急性蛛网膜下腔出血对左心室功能的影响及其与血浆脑钠素关系研究

A Study of the Effect of Acute Subarachnoid Hemorrhage on Left Ventricular Function and the Relationship Between Acute Subarachnoid Hemorrhage and Plasma Brain Natriuretic Peptide

目的通过超声心动图(echocardiography)进行心功能检查及血浆脑钠素(brain natriuretic peptide,BNP)测定,观察急性蛛网膜下腔出血(subarachnoid hemorrhage,SAH)患者心脏左心室功能(left ventricular function,LVF)的变化及其与血浆BNP的关系,并探讨其机制,为防治急性SAH所致心脏损害提供依据。方法选择发病24h内经临床和头颅CT检查确诊的急性SAH患者20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、心律失常等心脏并发症。选择性别和年龄匹配的21例正常人作为对照组。以上各组均行超声心动图检查,同时抽血检测血浆BNP,对结果进行分析。结果①急性SAH组患者的左室舒张末期内径、左室后壁厚度、室间隔厚度、相对室壁厚度、左室心肌重量、左室心肌重量指数均值与正常对照组比较无显著性差异(P>0.05);②急性SAH组每搏排出量(SV)、每分心排出量(CO)及心脏指数(CI)均值低于正常对照组(分别为33.46±11.33vs52.67±12.46,P<0.01;3.02±1.33vs3.87±1.33,P<0.05;1.75±0.76vs2.37±0.81,P<0.05);③急性SAH组左室射血分数(LVEF)均值明显低于正常对照组(46.95±9.36vs67.71±8.02,P<0.01)。急性SAH组E峰最大速度/A峰最大速度比值(E/A)均值显著低于正常对照组(1.04±0.48vs1.47±0.23,P<0.01);④急性SAH组血浆BNP浓度高于正常对照组(62.30,11.44～120.08vs1.90,0.15～21.50,P<0.01)。结论急性SAH可引起左心室收缩功能和舒张功能下降;急性SAH发病后血浆BNP浓度升高,可能与急性SAH本身的病理生理机制有关。

Objective The purpose of this study is to observe the changes of left ventricular function in patients with acute subarachnoid hemorrhage（SAH） and the relationship between SAH and plasma brain natriuretic peptide（BNP） by using echocardiography and determining plasma BNP concentration, and to approach the mechanism and find the evidences for preventing and treating cardiac impairment caused by acute SAH. Methods Twenty patients with acute SAH within 24 hours diagnosed by clinical manifestation and head computed tomography were selected. All enrolled patients had no history of heart diseases and no complications such as cardiac insufficiency and arrhythmia. And in the same period twenty - one sex and age matched healthy persons were selected as control group. All patients and controls were undergone echocardiographic investigation and in the same time blood was drawn for the quantitative determination of plasma BNP concentration. Results （1）There is no significant difference in the mean of LVIDd,PWT,IVST,RWT,LVM,LVMi between acute SAH group and healthy persons group（P 〉 0.05 ）. （2）The mean of SV, the mean of CO and the mean of CI in acute SAH group were lower than those in healthy persons group respectively （33.46 ± 11.33 vs 52.67 ± 12.46,P 〈 0.01 ; 3.02 ± 1.33 vs 3.87 ± 1.33, P 〈 0.05 ; 1.75 ± 0.76 vs 2.37 ± 0.81 ,P 〈 0.05 ）. （3）The mean of LVEF in acute SAH group was much lower than that in healthy persons group （46.95 ±9.36 vs 67.71 ± 8.02,P 〈0.01 ）. The mean of E/A ratio in acute SAH group was much lower than that in healthy persons group （1.04 ±0.48 vs 1.47 ± 0.23, P 〈 0.01 ）. （4）The plasma BNP concentration in acute SAH group was higher than that in healthy persons group （62.30, 11.44 -120.08 vs 1.90, 0.15 -21.50,P〈0.01）. Conclusions Acute SAH can cause left ventricular systolic and diastolic function to decrease. The plasma BNP concentration increases after the onset of acute SAH. The rise of plasma BNP concentration may be caused by the pathophysiologic mechanism of acute SAH.