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心肌运动定量技术在多囊卵巢合并胰岛素抵抗患者左室纵向心肌功能评价中的价值

2018-11-10杜启亘米香琴徐宏伟商玮珉周立平陈巍

中国医药导报 2018年19期
关键词:胰岛素抵抗左心室

杜启亘 米香琴 徐宏伟 商玮珉 周立平 陈巍

[摘要] 目的 探討心肌运动定量(CMQ)技术评价多囊卵巢合并胰岛素抵抗(PCOS-IR)患者左心室纵向运动的临床价值。 方法 选取2016年2月~2017年2月在黑龙江中医药大学附属第二医院妇科就诊的PCOS-IR患者55例为PCOS-IR组,另选择年龄相匹配的55名健康妇女为对照组。记录一般资料:腰臀比(WHR)、体重指数(BMI)、收缩压(SBP)、舒张压(DBP)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、空腹血糖(FPG)、空腹血浆胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR),进行常规超声心动图检查,测量左室舒张末期内径(LVDd)、左室收缩末期内径(LVDs)、舒张末期室间隔厚度(IVSTd)、舒张末期左室后壁厚度(LVPWTd)、左室射血分数(LVEF)、舒张早期二尖瓣口血流峰值速度(E)、舒张晚期二尖瓣口血流峰值速度(A)、舒张早期二尖瓣环运动峰值速度(Em),计算E/A及E/Em,测量E峰减速时间(DT)、等容舒张时间(IVRT)及等容收缩时间(IVCT)。应用CMQ技术跟踪描记心肌运动轨迹,获取左室18节段心肌收缩期纵向峰值应变(LS)及收缩期整体纵向峰值应变(GLS)。采用Pearson相关分析各参数之间的相关性。 结果 PCOS-IR组WHR、BMI、FINS、HOMA-IR、LDL-C高于对照组,差异有统计学意义(P < 0.05)。两组年龄、SBP、DBP、FPG、HDL-C、TG比较,差异无统计学意义(P > 0.05)。与对照组比较,PCOS-IR组DT、IVRT、E/Em增加,Em减小,差异有统计学意义(P < 0.05);两组LVDd、LVDs、IVSTd、LVPWTd、LVEF、E、A、E/A、IVCT比较,差异无统计学意义(P > 0.05)。PCOS-IR组各节段LS及GLS均较对照组减低,差异有统计学意义(P < 0.05)。GLS与FINS、WHR及LDL-C均呈负相关(r = -0.58、-0.46、-0.44,P < 0.05),与FPG、HOMA-IR、HDL-C、TG、BMI无相关性(P > 0.05)。 结论 PCOS-IR患者在LVEF正常情况下可出现早期纵向收缩功能下降。CMQ技术可早期检测出PCOS-IR患者左心室纵向运动异常,为临床及时干预治疗提供帮助。

[关键词] 多囊卵巢;胰岛素抵抗;心肌运动定量技术;左心室

[中图分类号] R711.75 [文献标识码] A [文章编号] 1673-7210(2018)07(a)-0071-05

Evaluation of left ventricular longitudinal myocardial function in patients with polycystic ovary syndrome associated with insulin resistance by cardiac motion quantification

DU Qigen MI Xiangqin XU Hongwei SHANG Weimin ZHOU Liping CHEN Wei

Department of Ultrasound, Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Heilongjiang Province, Harbin 150000, China

[Abstract] Objective To investigate the clinical value of myocardial motion quantification (CMQ) in evaluation of left ventricular longitudinal motion in patients with polycystic ovary combined with insulin resistance (PCOS-IR). Methods From the February 2016 to February 2017, 55 patients with PCOS-IR in Department of Gynecology, the Second Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine were selected, 55 age matched healthy women were selected as control group. The general data were recorded: waist-to-hipratio (WHR), body mass index (BMI), systolic pressure (SBP), diastolic pressure (DBP), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), fasting blood glucose (FPG), fasting plasma insulin (FINS), homeostasis model assessment for IR index (HOMA-IR), and all subjects were given routine echocardiography, the left ventricular end-diastolic dimension (LVDd) and left ventricular end-systolic diameter (LVDs), end-diastolic interventricular septum thickness (IVSTd), end-diastolic left ventricular posterior wall thickness (LVPWTd), and left ventricular ejection fractional (LVEF), early diastolic blood flow peak velocity (E), late diastolic blood flow peak velocity (A), mitral annular early diastolic motion peak velocity (Em) were measured, E/A and E/Em were calculated, E peak deceleration time (DT), isovolumic relaxation time (IVRT) and isovolumic contraction time (IVCT) were measured. CMQ technique was used to trace tracing of myocardial trajectory, and systolic longitudinal peak strain (LS) and systolic global longitudinal peak strain (GLS) of 18 left ventricular segments were obtained. Pearson correlation was used to analyze the correlation between the parameters. Results The WHR, BMI, FINS, HOMA-IR and LDL-C in the PCOS-IR group were higher than those in the control group, the differences were statistically significant (P < 0.05); there was no significant difference in age, SBP, DBP, FPG, HDL-C, TG between the two groups (P > 0.05). Compared with the control group, DT, IVRT, E/Em increased in the PCOS-IR group, and Em decreased, the differences were statistically significant (P < 0.05); there was no significant difference in LVDd, LVDs, IVSTd, LVPWTd, LVEF, E, A, E/A, IVCT between the two groups (P > 0.05). The LS and GLS in each segment of PCOS-IR group were lower than those in the control group, the differences were statistically significant (P < 0.05). There were negative correlations between GLS and FINS, WHR, LDL-C (r = -0.58, -0.46, -0.44, all P < 0.05). There was no correlation between GLS and FPG, HOMA-IR, HDL-C, TG, BMI (P > 0.05). Conclusion Patients with PCOS-IR may show a decline in early longitudinal systolic function under normal LVEF. CMQ technology can detect early left ventricular longitudinal movement abnormalities in patients with PCOS-IR, and provide clinical help for timely intervention.

[Key words] Polycystic ovary; Insulin resistance; Quantitative myocardial motion; Left ventricle

多囊卵巢综合征(PCOS)以稀发排卵和高雄激素血症为特点,在育龄妇女中发病比例高且多伴有胰岛素抵抗(IR)[1-2],罹患心血管疾病(CVD)的风险升高[3]。本研究目的为应用心肌运动定量(CMQ)技术定量评估PCOS-IR患者左心室纵向心肌运动,探讨PCOS-IR患者心肌局部及整体收缩功能,该方法能够在常规二维超声心动图未发现射血分数(LVEF)降低之前,早期发现左心室局部心肌功能障碍,对临床早期干预及治疗有着重要意义。

1 资料与方法

1.1 一般资料

选择2016年2月~2017年2月黑龙江中医药大学附属第二医院(以下简称“我院”)妇科就诊的PCOS-IR患者55例,患者年龄26~39岁,平均(30.13±5.26)岁,均符合2003年Rotterdam会议制订的PCOS诊断标准[4],以稳态模型评估的胰岛素抵抗指数(HOMA-IR)≥1.66为IR。HOMA-IR=FINS(空腹胰岛素)×FPG(空腹血浆血糖)/22.5[5]。剔除其他内分泌疾病如甲状腺功能亢进、库欣综合征、先天性肾上腺皮质增生等。另选取同期我院体检的年龄匹配的健康女性55例为对照组,年龄25~40岁,平均(29.47±6.32)岁,月经规律,超声显示双侧卵巢形态正常。两组均排除吸烟、酗酒、糖尿病、近6个月内妊娠或使用避孕药物、近6个月内有血栓或栓塞史者。本研究经医院医学伦理委员会批准,所有研究对象均知情同意并签署知情同意书。

1.2 观察指标及检测方法

选用飞利浦IU-22彩色多普勒超声诊断仪,S5-1心脏探头,频率1~5 MHz,帧频≥60帧/s,仪器内置QLAB分析软件。

1.2.1 记录受试对象一般资料 腰臀比(WHR)、体重指数(BMI)、收缩压(SBP)、舒張压(DBP)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)、空腹血糖(FPG)、空腹血浆胰岛素(FINS)、胰岛素抵抗指数(HOMA-IR)。

1.2.2 心脏超声评价 心脏超声检查:受检者取左侧卧位,平静呼吸,连接心电监测。行常规二维超声心动图检查,于胸骨左缘第2~4肋间获取左室长轴切面,测量左室舒张末期内径(LVDd)、左室收缩末期内径(LVDs)、舒张末期室间隔厚度(IVSTd)及舒张末期左室后壁厚度(LVPWTd),采用双平面Simpson法计算左室射血分数(LVEF)。于心尖四腔心切面测量二尖瓣口舒张早期血流峰值速度(E),舒张晚期血流峰值速度(A),并计算E/A;放置TDI取样容积于二尖瓣环,在室间隔及侧壁两个部位测量取平均值,测量舒张早期二尖瓣环峰值运动速度(Em),并计算E/Em,测量E峰减速时间(DT)、等容舒张时间(IVRT)及等容收缩时间(IVCT)。

1.2.3 CMQ技术对左心室纵向心肌运动的评价 采集并储存连续3个心动周期的左室心尖长轴四腔心切面、三腔心切面和两腔心切面的二维超声动态图像,将储存图像导入QLAB工作站中的CMQ模式进行分析,选取清晰图像,借助软件标记点勾画左心室心内膜及心外膜边界,软件自动将左室壁分为6个节段,追踪描记18节段各节段心肌斑点的运动,生成左室节段心肌的收缩期应变曲线,获取各节段收缩期峰值纵向应变(LS)及整体纵向应变(GLS)。

1.3 统计学方法

采用统计软件SPSS 20.0对数据进行分析,正态分布的计量资料以均数±标准差(x±s)表示,两组间比较采用t检验;计数资料以率表示,采用χ2检验。参数间相关性分析采用Pearson相关分析。以P < 0.05为差异有统计学意义。

2 结果

2.1 两组一般临床参数比较

PCOS-IR组WHR、BMI、FINS、HOMA-IR、LDL-C高于对照组,差异有统计学意义(P < 0.05)。PCOS-IR组年龄、SBP、DBP、FPG、HDL-C、TG与对照组比较,差异无统计学意义(P > 0.05)。见表1。

2.2 两组常规超声心动图参数比较

与对照组比较,PCOS-IR组DT、IVRT、E/Em增加,Em减小,差异有统计学意义(P < 0.05);PCOS-IR组LVDd、LVDs、IVSTd、LVPWTd、LVEF、E、A、E/A、IVCT与对照组比较,差异无统计学意义(P > 0.05)。见表2。

2.3 左心室各节段心肌LS及GLS比较

PCOS-IR组GLS(-15.39±1.58)与对照组(-17.74±2.03)比较,差异有统计学意义(P < 0.05)。PCOS-IR组各节段LS较对照组减低,差异均有统计学意义(P < 0.05)。见表3。

2.4 心肌GLS与常规临床指标的相关性分析

GLS与FINS、WHR及LDL-C呈负相关(r = -0.58、-0.46、-0.44,P < 0.05),与FPG、HOMA-IR、HDL-C、TG、BMI无相关性(P > 0.05)。见表4。

3 讨论

PCOS以慢性无排卵、高雄激素血症及多毛症为特征,是育龄期妇女常见的内分泌疾病[1-2]。PCOS患者极易罹患心血管疾病,有报道称PCOS患者心肌梗死发生率是正常人的7倍[3],冠状动脉硬化发生率远高于正常排卵女性[6]。PCOS患者多合并IR,IR是PCOS患者心血管疾病的重要危险因素[7]。PCOS患者出现亚临床左室收缩功能障碍呈现年轻化[8],因此检测左室纵向收缩功能异常对于降低PCOS患者心血管疾病发病率和死亡率有重要意义。CMQ技术是近年来无创定量评价左室心肌力学的新技术,它基于斑点追踪技术,可以追踪心内膜、心外膜及整体室壁的运动,从纵向、径向及圆周方向全方位评估不同区域心肌运动,可准确、定量评估局部及整体心肌功能。

以往研究证实PCOS患者多伴有心血管异常,包括:心脏收缩期峰值血流速度降低、舒张功能障碍、大动脉僵硬度增加,血管内皮功能障碍等[9-11]。本研究结果显示,PCOS-IR患者DT、IVRT、E/Em增加,Em减小,提示PCOS-IR患者早期心肌损害主要表现为左室舒张功能减低。原因可能为PCOS患者多伴有冠状动脉疾病、血脂异常、血管内皮功能障碍、轻度炎症和氧化应激[12-14],导致心肌细胞缺氧、纤维化。IR也可能是PCOS患者左室舒张功能减低的主要危险因素[15]。TlRA等[16]研究发现IR与左室舒张功能呈显著负相关。

心肌具有复杂的解剖结构以及复杂的运动形式,心肌收缩时产生沿长轴及短轴的运动[17]。左室长轴纵向运动在心脏力学中起重要作用,其机制为:收缩期左室纵向心肌将二尖瓣环向心尖部拉近,在长轴方向缩小左室容积,有助于心室射血[18-19];舒张早期纵向心肌释放在收缩期储存的势能,产生室性吸力,是心脏完成心室快速充盈的关键[20]。左室纵向收缩功能是心脏泵功能的重要组成部分,收缩期纵向心肌做功占LVEF的70%[21]。本研究显示PCOS-IR患者左室各节段LS及GLS减低,提示在LVEF正常情况下,左室局部及整体心肌纵向收缩功能下降,与Erdoan等[8]及Demirelli等[22]研究结果一致。Erdoan等[8]认为PCOS患者大动脉僵硬度上升可导致左室后负荷增加,破坏纵向心肌纤维结构,导致左室局部心肌纵向收缩功能下降。本研究结果显示,GLS与FINS、WHR、LDL-C呈负相关(r < 0,P < 0.05)。FINS、WHR、LDL-C均为心血管危险因子,导致PCOS患者左室心肌缺血、纤维化,心内膜下纵行心肌与中层及心外膜下心肌比较,对缺血更为敏感[23],因此纵向心肌收缩功能降低。

综上所述,PCOS-IR患者在LVEF正常情况下可出现早期纵向收缩功能下降。CMQ技术可早期检测出PCOS-IR患者左心室纵向运动异常,为临床及时干预治疗提供帮助。

[参考文献]

[1] Azziz R,Woods KS,Reyna R,et al. The Prevalence and features of the polycystic ovary syndrome in an unselected population [J]. J Clin Endocrinol Metab,2004,89(6):2745-2749.

[2] Hart R,Hickey M,Franks S. Definitions,prevalence and symptoms of polycystic ovaries and polycystic ovary syndrome [J]. Best Pract Res Clin Obstet Gynaecol,2004,18(5):671-683.

[3] Dahlgren E,Janson PO,Johansson S,et al. Polycystic ovary syndrome and risk for myocardial infarction:Evaluated from a risk factor model based on a prospective population study of women [J]. Acta Obstet Gynecol Scand,1992, 71(8):599-604.

[4] The Rotterdam ESHRE/ASRM-sponsored PCOS consensus workshop group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS) [J]. Hum Reprod,2004,19(1):41-47.

[5] 李昕,林金芳.肥胖型多囊卵巢综合征患者临床及内分泌代谢特征的研究[J].中華医学杂志,2005,85(46):3266-3271.

[6] Birdsall MA,Farquhar CM,White HD. Association between polycystic ovaries and extent of coronary artery disease in women having cardiac catheterization [J]. Ann Inter Med,1997,126(1):32-35.

[7] Dunaif A,Segal KR,Futterweit W,et al. Profound peripheral insulin resistance,independent of obesity,in polycystic ovary syndrome [J]. Diabetes,1989,38(9):1165.

[8] Erdoan E,Akkaya M,Bacaks?覦z A,et al. Subclinical left ventricular dysfunction in women with polycystic ovary syndrome:an observational study [J]. Anadolu Kardiyol Derg,2013,13(8):784-790.

[9] Prelevic G M,Beljic T,Balintperic L,et al. Cardiac flow velocity in women with the polycystic ovary syndrome [J]. Clin Endocrinol,1995,43(6):677-681.

[10] Paradisi G,Steinberg HO,Hempfling A,et al. Polycystic ovary syndrome is associated with endothelial dysfunction [J]. Circulation,2001,103(10):1410-1405.

[11] Birdsall MA,Farquhar CM,White HD. Association between polycystic ovaries and extent of coronary artery disease in women having cardiac catheterization [J]. Ann Inter Med,1997,126(1):32-35.

[12] Watts GF,Marwick TH. Ventricular dysfunction in early diabetic heart disease: Detection,mechanisms and significance [J]. Clin Sci(Lond),2003,105(5):537-540.

[13] Kelly CC,Lyall H,Petrie JR,et al. Low grade chronic inflammation in women with polycystic ovarian syndrome [J]. J Clin Endocrinol Metab,2001,86(6):2453-2455.

[14] Paradisi G,Steinberg HO,Hempfling A,et al. Polycystic ovary syndrome is associated with endothelial dysfunction [J]. Circulation,2001,103(10):1410-1405.

[15] Dunaif A. Insulin resistance and the polycystic ovary syndrome:mechanism and implications for pathogenesis [J]. Endocrine Reviews,1997,18(6):774.

[16] Tlra MB,Yal?觭?覦n R,Noyan V,et al. Alterations in cardiac flow parameters in patients with polycystic ovarian syndrome [J]. Hum Reprod,1999,14:1949-19452.

[17] Jung B,Odening KE,Dall'Armellina E,et al. A quantitative comparison of regional myocardial motion in mice,rabbits and humans using in-vivo phase contrast CMR [J]. J Cardiovasc Magn Reson,2012,14(1):87.

[18] Carlsson M,Ugander M,Heiberg E,et al. The quantitative relationship between longitudinal and radial function in left,right,and total heart pumping in humans [J]. Am J Physiol Heart Circ Physiol,2007,293(1):H636.

[19] Henein MY,Gibson DG. Normal long axis function [J]. Heart,1999,81(2):111.

[20] Riordan MM,Kovács SJ. Relationship of pulmonary vein flow to left ventricular short-axis epicardial displacement in diastole:model-based prediction with in vivo validation [J]. Am J Physiol Heart Circ Physiol,2006,291(3):H1210-H1215.

[21] Brecker SJ. The importance of long axis ventricular function [J]. Heart,2000,84(6):577-579.

[22] Demirelli S,Deirmenci H,Ermi E,et al. OP-174 the importance of speckle tracking echocardiography in the early detection of left ventricular dysfunction in patients with polycystic ovary syndrome [J]. Am J Cardiol,2015, 115(4):S77-S78.

[23] Henein MY,Gibson DG. Long axis function in disease [J]. Heart,1999,81(3):229-231.

(收稿日期:2018-02-25 本文編辑:苏 畅)

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