中华老年多器官疾病杂志
中華老年多器官疾病雜誌
중화노년다기관질병잡지
CHINESE JOURNAL OF MULTIPLE ORGAN DISEASES IN THE ELDERLY
2013年
9期
710-713
,共4页
心力衰竭%缬沙坦%N端脑钠肽前体%和肽素%老年人
心力衰竭%纈沙坦%N耑腦鈉肽前體%和肽素%老年人
심력쇠갈%힐사탄%N단뇌납태전체%화태소%노년인
heart failure%valsartan%N-terminal pro-B-type natriuretic peptide (NT-pro BNP)%copeptin%elderly
目的观察老年慢性心力衰竭(简称“心衰”)患者缬沙坦治疗前后血浆N端脑钠肽前体(NT-proBNP)及和肽素的变化,探讨缬沙坦抑制心室重构的作用机制。方法纳入2011年6月至2012年9月在湖南株洲凯德心血管病医院心内科就诊的老年慢性心衰患者99例,随机分为治疗组(常规治疗+缬沙坦,n=50)和对照组(仅常规治疗,n=49),分别检测两组治疗前、治疗1个月、治疗6个月,血浆NT-proBNP、和肽素水平及心室结构功能的变化。结果两组患者治疗1个月与治疗前、治疗6个月与1个月比较,血浆NT-proBNP及和肽素水平均下降,差异均有统计学意义(P<0.05或P<0.01);治疗组患者治疗1个月、6个月的血浆NT-proBNP、和肽素水平与同时间段对照组相比均下降,差异均有统计学意义(P<0.05或P<0.01)。治疗1个月,两组患者左室射血分数(LVEF)、左心室收缩末期内径(LVESD)及左心室舒张末期内径(LVEDD)与治疗前比较,以及两组间比较,差异均无统计学意义(P>0.05);治疗6个月,治疗组LVEF较对照组明显升高(P<0.01),LVESD及LVEDD较对照组明显减小(均P<0.01)。结论血管紧张素Ⅱ受体拮抗剂缬沙坦能够抑制老年慢性心衰患者血浆NT-proBNP、和肽素的分泌,抑制神经内分泌因子,抑制心室重构,改善心功能。
目的觀察老年慢性心力衰竭(簡稱“心衰”)患者纈沙坦治療前後血漿N耑腦鈉肽前體(NT-proBNP)及和肽素的變化,探討纈沙坦抑製心室重構的作用機製。方法納入2011年6月至2012年9月在湖南株洲凱德心血管病醫院心內科就診的老年慢性心衰患者99例,隨機分為治療組(常規治療+纈沙坦,n=50)和對照組(僅常規治療,n=49),分彆檢測兩組治療前、治療1箇月、治療6箇月,血漿NT-proBNP、和肽素水平及心室結構功能的變化。結果兩組患者治療1箇月與治療前、治療6箇月與1箇月比較,血漿NT-proBNP及和肽素水平均下降,差異均有統計學意義(P<0.05或P<0.01);治療組患者治療1箇月、6箇月的血漿NT-proBNP、和肽素水平與同時間段對照組相比均下降,差異均有統計學意義(P<0.05或P<0.01)。治療1箇月,兩組患者左室射血分數(LVEF)、左心室收縮末期內徑(LVESD)及左心室舒張末期內徑(LVEDD)與治療前比較,以及兩組間比較,差異均無統計學意義(P>0.05);治療6箇月,治療組LVEF較對照組明顯升高(P<0.01),LVESD及LVEDD較對照組明顯減小(均P<0.01)。結論血管緊張素Ⅱ受體拮抗劑纈沙坦能夠抑製老年慢性心衰患者血漿NT-proBNP、和肽素的分泌,抑製神經內分泌因子,抑製心室重構,改善心功能。
목적관찰노년만성심력쇠갈(간칭“심쇠”)환자힐사탄치료전후혈장N단뇌납태전체(NT-proBNP)급화태소적변화,탐토힐사탄억제심실중구적작용궤제。방법납입2011년6월지2012년9월재호남주주개덕심혈관병의원심내과취진적노년만성심쇠환자99례,수궤분위치료조(상규치료+힐사탄,n=50)화대조조(부상규치료,n=49),분별검측량조치료전、치료1개월、치료6개월,혈장NT-proBNP、화태소수평급심실결구공능적변화。결과량조환자치료1개월여치료전、치료6개월여1개월비교,혈장NT-proBNP급화태소수평균하강,차이균유통계학의의(P<0.05혹P<0.01);치료조환자치료1개월、6개월적혈장NT-proBNP、화태소수평여동시간단대조조상비균하강,차이균유통계학의의(P<0.05혹P<0.01)。치료1개월,량조환자좌실사혈분수(LVEF)、좌심실수축말기내경(LVESD)급좌심실서장말기내경(LVEDD)여치료전비교,이급량조간비교,차이균무통계학의의(P>0.05);치료6개월,치료조LVEF교대조조명현승고(P<0.01),LVESD급LVEDD교대조조명현감소(균P<0.01)。결론혈관긴장소Ⅱ수체길항제힐사탄능구억제노년만성심쇠환자혈장NT-proBNP、화태소적분비,억제신경내분비인자,억제심실중구,개선심공능。
Objective To determine the effects of valsartan on the plasma levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and copeptin in the elderly patients with chronic heart failure (CHF), and to investigate the possible mechanism of valsartan to prevent ventricular remodeling. Methods A total of 99 CHF elderly patients aged from 60~81(68±12)years who were hospitalized in our department from June 2011 to September 2012 were recruited in this study. They were randomly divided into 2 groups:valsartan and conventional treatment group (valsartan group, n=50), and conventional treatment (control group, n=49). The plasma levels of NT-proBNP and copeptin, and the structural function of left ventricle were measured at the baseline, 1 and 6 months after valsartan treatment. Results The levels of NT-proBNP and copeptin were decreased in both groups at 1 month after treatment, and more significantly at 6 months (P<0.05 or 0.01). Their levels were significantly lower in the valsartan treatment group than in the control group at 1 and 6 months after treatment respectively (P<0.05 or 0.01). No significant difference was found in the left ventricular ejection fraction (LVEF), left ventricular end systolic diameter (LVESD) and left ventricular end diastolic diameter (LVEDD) in the 2 groups at 1 month after treatment, and between the 2 groups before and at 1 month after treatment (P>0.05). But at 6 months after treatment, the LVEF was significantly higher (P<0.01), while the LVESD and LVEDD were significantly lower in the valsartan treatment group than in the control group (P<0.01). Conclusion Angiotensin Ⅱ receptor antagonist valsartan could inhibit the secretion of NT-proBNP and copeptin in the plasma of elderly patients with CHF, and then suppresses neuroendocrine factors, prevents ventricular remodeling, and therefore improves the heart function.