国产日韩欧美一区二区三区三州_亚洲少妇熟女av_久久久久亚洲av国产精品_波多野结衣网站一区二区_亚洲欧美色片在线91_国产亚洲精品精品国产优播av_日本一区二区三区波多野结衣 _久久国产av不卡

?

中國(guó)血管病變?cè)缙跈z測(cè)技術(shù)應(yīng)用指南(2011第二次報(bào)告)

2011-08-15 00:53:27中國(guó)社工協(xié)會(huì)康復(fù)醫(yī)學(xué)工作委員會(huì)血管專業(yè)委員會(huì)國(guó)際血管健康學(xué)會(huì)中國(guó)分會(huì)
關(guān)鍵詞:袖帶受檢者動(dòng)脈

中國(guó)社工協(xié)會(huì)康復(fù)醫(yī)學(xué)工作委員會(huì)血管專業(yè)委員會(huì)國(guó)際血管健康學(xué)會(huì)中國(guó)分會(huì)

北京大學(xué)首鋼醫(yī)院血管醫(yī)學(xué)中心

1 背景

隨著社會(huì)經(jīng)濟(jì)的發(fā)展,人們生活水平的提高以及社會(huì)人口老齡化進(jìn)程的加快,血管性疾病日益成為威脅人類健康的嚴(yán)重問(wèn)題,越來(lái)越引起國(guó)內(nèi)外醫(yī)學(xué)界的廣泛重視。

在我國(guó),腦血管病每年發(fā)病率為150/10萬(wàn),病死率為120/10萬(wàn),致殘率高達(dá)50%以上,因此,每年約有近200萬(wàn)的新發(fā)病例,約有150萬(wàn)人死于腦血管病,生存者約600萬(wàn)~700萬(wàn),近半數(shù)的患者有不同程度的殘疾。我國(guó)每年用于腦血管病患者的直接住院費(fèi)用約為97億,間接花費(fèi)則達(dá)數(shù)百億元,給國(guó)家和家庭帶來(lái)沉重的經(jīng)濟(jì)負(fù)擔(dān),因此,腦血管病的防治已經(jīng)成為我國(guó)衛(wèi)生工作的一項(xiàng)重要課題。實(shí)際上,血管疾病是累及全身的一組病變,它包括冠狀動(dòng)脈疾病、腦血管疾病、腎血管疾病和外周血管疾病,上述疾病導(dǎo)致的致死和致殘給國(guó)家和個(gè)人家庭造成巨大財(cái)產(chǎn)和精神損失。動(dòng)脈功能和結(jié)構(gòu)損害是包括高血壓、血脂異常和糖尿病在內(nèi)的許多心血管危險(xiǎn)因素導(dǎo)致的早期血管改變,其與預(yù)后的確切關(guān)系已引起學(xué)術(shù)界的高度重視。探討無(wú)創(chuàng)測(cè)定亞臨床血管病變的方法以及其與預(yù)后心血管事件的關(guān)系,不僅為早期和方便地檢出預(yù)后發(fā)生心血管事件高危患者提供了一項(xiàng)指標(biāo),同時(shí)可為判斷臨床干預(yù)效果提供可靠的替代終點(diǎn)。目前介入治療已成為解除由于粥樣硬化導(dǎo)致的動(dòng)脈管腔堵塞的直接和起效快速的方法。但是面對(duì)世界范圍內(nèi)與日劇增的血管疾病患者,血管病變的臨床前期發(fā)現(xiàn)并進(jìn)行強(qiáng)化干預(yù)是最終降低臨床心血管事件發(fā)生率的唯一出路。2004年6月國(guó)家衛(wèi)生部批準(zhǔn)將血管病變?cè)缙跈z測(cè)技術(shù)作為十年百項(xiàng)計(jì)劃向全國(guó)推廣,2005年我國(guó)制訂了國(guó)際上首個(gè)關(guān)于血管病變?cè)缙跈z測(cè)技術(shù)的應(yīng)用指南,這一指南的制訂有利于規(guī)范使用血管病變?cè)缙跈z測(cè)技術(shù),我國(guó)在血管疾病預(yù)防領(lǐng)域的經(jīng)驗(yàn)受到國(guó)際學(xué)術(shù)界的關(guān)注,歐美發(fā)達(dá)國(guó)家對(duì)我國(guó)的經(jīng)驗(yàn)進(jìn)行了借鑒[1-2]。2010年4月北京大學(xué)首鋼醫(yī)院成立了我國(guó)第一個(gè)血管醫(yī)學(xué)中心,集血管病早期預(yù)防、血管健康維護(hù)、血管疾病綜合治療于一體,為推動(dòng)血管醫(yī)學(xué)學(xué)科的發(fā)展發(fā)揮重要的作用[3-10]。2011新版指南更注重其在血管病變?cè)缙诰C合評(píng)價(jià)的臨床實(shí)用性和可推廣性進(jìn)行了修訂。

2 血管病變?cè)缙跈z測(cè)適用范圍

(1)年滿14周歲以上;

(2)有早發(fā)心腦血管疾病家族史者;

(3)有長(zhǎng)期頭暈,活動(dòng)后或靜息狀態(tài)下胸悶、心悸以及間歇性跛行等癥狀,尚未明確診斷者;

(4)已被診斷為高血壓(包括臨界高血壓)、高脂血癥、高尿酸血癥、糖尿病(包括空腹血糖升高和糖耐量減低)或具有肥胖、長(zhǎng)期吸煙、高脂飲食、缺乏體育運(yùn)動(dòng)等存在心腦血管疾病高危因素者;

(5)冠心病、腦卒中、缺血性腎病、下肢動(dòng)脈缺血性疾病、缺血性腸病等病史明確者。

3 血管病變?cè)缙跈z測(cè)項(xiàng)目

3.1 脈壓

3.1.1 受檢者要求:(1)安靜休息5min;(2)測(cè)量當(dāng)天禁止飲酒,測(cè)量前30 min內(nèi)禁止吸煙和飲用咖啡,排空膀胱。

3.1.2 受檢者檢查前準(zhǔn)備:取坐位,裸露右上臂,肘部置于與心臟同一水平。

3.1.3 儀器選擇:選擇符合計(jì)量標(biāo)準(zhǔn)的水銀柱式血壓計(jì)以及大小合適的袖帶。

3.1.4 檢查方法:(1)將袖帶緊貼縛在被測(cè)者右側(cè)上臂,袖帶下緣應(yīng)在肘彎上2~3cm。將聽(tīng)診器的探頭置于肘窩肱動(dòng)脈處。測(cè)量時(shí)快速充氣,氣囊內(nèi)壓力應(yīng)達(dá)到橈動(dòng)脈搏動(dòng)消失并再升高30 mmHg(4.0 kPa)(1 mmHg=0.1333kPa),然后以恒定速率(2~6mmHg/s)緩慢放氣。獲取舒張壓讀數(shù)后快速放氣至零。在放氣過(guò)程中仔細(xì)聽(tīng)取柯氏音,觀察柯氏音第Ⅰ時(shí)相與第Ⅴ時(shí)相水銀柱凸面的垂直高度。收縮壓讀數(shù)取柯氏音第Ⅰ時(shí)相,舒張壓讀數(shù)取柯氏音第Ⅴ時(shí)相(消失音)。兒童、妊娠婦女、嚴(yán)重貧血、主動(dòng)脈瓣關(guān)閉不全或柯氏音不消失者,以柯氏音第Ⅳ時(shí)相(變音)定為舒張壓;(2)相隔2min重復(fù)測(cè)量,取2次讀數(shù)的平均值記錄[11-22]。

3.1.5 測(cè)定指標(biāo)及其范圍:(1)脈壓:脈壓=收縮壓-舒張壓(單位:mmHg);(2)脈壓正常值:30~40 mmHg。

3.2 頸動(dòng)脈超聲

3.2.1 受檢者檢查前準(zhǔn)備:檢查前一天及檢查當(dāng)天禁止飲酒,檢查當(dāng)天禁止飲用咖啡及濃茶,檢查當(dāng)天禁止吸煙。(1)取坐位或平臥位,安靜狀態(tài)下休息5min方可開(kāi)始進(jìn)行檢測(cè);(2)取下項(xiàng)鏈等頸部飾物,避免穿著高領(lǐng)衣服。

3.2.2 儀器選擇:超聲探頭采用7.0~12.0 MHz線陣探頭。

3.2.3 檢查方法

3.2.3.1 受檢者體位:受檢者取仰臥位,去枕平臥,雙臂置于身體兩側(cè),頭頸部盡量仰伸使頸部充分顯露,頭轉(zhuǎn)向被檢側(cè)的對(duì)側(cè)。連接肢體導(dǎo)聯(lián)心電監(jiān)測(cè),同步實(shí)時(shí)監(jiān)測(cè)肢體導(dǎo)聯(lián)心電圖。

3.2.3.2 B型超聲測(cè)定

3.2.3.2.1 測(cè)定方法:首先進(jìn)行縱行掃描:從頸根部開(kāi)始,探頭置于胸鎖關(guān)節(jié)上方胸鎖乳突肌前緣確定頸總動(dòng)脈,沿動(dòng)脈走行逐次向頭側(cè)掃查至下頜角,顯示頸總動(dòng)脈主干、頸總動(dòng)脈分叉部及頸內(nèi)、頸外動(dòng)脈近段,然后采用相同方法沿橫斷面向上掃查。

3.2.3.2.2 測(cè)量指標(biāo)及其參考標(biāo)準(zhǔn)

(1)血管內(nèi)徑:①測(cè)定方法:取頸總動(dòng)脈分叉處近端1.5cm處測(cè)量頸總動(dòng)脈內(nèi)徑,試驗(yàn)同步記錄受試者心電圖,在心室舒張末期(即心電圖顯示R波頂端時(shí))測(cè)量頸總動(dòng)脈前壁中膜~外膜交界區(qū)與后壁血管腔~內(nèi)膜之間的距離,每次測(cè)量3個(gè)心動(dòng)周期,取其平均值為測(cè)定結(jié)果。②正常值:20~39歲<7.0 mm;40~59歲<7.5mm;>60歲<8.0 mm 。

(2)血管壁內(nèi)膜~中層厚度:①測(cè)定方法:取頸總動(dòng)脈分叉處近端后壁1.5cm處測(cè)量頸總動(dòng)脈內(nèi)膜~中層厚度,若該處存在粥樣硬化斑塊病變則取病變近端1.5cm處測(cè)量頸總動(dòng)脈內(nèi)膜~中層厚度。

②正常值:20~39歲<0.65mm;40~59歲<0.75mm;>60歲<0.85mm,高于該年齡段正常值則被判定為內(nèi)膜~中層增厚。

(3)動(dòng)脈硬化斑塊判定標(biāo)準(zhǔn):血管縱行掃描及橫斷面掃描時(shí)均可見(jiàn)該位置存在突入管腔的回聲結(jié)構(gòu),或突入管腔的血流異常缺損,或局部頸動(dòng)脈內(nèi)膜~中層厚度>1.3mm。

3.3 動(dòng)脈內(nèi)皮功能

3.3.1 受檢者要求:(1)空腹或餐后8h以上;(2)12h以內(nèi)禁止飲酒、咖啡及濃茶,禁止吸煙,避免進(jìn)行劇烈運(yùn)動(dòng)。

3.3.2 檢查前準(zhǔn)備:受檢者平臥位,安靜狀態(tài)下休息5min方可開(kāi)始進(jìn)行檢測(cè)。檢測(cè)時(shí)環(huán)境應(yīng)保持安靜,溫度在20~25℃之間并保持相對(duì)穩(wěn)定。

3.3.3 檢查方法:(1)受檢者體位:受檢者取仰臥位,去枕平臥,雙臂置于身體兩側(cè),選擇一側(cè)(一般為右側(cè))上臂肱動(dòng)脈為受檢動(dòng)脈,該側(cè)手臂輕度外展15°,手心向上(前),并保持該側(cè)上臂肌肉放松。連接肢體導(dǎo)聯(lián)心電監(jiān)測(cè),同步實(shí)時(shí)監(jiān)測(cè)肢體導(dǎo)聯(lián)心電圖。(2)測(cè)量方法:按照測(cè)量血壓標(biāo)準(zhǔn)方法將血壓計(jì)袖帶縛于該側(cè)上臂,袖帶下緣位于肘橫紋以上5cm處,以縱切面掃描肱動(dòng)脈,掃描位置取肘橫紋處至肘上3~5cm之間,探頭輕壓在皮膚表面,以能夠清晰顯示動(dòng)脈前后壁而不致令動(dòng)脈受壓變形為準(zhǔn)。在整個(gè)測(cè)試過(guò)程中,超聲探頭位置固定(可使用專用探頭固定裝置,或在皮膚表面作標(biāo)記),每次測(cè)量肱動(dòng)脈內(nèi)徑均取同一部位。首先記錄基礎(chǔ)肱動(dòng)脈二維圖像及其多普勒血流頻譜(測(cè)定方法同上),然后將袖帶充氣至高于收縮壓50 mmHg并完全阻斷血流5min,5min內(nèi)監(jiān)測(cè)袖帶內(nèi)壓力,使壓力波動(dòng)不超過(guò)10 mmHg。血流阻斷過(guò)程中囑受檢者安靜并保持上述體位不變。5min后迅速放氣,記錄放氣前30 s至放氣后2min內(nèi)肱動(dòng)脈二維圖像及放氣后15s內(nèi)肱動(dòng)脈多普勒血流信號(hào)圖像[23-64]。

3.3.4 測(cè)定指標(biāo):血流介導(dǎo)的血管擴(kuò)張(f l o wmediated dilatation,F(xiàn)MD)FMD=(動(dòng)脈反應(yīng)性充血后內(nèi)徑-動(dòng)脈基礎(chǔ)內(nèi)徑)/動(dòng)脈基礎(chǔ)內(nèi)徑 ×100%;正常值FMD>10%。

3.4 脈搏波傳導(dǎo)速度(pulse wave velocity,PWV)

3.4.1 受檢者要求:(1)空腹或餐后2h以上;(2)檢查前一天及檢查當(dāng)天禁止飲酒,檢查當(dāng)天禁止飲用咖啡及濃茶,檢查當(dāng)天禁止吸煙;(3)避免穿著高領(lǐng)衣服。

3.4.2 檢查前準(zhǔn)備:受試者取坐位或平臥位,安靜狀態(tài)下休息5min方可開(kāi)始進(jìn)行檢測(cè);目前國(guó)外和國(guó)內(nèi)有多種檢測(cè)裝置可以應(yīng)用,可自動(dòng)測(cè)量不同動(dòng)脈節(jié)段的脈搏波速度。

3.4.3 測(cè)定指標(biāo):PWV=測(cè)量動(dòng)脈節(jié)段的體表距離/波傳導(dǎo)時(shí)間(m/s);正常值:頸-股PWV<9m/s,踝-肱PWV<14m/s[65-81]。

3.5 心踝血管指數(shù)(cardio ankle vascular index, CAVI)

3.5.1 受試者檢查前準(zhǔn)備:(1)避免身著緊身衣褲;(2)檢查前脫去外衣及厚毛衣類服裝,可著薄夏裝;脫去緊身褲并將寬松褲子挽至膝水平,寬松褲子與膝之間至少能夠容納一指;除去襪子,女士可著薄絲襪;(3)保持安靜并平臥位5min。

3.5.2 檢測(cè)方法:(1)受試者體位:去枕仰臥體位,雙手手心向上置于身體兩側(cè);(2)檢測(cè)過(guò)程:將四肢血壓袖帶縛于上臂及下肢踝部。上臂袖帶下緣距肘窩橫紋2~3cm,袖帶松緊度以恰好能放進(jìn)一指為宜,下肢袖帶下緣距內(nèi)踝5cm,袖帶松緊度同上;2個(gè)電極分別置于雙腕部以采集心電信號(hào);微型麥克風(fēng)置于胸骨體以采集心音信號(hào)。首先加壓袖帶壓力至30~50 mmHg,儀器自動(dòng)檢測(cè)心踝脈搏波速度(haPWV),然后采用壓力振蕩法分別測(cè)定雙側(cè)上下肢收縮壓及舒張壓。最后儀器根據(jù)測(cè)得的數(shù)據(jù)自動(dòng)計(jì)算CAVI。

3.5.3 測(cè)定指標(biāo):CAVI=a×[2ρ×ln(SBP/DBP)×haPWV2/PP]+b [a、b:常數(shù);ρ:血液密度(常數(shù));SBP:收縮壓;DBP:舒張壓;haPWV:心踝脈搏波速度;PP:脈壓] ;正常值<9。

3.6 踝臂指數(shù)

3.6.1 受檢者要求:(1)測(cè)量當(dāng)天禁止飲酒,測(cè)量前30 min內(nèi)禁止吸煙和飲用咖啡,排空膀胱。(2)保持安靜并平臥位3min,避免身著緊身衣褲。

3.6.2 檢測(cè)裝置:選擇符合計(jì)量標(biāo)準(zhǔn)的水銀柱式血壓計(jì)以及大小合適的袖帶。

3.6.3 檢測(cè)方法:將四肢血壓袖帶縛于上臂及下肢踝部。上臂袖帶下緣距肘窩橫紋2~3cm,袖帶松緊度以恰好能放進(jìn)一指為宜,聽(tīng)診器置于肘窩肱動(dòng)脈搏動(dòng)處;下肢袖帶下緣距內(nèi)踝5cm,袖帶松緊度同上,聽(tīng)診器置于足背動(dòng)脈搏動(dòng)處;采用超聲多普勒或壓力振蕩法分別測(cè)定雙側(cè)上肢、下肢的收縮壓。對(duì)每位受試者均設(shè)定采集2次,2次間隔1 min以上,取其平均值資料為最后結(jié)果。

3.6.4 測(cè)定指標(biāo):踝臂指數(shù)(ABI)。計(jì)算方法:分別以測(cè)定的下肢收縮壓與上肢收縮壓中較高的一側(cè)收縮壓相除,所得結(jié)果即為雙側(cè)ABI[82-86]。

3.6.5 參考范圍:

0.9 <ABI<1.3 正常

ABI>1.3 動(dòng)脈鈣化

0.8 <ABI<0.9 動(dòng)脈阻塞的可能性高

0.5 <ABI<0.8 有一處存在動(dòng)脈阻塞

ABI<0.5 有多處存在動(dòng)脈阻塞

3.7 橈動(dòng)脈脈搏波形分析

3.7.1 受檢者要求:(1)空腹或餐后8h以上;(2)12h以內(nèi)禁止飲酒、咖啡及濃茶,禁止吸煙,避免進(jìn)行劇烈運(yùn)動(dòng)。

3.7.2 檢查前準(zhǔn)備:受檢者平臥位,安靜狀態(tài)下休息5min方可開(kāi)始進(jìn)行檢測(cè)。檢測(cè)時(shí)環(huán)境應(yīng)保持安靜,溫度在20~25℃之間并保持相對(duì)穩(wěn)定。

3.7.3 檢查方法:將合適大小的袖帶置于受檢者左上臂,觸摸右側(cè)橈動(dòng)脈搏動(dòng)最強(qiáng)處并做標(biāo)記。橈動(dòng)脈搏動(dòng)最強(qiáng)處一般在橈骨遠(yuǎn)端外側(cè)隆突與肌腱之間,約距拇指基底部2cm。然后將腕部固定裝置縛在右前臂和腕部,使固定裝置支架上的平面壓力波測(cè)定探頭置于右側(cè)橈動(dòng)脈搏動(dòng)最強(qiáng)處。緩慢調(diào)節(jié)固定裝置支架上的旋鈕,直到獲得理想的橈動(dòng)脈脈搏壓力波形和最大的信號(hào)強(qiáng)度。同步啟動(dòng)左上臂血壓測(cè)量和右側(cè)橈動(dòng)脈脈搏壓力波記錄(共30 s)。儀器內(nèi)的軟件系統(tǒng)以每秒采集200個(gè)數(shù)據(jù)的速度自動(dòng)識(shí)別、計(jì)算并顯示壓力波形和動(dòng)脈彈性功能數(shù)據(jù)。

3.7.4 測(cè)定指標(biāo):大動(dòng)脈彈性指數(shù)C1(ml/mmHg×10),小動(dòng)脈彈性指數(shù)C2(ml/mmHg×100)[87-94]。

3.7.5 正常標(biāo)準(zhǔn)(僅供參考):

C1: 15~30歲>18(ml/mmHg×10);31~45

歲>16(ml/mmHg×10);

46~60歲>14(ml/mmHg×10);60歲以 上>10(ml/mmHg×10)。

C2: 15~30歲>8(ml/mmHg×100);31~45

歲>7(ml/mmHg×100);

46~60歲>6(ml/mmHg×100);60歲以 上>5(ml/mmHg×100)。

3.8 冠狀動(dòng)脈鈣化積分(coronary artery calcification score)

冠狀動(dòng)脈CT(包括電子束CT,electron-beam computed tomography及螺旋CT,spiral or helica computed tomography)作為一種無(wú)創(chuàng)性方法,可以檢測(cè)冠狀動(dòng)脈鈣化的位置及范圍,近10年來(lái)在我國(guó)得到了越來(lái)越廣泛的應(yīng)用。

目前臨床上評(píng)價(jià)冠狀動(dòng)脈鈣化采用Agatston積分系統(tǒng),當(dāng)CT值≥130 HU(Hounsfield Unit)、面積≥1 mm2時(shí),即認(rèn)為鈣化存在,即:

Agatston積分=CT值≥130 HU的像素面積×鈣化灶CT峰值系數(shù)。

其中:

鈣化CT值130~199HU:鈣化灶CT峰值系數(shù)=1

鈣化CT值200~299HU:鈣化灶CT峰值系數(shù)=2

鈣化CT值300~399HU:鈣化灶CT峰值系數(shù)=3

鈣化CT值>400 HU:鈣化灶CT峰值系數(shù)=4

3.9 生物標(biāo)志物

越來(lái)越多的證據(jù)顯示內(nèi)皮功能障礙是動(dòng)脈粥樣硬化性血管病變的早期表現(xiàn),其發(fā)生時(shí)間遠(yuǎn)遠(yuǎn)早于血管造影能夠得到動(dòng)脈粥樣硬化證據(jù)。采用多種實(shí)驗(yàn)室方法能夠直接分析血液中血管內(nèi)皮細(xì)胞釋放的各種生物活性介質(zhì)的水平以評(píng)價(jià)內(nèi)皮功能,包括超敏C-反應(yīng)蛋白、同型半胱氨酸、B-型腦鈉肽、纖維蛋白原、血管性血友病因子、可溶性血栓調(diào)節(jié)蛋白、E選擇素以及非對(duì)稱性二甲基精氨酸等等。

4 未來(lái)發(fā)展方向

代謝異常相關(guān)的疾病如高血壓、高血脂、高尿酸和糖尿病等主要損害人體動(dòng)脈血管并引發(fā)靶器官損害。其臨床結(jié)果主要包括心絞痛、心肌梗死、致命性心律失常、腦卒中、晚期腎病、周圍動(dòng)脈閉塞和猝死等。心血管疾病是累及全身的病變,因此,整體干預(yù)血管病變的策略才是降低各種心血管事件和改善患者遠(yuǎn)期預(yù)后的根本措施。動(dòng)脈僵硬度增加和內(nèi)皮功能障礙等早期血管病變是基于個(gè)體遺傳背景并受后天包括血壓,血脂等多種因素影響的病變。目前動(dòng)脈功能的檢測(cè)操作簡(jiǎn)便,有助于我們對(duì)亞臨床期的潛在高?;颊弑M早采取積極有效的治療,并選擇更為合理有效的藥物,從而全面控制心血管病的發(fā)病率和死亡率。越來(lái)越多的流行病學(xué)資料及臨床和病理生理學(xué)研究結(jié)果將為我們開(kāi)辟認(rèn)識(shí)各種危險(xiǎn)因素及其所致的包括動(dòng)脈僵硬度在內(nèi)的其它增加心血管事件發(fā)生發(fā)展危險(xiǎn)性的新領(lǐng)域。積極控制血壓達(dá)目標(biāo)值,并進(jìn)一步控制SBP和PP;早期對(duì)亞臨床血管病變進(jìn)行評(píng)價(jià)和保護(hù)血管功能;針對(duì)多種危險(xiǎn)因素的控制和高?;颊叩奶幚?;探討血管病變的分子遺傳機(jī)制,認(rèn)識(shí)高血壓相關(guān)基因與環(huán)境因素相互作用的機(jī)理,采用基因檢測(cè)高血壓及相關(guān)心血管高?;颊?,并指導(dǎo)靶向治療;開(kāi)發(fā)新的降低血壓和針對(duì)動(dòng)脈病變的藥物如血管肽酶抑制劑、內(nèi)皮素轉(zhuǎn)換酶抑制劑或其受體拮抗劑,膠原交聯(lián)抑制劑等都將為人類戰(zhàn)勝心血管疾病作出新貢獻(xiàn)[95-109]。

目前,用于血管病變?cè)缙谠u(píng)價(jià)各項(xiàng)指標(biāo)仍存在其局限性,尤其是我國(guó)國(guó)人的資料還不完善,未來(lái)我們?nèi)孕鑼?duì)反映早期血管病變的各項(xiàng)參數(shù)進(jìn)行系統(tǒng)評(píng)估,并通過(guò)大規(guī)模人群研究對(duì)其預(yù)后預(yù)測(cè)價(jià)值的綜合評(píng)價(jià),最終為臨床尋找和確立逆轉(zhuǎn)早期血管病變的策略提供新思路,探索預(yù)防心腦血管疾病的新模式。

[1] 中國(guó)血管病變?cè)缙跈z測(cè)技術(shù)標(biāo)準(zhǔn)化建議(草案)專家工作組. 中國(guó)血管病變?cè)缙跈z測(cè)技術(shù)標(biāo)準(zhǔn)化建議(草案)[J]. 中國(guó)民康醫(yī)學(xué), 2005, 17(增刊1): 1-4.

[2] 王宏宇. 血管病學(xué)[M]. 第一版. 北京: 人民軍醫(yī)出版社, 2006: 1-8.

[3] 王宏宇, 王靖, 劉望彭, 等. 血管病變?cè)缙跈z測(cè)系統(tǒng)在心血管疾病患者中的應(yīng)用[J]. 中國(guó)民康醫(yī)學(xué), 2006, 18(9): 336-339.

[4] 王宏宇, 王靖, 劉望彭, 等. 回波跟蹤技術(shù)評(píng)價(jià)高血壓和冠心病患者外周血管功能[J]. 中華超聲影像學(xué)雜志, 2006, 15(7): 501-503.

[5] 王宏宇, Asmar R, 倪永斌, 等. 中國(guó)僧侶素食時(shí)間對(duì)動(dòng)脈僵硬度的影響[J]. 中國(guó)臨床實(shí)用醫(yī)學(xué)雜志, 2007, 1(2): 1-3.

[6] 王宏宇, 郭遠(yuǎn), 蘆娜. 我國(guó)醫(yī)院醫(yī)務(wù)人員對(duì)早期血管病變認(rèn)識(shí)的初步調(diào)查[J].中國(guó)民康醫(yī)學(xué), 2008, 20(9): 859-861.

[7] 王宏宇, 蘆那, 李麗紅. 脈搏波速度、心-踝血管指數(shù)和踝臂指數(shù)評(píng)價(jià)血管早期病變[J]. 中國(guó)民康醫(yī)學(xué), 2009, 21(9): 953-956.

[8] 黃健, 劉康, 龍勝利,等. 中國(guó)貴州苗族人群血管功能狀態(tài)及其影響因素分析[J]. 中國(guó)綜合臨床, 2009, 25(8): 790-793.

[9] 王宏宇, 洪永強(qiáng), 李朝軍, 等. 中國(guó)福建畬族自然人群血管功能評(píng)價(jià)及其危險(xiǎn)因素分析-中國(guó)動(dòng)脈僵硬度評(píng)價(jià)研究-4[J]. 中國(guó)民康醫(yī)學(xué), 2009, 21(21): 2635-2641.

[10] 王宏宇, 蘆娜. 代謝綜合征與大血管病變[J]. 心血管病學(xué)進(jìn)展, 2008, 29(4): 511-513.

[11] Franklin SS, Gustin W 4th, Wong ND, et al. Hemodynamic patterns of age-related changes in blood pressure: The Framingham Heart Study[J]. Circulation, 1997, 96(1): 308-315.

[12] Blacher J, Staessen JA, Girerd X, et al. Pulse pressure not mean pressure determines cardiovascular risk in older hypertensive patients[J]. Arch Intern Med, 2000, 160(8): 1085-1089.

[13] Benetos A. Pulse pressure and cardiovascular risk[J]. J Hypertens suppl, 1999, 17(5): S21-S24.

[14] Benetos A, Zureik M, Morcet J, et al. A decrease in diastolic blood pressure combined with an increase in systolic blood pressure is associated with a higher cardiovascular mortality in men[J]. J Am Coll Cardiol, 2000, 35(3): 673-680.

[15] Domanski MJ, Davis BR, Pfeffer MA, et al. Isolated systolic hypertension. Prognostic information provided by pulse pressure[J]. Hypertens, 1999, 34(3): 375-380.

[16] Franklin SS, Khan SA, Wong ND, et al. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham heart study[J]. Circulation, 1999, 100(4): 354-360.

[17] Haider AW, Larson MG, Franklin SS, et al. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study[J]. Ann Intern Med, 2003, 138(1): 10-16.

[18] Mitchell GF, Moye LA, Braunwald E, et al. Sphygmomanometrically determined pulse pressure is a powerful independent predictor of recurrent events after myocardial infarction in patients with impaired left ventricular function. SAVE investigators. Survival and Ventricular Enlargement[J]. Circulation, 1997, 96(12): 4254-4260.

[19] O’Rourke M, Frohlich ED. Pulse pressure: Is this a clinically useful risk factor[J]? Hypertension, 1999, 34: 372-374.

[20] Safar ME. Pulse pressure in essential hypertension: clinical and therapeutic implications[J]. J Hypertens, 1989, 7(10): 769-776.

[21] Schram MT, Kostense PJ, van Dijk RA, et al. Diabetes, pulse pressure and cardiovascular mortality: the Hoorn Study[J]. J Hypertens, 2002, 20(9): 1743-1751.

[22] 王宏宇, 胡大一, 馬志敏, 等. 脈壓與冠狀動(dòng)脈病變嚴(yán)重性的關(guān)系研究[J]. 中華心血管病雜志,2003, 31(2): 83-86.

[23] Anderson EA, Mark AL. Flow-mediated and reflex changes in large peripheral artery tong in humans[J]. Circulation, 1989, 79(1): 93-100.

[24] Anderson TJ. Assessment and treatment of endothelium dysfunction in humans[J]. J Am Coll Cardiol, 1999, 34(3): 631-638.

[25] Corretti MC, Anderson TJ, Benjamin EJ, et al. Guidelines for the ultrasound assessment of endothelial dependent flow-mediated vasodilation of the brachial artery. A report of the international brachial artery reactivity task force[J]. J Am Coll Cardiol, 2002, 39(2): 257-265.

[26] Celermajar DS, Sorensen KE, Gooch VM, et al. Non-invasive detection of endothelial dysfunction in child and adults at risk of atherosclerosis[J]. Lancet, 1992, 340(8828): 1111-1115.

[27] Djuric D, Popovic Z, Petrovic J. Age related progressive brachial artery endothelial dysfunction precedes the changed carotid and left ventricular geometry in healthy humans[J]. Angiology, 1999, 50(7): 555-561.

[28] Enderle MD, Schroeder S, Ossen R, et al. Comparison of peripheral endothelial dysfunction and intimal media thickness in patients with suspected coronary artery disease[J]. Heart, 1998, 80(4): 349-354.

[29] Halcox JP, Schenke WH, Zalos G, et al. Prognostic value of coronary vascular endothelial dysfunction[J]. Circulation, 2002, 106(6): 653-658.

[30] Iiyama K, Nagano M, Yo Y, et al. Impaired endothelial function with essential hypertension assessed by ultrasonography[J]. Am Heart J, 1996, 132(4): 779-782.

[31] Khder Y, Briancon S, Petermann R, et al. Shear stress abnormalities contribute to endothelial dysfunction in hypertension but not in type II diabetes[J]. J Hypertens, 1998, 16(11): 1619-1625.

[32] Leeson P, Thorne S, Donald A, et al. Non-invasive measurement of endothelial function: effect on brachial artery dilatation of graded endothelial dependent and independent stimuli[J]. Heart, 1997, 78(1): 22-27.

[33] Ludmer PL, Selwyn AP, Shook TL, et al. Paradoxical vasoconstriction induced by acetylcholine in atherosclerotic coronary arteries[J]. N Engl J Med, 1986, 315(17): 1046-1051.

[34] Nabel EG, Selwyn AP, Ganz P. Large coronary arteries in humans are responsive to changing blood flow: an endothelium-dependent mechanism that fails in patients with atherosclerosis[J]. J Am Coll Cardiol, 1990, 16(2): 349-356.

[35] Neuntuefl T, Heher S, Katzenschlager R, et al. Late prognostic value of flow-mediated dilation in the brachial artery of patients with chest pain[J]. Am J Cardio, 2000, 86(2): 207-210.

[36] Okumura K, Yasue H, Matsuyama K, et al. Effect of acetylcholine on the highly stenotic coronary artery: difference between the constrictor response of the infarct-related coronary artery and the non infarct-related artery[J]. J Am Coll Cardiol, 1992, 19(4): 752-758.

[37] Suwaidi JA, Hamasaki S, Higano ST, et al. Long-term follow-up of patients with mild coronary artery disease and endothelial dysfunction[J]. Circulation, 2000, 101(9): 948-954.

[38] Treasure CB, Manoukian SV, Klein JL, et al. Epicardial coronary artery responses to acetylcholine are impaired in hypertensive patients[J]. Circ Res, 1992, 71(4): 776-781.

[39] Barth JD. Which tools are in your cardiac workshop? Carotid ultrasound, endothelial function, and magnetic resonance imaging[J]. Am J Cardiol, 2001, 87(4A): 8A-14A.

[40] Bots ML, Hoes AW, Koudstaal PJ, et al. Common carotid intima-media thickness and risk of stroke and myocardial infarction: the Rotterdam Study[J]. Circulation, 1997, 96(5): 1432-1437.

[41] Lemne C, Jogestrand T. Carotid intima-media thickness and plaque in borderline hypertension[J]. Stoke, 1995, 26(1): 34-39.

[42] Bonithon-Kopp C, Touboul PJ, Berr C, et al. Relation of intima-media thickness to atherosclerotic plaque in carotid arteries. The Vascular Aging (EVA)Study[J]. Arterioscler Thromb Vasc Biol, 1996, 16(2): 310-316.

[43] Bonithon-Kopp C, Jouven X, Taquet A, et al. Early carotid atherosclerosis in healthy middle-aged women. A follow-up study[J]. Stroke, 1993, 24(12): 1837-1843.

[44] Chanbless LE, Heiss G, Folsom AR, et al. Association of coronary heart disease incidence with carotid arterial wall thickness and major risk factors: the Atherosclerosis Risk in Communities (ARIC) Study, 1987-1993[J]. Am J Epidemiol, 1997, 146(6): 483-494.

[45] Craven TE, Ryu JE, Espeland MA, et al. Evaluation of the associations between carotid artery atherosclerosis and coronary artery stenosis. A case-control study[J]. Circulation, 1990, 82(4): 1230-1242.

[46] Crouse Jr, Thompson C. An evaluation of methods for imaging and qualifying coronary and carotid lumen stenosis and atherosclerosis[J]. Circulation, 1993, 87(3Suppl II): 17-33.

[47] Ferrara LA, Mancini M, Celentano M, et al. Early changes of the arterial wall in uncomplicated primary hypertensive patients. Study by ultra sound high-resolution B-mode imaging[J]. Arterioscler Thromb, 1994, 14(8): 1290-1296.

[48] Folsom AR, Eckfeldt JH, Weitzman S, et al. Relation of carotid artery wall thickness to diabetes mellitus, fasting glucose and insulin, body size, and physical activity. Atherosclerosis Risk in Communities (ARIC) Study Investigators[J]. Stroke, 1994, 25(1): 66-73.

[49] Geroulakos G, O’Gorman DJ, Kalodiki E, et al. The carotid intimamedia thickness as a marker of the presence of severe symptomatic coronary artery disease[J]. Eur Heart J, 1994, 15(6): 781-785.

[50] Grobbee DE, Bots ML. Carotid artery intima-media thickness as an indicator of generalized atherosclerosis[J]. J Intern Med, 1994, 236(5): 567-573.

[51] Handa N, Matsumoto M, Maeda H, et al. Ultrasonic evaluation of early carotid atherosclerosis[J]. Stroke, 1990, 21(11): 1567-1572.

[52] Hodis HN, Mack WJ, LaBree L, et al. The role of carotid arterial intimamedia thickness in predicting clinical coronary events[J]. Ann Intern Med, 1998, 128(4): 262-269.

[53] Laurent S. Arterial wall hypertrophy and stiffness in essential hypertensive patients[J]. J Hypertens, 1995, 26(2): 355-362.

[54] Simons PC, Algra A, Bots ML, et al. Common carotid intima-media thickness and arterial stiffness: Indictors of cardiovascular risk in high risk patients. The SMART Study (Second Manifestion of ARTeria disease) [J]. Circulation, 1999, 100(9): 951-957.

[55] Hulthe J, Wikstrand J, Emanuelsson H, et al. Atherosclerosis change in the carotid artery bulb as measured by B-mode ultrasound ar associated with the extent of coronary atherosclerosis[J]. Stroke, 199728(6): 1189-1194.

[56] O’Leary DH, Polak JF, Kronmal RA, et al. Carotid artery intima an media thickness as a risk factor for myocardial infarction and strok in older adults. Cardiovascular Health Study Collaborative Researc Group[J]. N Engl J Med, 1999, 340(1): 14-22.

[57] Selzer RH, Mack WJ, Lee PL, et al. Improved common carotid elasticit and intima-media thickness measurements from computer analysis o sequential ultrasound frames[J]. Atherosclerosis, 2001, 154(1): 185-193

[58] Salonen JT, Salonen R. Ultrasound B-mode imaging in observationa studies of atherosclerotic progress[J]. Circulation, 1993, 87(3Suppl II56-65.

[59] Salonen R, Haapanen A, Salonen JT, et al. Measurement of intima media thickness of common carotid arteries with high resolution B-mod ultrasonography: inter- and intra-observer variability[J]. Ultrasound Me Biol, 1991, 17(3): 225-230.

[60] Simon A, Gariepy J, Ghironi G, et al. Intima-media thickness: a new too for diagnosis and treatment of cardiovascular risk[J]. J Hypertens, 200220(2): 159-169.

[61] Taniwaki H, Kawagishi T, Emoto M, et al. Correlation between the intima media thickness of the carotid artery and aortic pulse wave velocity i patients with type2diabetes. Vessel wall properties in type2diabetes[J Diabetes Care, 1999, 22(11): 1851-1857.

[62] Woo KS, Chook P, Raitakari OT, et al. Westernization of Chinese adult and increased subclinical atherosclerosis[J]. Arterioscler Thromb Vas Biol, 1999, 19(10): 2487-2493.

[63] Arcaro G, Laurent S, Jondeau G, et al. Stiffness of the common caroti artery in treated hypertensive patients[J]. J Hypertens, 1991, 9(10): 947954.

[64] 王宏宇, 張維忠, 龔蘭生. 超聲評(píng)價(jià)高血壓患者動(dòng)脈緩沖功能[J]. 高血壓雜志, 2000, 8: 15-17.

[65] Blacher J, Safar ME, Pannier B, et al. Prognostic significance of arteria stiffness measurements in end-stage renal disease patients[J]. Curr Opi Nephrol Hypertens, 2002, 11(16): 629-634.

[66] Asmar R, Benetos A, Topouchian J, et al. Assessment of arteria distensibility by automatic pulse wave velocity measurement. Validatio and clinical application studies[J]. Hypertension, 1995, 26(3): 485-490.

[67] Asmar R, Topouchian J, Pannier B, et al. Pulse wave velocity as endpoin in large-scale intervention trial. The Complior study. Scientific, Qualit Control, Coordination and Investigation Committees of the Complio Study[J]. J Hypertens, 2001, 19(4): 813-818.

[68] Blacher J, Asmar R, Djane S, et al. Aortic pulse wave velocity as marker of cardiovascular risk in hypertensive patients[J]. Hypertension 1999, 33(5): 1111-1117.

[69] Isnard RN, Pannier BM, Laurent S, et al. Pulsatile diameter and elast modulus of the aortic arch in essential hypertension: a noninvasiv study[J]. J Am Coll Cardiol, 1989, 13(2): 399-405.

[70] Boutouyrie P, Tropeano AI, Asmar R, et al. Aortic stiffness is a independent predictor of primary coronary events in hypertensiv patients: a longitudinal study[J]. Hypertension, 2002, 39(1): 10-15.

[71] Kimoto E, Shoji T, Shinohara K, et al. Preferential stiffening of centra over peripheral arteries in type 2diabetes[J]. Diabetes, 2003, 52(2): 448-452.

[72] Laurent S, Boutouyrie P, Asmar R, et al. Aortic stiffness is an independen predictor of all-cause and cardiovascular mortality in hypertensiv patients[J]. Hypertension, 2001, 37(5): 1236-1241.

[73] Liao D, Arnett DK, Tyroler HA, et al. Arterial stiffness and th development of hypertension The Atherosclerosis Risk in Communitie(ARIC) study[J]. Hypertension, 1999, 34(2): 201-206.

[74] Philippe F, Chemaly E, Blacher J, et al. Aortic pulse pressure and extent of coronary artery disease in percutaneous transluminal coronary angioplasty candidates[J]. Am J Hyertens, 2002, 15(8): 672-677.

[75] Safar ME, Siche JP, Mallion JM, et al. Arterial mechanics predict cardiovascular risk in hypertension[J]. J Hypertens, 1997, 15(12Pt 2): 1605-1611.

[76] Stefanadis C, Dernellis J, Tsiamis E, et al. Aortic stiffness as a risk factor for recurrent acute coronary events in patients with ischemic heart disease[J]. Eur Heart J, 2000, 21(5): 390-396.

[77] Safar ME, London GM, Asmar R, et al. Recent advances on large arteries in hypertension[J]. Hypertension, 1998, 32(1): 156-161.

[78] Wang HY, Hu DY, Sun NL, et al. Effect of long-acting isosorbide-5-mononitrate administration on large arterial distensibility in patients with essential hypertension[J]. Hypertension Research, 2001, 24(3): 311-314.

[79] 王宏宇, 張維忠, 龔蘭生,等. 高血壓合并動(dòng)脈粥樣硬化與大動(dòng)脈緩沖功能關(guān)系的研究[J]. 中華心血管病雜志, 2001, 29(4): 206-209.

[80] 王宏宇, 張維忠, 龔蘭生, 等. 高血壓病大動(dòng)脈擴(kuò)張性與左室肥厚的關(guān)系探討[J]. 中華心血管病雜志, 2000, 28(3): 177-180.

[81] 倪永斌, 張維忠, 王宏宇, 等. 高血壓病脈搏波速度與脈壓關(guān)系的研究[J]. 中華心血管病雜志,2003, 31(4): 257-259.

[82] Dieter RS, Chu WW, Pacanowski JP Jr, et al. The significance of lower extremity peripheral disease[J]. Clin Cardiol, 2002, 25(1): 3-10.

[83] Hirsch AT, Criqui MH, Treat-Jacobson D, et al. Peripheral arterial disease detection, awareness, and treatment in primary care[J]. JAMA, 2001, 286(11): 1317-1324.

[84] Megnien JL, Sene V, Jeannin S, et al. Coronary calcification and its relation to extracoronary atherosclerosis in asymptomatic hypercholesterolemic men[J]. Circulation, 1992, 85(5): 1799-1807.

[85] Finkelstein SM, Collins VR, Cohn JN. Arterial vascular compliance response to vasodilators by Fourier and pulse contour analysis[J].Hypertension, 1988, 12(4): 380-387.

[86] Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease[J]. N Engl J, 1992, 326(6): 381-386.

[87] Cohn JN, Finkelstein S, McVeigh G, et al. Noninvasive pulse wave analysis for the early detection of the vascular disease[J]. Hypertension, 1995, 26(3): 503-508.

[88] Cohn JN. Vascular wall function as a risk marker for cardiovascular disease[J]. J Hypertens Suppl, 1999, 17(5): S41-S44.

[89] Grey E, Bratteli C, Glasser SP, et al. Reduced small artery but not large artery elasticity is an independent risk marker for cardiovascular events[J]. Am J Hypertens, 2003, 16(4): 265-269.

[90] 動(dòng)脈功能臨床研究協(xié)作組. 中國(guó)健康人群動(dòng)脈彈性功能參數(shù)研究[J]. 中華心血管病雜志, 2003, 31(4): 245-249.

[91] McVeigh G, Brennan G, Hayes R, et al. Vascular abnormalities in noninsulin-dependent diabetes mellitus identified by arterial waveform analysis[J]. Am J Med, 1993, 95(4): 424-30.

[92] McVeigh GE, Burns DE, Finkelstein SM, et al. Reduced vascular compliance as a marker for essential hypertension[J]. Am J Hypertens, 1991, 4(3Pt 1): 245-251.

[93] Prisant LM, Resnick LM, Hollenberg SM. Arterial elasticity among normotensive subjects and treated and untreated hypertensive subjects[J]. Blood Press Monit, 2001, 6(5): 233-237.

[94] Cohn JN. Arteries, myocardium, blood pressure and cardiovascular risk: towards a revised definition of hypertension[J]. J Hypertens, 1998, 16(12Pt 2): 2117-2124.

[95] Woodman RJ, Watts GF. Measurement and application of arterial stiffness in clinical research: focus on new methodologies and diabetes mellitus[J]. Med Sci Monit, 2003, 9(5): RA81-89.

[96] Guidelines Committee. 2003European Society of hypertension-European Society of Cardiology guidelines for the management of arterial hypertension[J]. J Hypertens, 2003, 21(6): 1011-1053.

[97] Oliver JJ, Webb DJ. Noninvasive Assessment of Arterial Stiffness and Risk of Atherosclerotic Events[J]. Arterioscler Thromb Vasc Biol, 2003, 23(4): 554-566.

[98] Wendelhag I, Wiklund O, Wikstrand J. Arterial wall thickness in familial hypercholesterolemia. Ultrasound measurement of intima-media thickness in the common carotid artery[J]. Arterioscler Thromb Vasc Biol, 1992, 12(1): 70-77.

[99] Persson J, Stavenow L, Wikstrand J, et al. Noninvasive quantification of atherosclerotic lesions. Reproducibility of ultrasonographic measurement of arterial wall thickness and plaque size[J]. Arterioscler Thromb Vasc Biol, 1992, 12(2): 261-266.

[100] Yasmin, Brown MJ. Similarities and differences between augmentation index and pulse wave velocity in the assessment of arterial stiffness[J]. Q J Med, 1999, 92(10): 595-600.

[101] Riley WA, Barnes RW, Evans GW, et al. Ultrasonic measurement of the elastic modulus of the common carotid artery. The Atherosclerosis Risk in Communities (ARIC) Study[J]. Stroke, 1992, 23(7), 952-956.

[102] Al-Qaisi M, Nott DM, King DH, et al. Ankle Brachial Pressure Index (ABPI): An update for practitioners[J]. Vascular Health and Risk Management, 2009, 5: 833-841.

[103] Rietzschel ER, Boeykens E, de Buyzere ML, et al. A Comparison between systolic and diastolic pulse contour analysis in the evaluation of arterial stiffness[J]. Hypertension, 2001, 37(6): e15-e22.

[104] Corretti MC, Anderson TJ, Benjamin EJ, et al. Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery[J]. J Am Coll Cardiol, 2002, 39(2): 257-265.

[105] Oliver JJ, Webb DJ. Noninvasive assessment of arterial stiffness and risk of atherosclerotic events[J]. Arterioscler Thromb Vasc Biol, 2003, 23(4): 554-566.

[106] Lane HA, Smith JC, Davies JS. Noninvasive assessment of preclinical atherosclerosis[J]. Vascular Health and Risk Management, 2006, 2(1): 19-30.

[107] 王宏宇. 血管病變?cè)缙谠u(píng)價(jià)技術(shù)系統(tǒng)的臨床應(yīng)用[J]. 心血管病學(xué)進(jìn)展, 2009, 30(2): 194-196.

[108] 王宏宇. 青少年血管病變?cè)缙谠u(píng)價(jià)的價(jià)值[J]. 心血管病學(xué)進(jìn)展, 2010, 31(2): 161-163.

[109] 王宏宇. 血管醫(yī)學(xué):血管健康評(píng)價(jià)與血管疾病綜合防治[J]. 中華醫(yī)學(xué)雜志, 2010, 90(30): 2092-2093.

猜你喜歡
袖帶受檢者動(dòng)脈
胰十二指腸上動(dòng)脈前支假性動(dòng)脈瘤1例
介紹一種防止股部止血袖帶下滑的新方法
細(xì)節(jié)護(hù)理在健康體檢中心護(hù)理服務(wù)中的應(yīng)用及體檢滿意率分析
冠狀動(dòng)脈CTA檢查前需做哪些準(zhǔn)備?
說(shuō)說(shuō)健康體檢中的溝通技巧
幸福家庭(2020年15期)2020-11-23 01:54:56
健康管理對(duì)糾正體檢人群不良生活方式的效果評(píng)價(jià)
監(jiān)護(hù)儀不同袖帶綁扎方法對(duì)血壓測(cè)量及袖帶破損的觀察
單純吻合指動(dòng)脈在末節(jié)斷指再植術(shù)中的應(yīng)用
介入栓塞治療腎上腺轉(zhuǎn)移癌供血?jiǎng)用}的初步探討
12例閉合性腘動(dòng)脈損傷的治療
海晏县| 大洼县| 诸城市| 通城县| 武宁县| 常山县| 宁强县| 绩溪县| 泸水县| 东台市| 沐川县| 三原县| 庆城县| 左云县| 郎溪县| 郯城县| 郸城县| 洪泽县| 宣武区| 买车| 镇康县| 陆川县| 巨野县| 临安市| 镇原县| 安阳市| 澳门| 四子王旗| 巩义市| 宝坻区| 澄江县| 汾阳市| 于都县| 彩票| 建昌县| 上杭县| 襄城县| 岳池县| 遂溪县| 铅山县| 太原市|