/min and (71.9±10.4), (73.8± 12.2)times/min, t=1.77,1.74, all P>0.05]. After treatment, both SBP and DBP of captopril group were significantly lower than that in the control group (q=3.52,3.56, all P<0.05); HR was reduced in metoprolol group, lower than that in captopril group and control group(q=5.44,3.73, all P<0.01). Conclusions Having a tendency of depressing mortality, captopril and metoprolol can reverse or delay myocardial remodeling and reduce admission rate in a safe,reliable and economic way, and are worth to be widely used in the treatment of chronic Keshan disease.
