急性脑出血对左心室功能的影响及其与血浆脑钠素的关系

目的观察急性脑出血(acute cerebral hemorrhage)患者心脏左心室功能(left ventricu lar function,LVF)的变化及其与血浆脑钠素(brain natriuretic peptide,BNP)的关系并探讨其机制,为防治急性脑出血所致心脏损伤提供依据。方法选择发病24 h内经临床和头颅CT检查确诊的急性脑出血患者30例作为研究对象,所有患者既往无心脏病史,并除外心功能不全、心律失常等并发症。选择性别和年龄匹配的20例高血压患者及21例正常人作为对照组。以上各组受试者均行超声心动图检查,同时用ELISA法检测血浆BNP,并对结果进行分析。结果1)急性脑出血组左心室射血分数(left ventricu lar ejection fraction,LVEF)均值明显低于高血压组及正常对照组〔分别为(41.33±15.03)%vs(59.20±15.03)%,P<0.01;(41.33±15.03)%vs(67.71±8.02)%,P<0.01〕;高血压组LVEF均值与正常对照组比较差异无统计学意义(P>0.05)。急性脑出血组舒张早期最大血流速度/舒张晚期最大血流速度(E/A)均值低于高血压组及正常对照组,与高血压组比较差异无统计学意义(P>0.05),与正常对照组比较差异有统计学意义(1.00±0.46vs1.47±0.23,P<0.01),高血压组E/A均值低于正常对照组,二者比较差异有统计学意义(1.09±0.37vs1.47±0.23,P<0.01)。2)急性脑出血组血浆BNP浓度高于正常对照组〔(49.62 ng/L(17.18~85.25)ng/Lvs1.90 ng/L(0.15~21.50)ng/L,P<0.01)〕。3)急性脑出血组脑出血量与血浆BNP浓度的相关系数r=0.13(P>0.05);急性脑出血组脑出血量与各心功能参数间无相关性(P>0.05)。急性脑出血组血浆BNP浓度与左心室各结构与功能参数间无相关性(P>0.05)。结论急性脑出血可引起左心室收缩功能和舒张功能下降;脑出血量与心功能参数之间无相关性;急性脑出血发病后血浆BNP浓度升高,但与心脏结构和功能参数间无相关性,可能与急性脑出血本身的病理生理机制有关。

Study on the Effect of Acute Cerebral Hemorrhage on Left Ventricular Function and the Relationship between Acute Cerebral Hemorrhage and Plasma Brain Natriuretic Peptide

Objective The purpose of this study is to investigate the alterations of left ventricular function in patients with acute cerebral hemorrhage and the relationship between acute cerebral hemorrhage and plasma brain natreuretic peptide(BNP) by way of echocardiography and plasma BNP concentration determination and to bring to light the mechanism and to provide the basics for preventing and treating cardiac impairment caused by acute cerebral hemorrhage.Methods Thirty patients with acute cerebral hemorrhage within 24h having been diagnosed by clinical manifestations and head computed tomography were recruited.All enrolled patients had no history of heart diseases and no complications such as cardiac insufficiency and arrhythmia.And concurrently twenty sex and age matched patients with essential hypertension,and twenty-one sex and age matched healthy persons were selected as control groups.All patients and controls underwent echocardiographic investigation and at the same time blood was drawn for the quantitative determination of plasma BNP concentration.Results 1) The mean of LVEF in acute cerebral hemorrhage group was much lower than those in hypertension group and healthy control group((41.33±15.03)% vs(59.20±15.03)%,P<0.01;(41.33±15.03)% vs(67.71±8.02)%,P<0.01,respectively);There was no significant difference in the mean of LVEF between hypertension and healthy control groups(P>0.05).The mean E/A ratio in acute cerebral hemorrhage group was lower than those in hypertension group and healthy control groups.There was no significant difference in the mean E/A ratio between acute cerebral hemorrhage group and hypertension group(P>0.05),but there was significant difference between acute hemorrhage group and healthy control group(1.00±0.46 vs 1.47±0.23,P<0.01).The mean E/A ratio in hypertension group was lower than that in healthy control group, the difference was significant(1.09±0.37 vs 1.47±0.23,P<0.01).2) The plasma BNP concentration in acute cerebral hemorrhage group was higher than that in healthy control group((49.62 ng/L,(17.18～85.25)ng/L vs(1.90 ng/L,(0.15～21.50)ng/L,P<0.01).3) The correlation coefficient between volume of cerebral hemorrhage and plasma BNP concentration was 0.13(P>0.05).There was no correlation between volume of cerebral hemorrhage and all cardiac functional parameters in acute cerebral hemorrhage group(P>0.05).There was no correlation between plasma BNP concentration in acute hemorrhage group and cardiac structural and functional parameters(P>0.05).Conclusion Acute cerebral hemorrhage can cause left ventricular systolic dys function.Acute cerebral hemorrhage may cause left ventricular diastolic dys function as well.There was no correlation between the volume of cerebral hemorrhage and all cardiac functional parameters in acute cerebral hemorrhage group.The plasma BNP concentration increases after the onset of acute hemorrhage,but there was no correlation between the BNP concentration and changes in cardiac structural and functional parameters.The rise of plasma BNP concentration may be caused by the pathophysiologic mechanism of acute hemorrhage.