磷酸肌酸钠对创伤性脑心综合征患者心脏局部室壁运动异常和射血分数值的影响
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摘要
目的:观察磷酸肌酸钠(creatine phosphate sodium,CP)对创伤性脑心综合征患者心脏局部室壁运动异常、射血分数值、心肌酶及血浆脑钠肽(brain natriuretic peptide,BNP)的影响。方法:选择创伤性脑损伤患者45例,年龄18～65岁,均行手术治疗后入ICU,随机数字表法分为对照组(C组)22例和治疗组(CP组)23例。C组进行常规治疗。CP组在接受常规治疗基础上,加用磷酸肌酸钠治疗:1.0 g/次,2次/d,静脉滴注3 d。分别于治疗前、治疗后3 d由同一位医师行床旁超声心动图检查,测定左室射血分数(LVEF)和局部室壁运动异常值(RWMA),同时抽取患者静脉血测定乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、天冬氨酸氨基转移酶(AST)以及血浆脑钠肽(BNP)的水平。结果:治疗后超声心动图检查提示,CP组室壁运动较C组明显改善。CP组心肌酶和BNP水平较C组明显降低,差异有统计学意义(P<0.05)。结论:磷酸肌酸钠能减轻心脏局部室壁运动障碍,改善心肌收缩力,降低创伤性脑损伤患者心肌酶和血浆BNP水平,对防治脑心综合征有益。
Objective:To inv estigate the effect of creatine phosphate sodium on regional wall motion abnormality,ejection fraction(EF),myocardial enzymes and plasma brain natriuretic peptide in patients with traumatic brain heart syndrome.Methods:A total of 45 patients with traumatic brain injury in ICU after surgical operation,aged 18 to 65,were randomly divided into control group(group C) and treatment group(group CP)(n=22 for Group C,n=23 for Group CP).Patients in group C received routine treatment.Patients in group CP were given creatine 1.0 g·d-1phosphate sodium ivgtt,bid for 3 days on the basis of routine treatment.The left ventricular ejection fraction and regional wall motion abnormality was measured under echocardiography by the same physician.The plasma levels of LDH,CK,CK-MB,AST and BNP were determined in both two groups.Results:Echocardiographic examination showed that the grade of RWMA in group CP was significantly decreased compared with that in group C.Compared with group C,the plasma levels of myocardial enzymes and BNP were significantly decreased in group CP(P<0.05).Conclusion:Creatine phosphate sodium can improve myocardial contractility,then reduce the levels of myocardial enzymes and plasma BNP in patients with traumatic brain injury,and prevent brain heart syndrome.
Objective:To inv estigate the effect of creatine phosphate sodium on regional wall motion abnormality,ejection fraction(EF),myocardial enzymes and plasma brain natriuretic peptide in patients with traumatic brain heart syndrome.Methods:A total of 45 patients with traumatic brain injury in ICU after surgical operation,aged 18 to 65,were randomly divided into control group(group C) and treatment group(group CP)(n=22 for Group C,n=23 for Group CP).Patients in group C received routine treatment.Patients in group CP were given creatine 1.0 g·d-1phosphate sodium ivgtt,bid for 3 days on the basis of routine treatment.The left ventricular ejection fraction and regional wall motion abnormality was measured under echocardiography by the same physician.The plasma levels of LDH,CK,CK-MB,AST and BNP were determined in both two groups.Results:Echocardiographic examination showed that the grade of RWMA in group CP was significantly decreased compared with that in group C.Compared with group C,the plasma levels of myocardial enzymes and BNP were significantly decreased in group CP(P<0.05).Conclusion:Creatine phosphate sodium can improve myocardial contractility,then reduce the levels of myocardial enzymes and plasma BNP in patients with traumatic brain injury,and prevent brain heart syndrome.
引文
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[12]Xu Y,Jiang L,Huang Y,et al.Solid-state characterization and transformation of various creatine phosphate sodium hydrates[J].J Pharm Sci,2014,103(11):3688-95.
[13]Kewu D,Xubo S,Yingxin Z,et al.The effect of exogenous creatine phosphate on myocardial injury after percutaneous coronary intervention[J].Angiology,2015,66(2):163-8.
[2]Strumia E,Pelliccia F,D'Ambrosio G.Creatine phosphate:pharmacological and clinical perspectives[J].Adv Ther,2012,29(2):99-123.
[3]Flynn M,Curtin R,Nowicki ER,et al.Regional wal motion abnormalities and scarring in severefunctiona ischemic mitral regurgitation:A pilot cardiovascular magnetic resonance imaging study[J].Thorac Cardiovasc Surg,2009,137:1063-70.
[4]Samuels MA.The brain-heart connection[J].Circulation2007,116(1):77-84.
[5]Krishnamoorthy V,Rowhani-Rahbar A,Chaikittisilpa Net al.Association of early hemodynamic profile and the development of systolic dysfunction following traumatic brain injury[J].Neurocril Care,2017,26(3):379-87.
[6]Mashaly HA,Provencio JJ.Inflammation as a link between brain injury and heart damage:the model o subarachnoid hemorrhage[J].Cleve Clin J Med,200875 Suppl 2(Suppl_2):S26-30.
[7]Davison DL,Terek M,Chawla LS.Neurogenic pulmonary edema[J].Crit Care,2012,16(2):212.
[8]Richard C.Stress-related cardiomyopathies[J].Ann Intensive Care,2011,1(1):1-8.
[9]Kilbourn KJ,Ching G,Silverman DI,et al.Clinical outcomes after neurogenic stress induced cardiomyopathy in aneurysmal sub-arachnoid hemorrhage:a prospective cohort study[J].Clin Neurol Neurosurg,2015,128:4-9.
[10]Chida K,Otani H,Kohzuki M,et al.The relationship between plasma BNP level and the myocardial phosphocreatine/adenosine triphosphate ratio determined by phosphorus-31 magnetic resonance spectroscopy in patients with dilated cardiomyopathy[J].Cardiology,2006,106:132-6.
[11]Humphrey SM,Vanderwee MA,Gavin JB.Transmural differences in the postischemic recovery of cardiac energy metabolism[J].Am J Pathol,1988,131(1):5-11.
[12]Xu Y,Jiang L,Huang Y,et al.Solid-state characterization and transformation of various creatine phosphate sodium hydrates[J].J Pharm Sci,2014,103(11):3688-95.
[13]Kewu D,Xubo S,Yingxin Z,et al.The effect of exogenous creatine phosphate on myocardial injury after percutaneous coronary intervention[J].Angiology,2015,66(2):163-8.