張曉暉 曾 偉
泰山醫(yī)學(xué)院附屬醫(yī)院心電圖室,山東泰安 271000
aVR導(dǎo)聯(lián)ST段抬高結(jié)合肌鈣蛋白I預(yù)測非ST段抬高型急性冠狀動脈綜合征患者預(yù)后
張曉暉曾 偉
泰山醫(yī)學(xué)院附屬醫(yī)院心電圖室,山東泰安 271000
目的 探討心電圖aVR導(dǎo)聯(lián)ST段抬高結(jié)合肌鈣蛋白Ⅰ(cTnI)在預(yù)測非ST段抬高型急性冠狀動脈綜合征(NSTE-ACS)患者預(yù)后中的價值。 方法 選擇本院自2014年1月~2015年1月收集205例NSTEACS患者,對所有患者均測定cTnⅠ,測量心電圖aVR導(dǎo)聯(lián)ST段抬高程度并行冠脈造影,并根據(jù)結(jié)果分別行冠脈介入治療或藥物保守治療,出院后隨訪6個月。205例患者分成四組:A組,cTnI陰性結(jié)合aVR-ST不抬高組(100例);B組,cTnI陰性結(jié)合aVR-ST抬高組(31例);C組,cTnI陽性結(jié)合aVR-ST不抬高組(43例);D組,cTnI陽性結(jié)合aVR-ST抬高組(31例)。觀察分析四組間左主干病變或三支冠脈病變發(fā)生率及不良心血管事件(包括死亡、心肌梗死、再梗、血運重建)的發(fā)生率,P<0.05為差異有統(tǒng)計學(xué)意義。結(jié)果 (1)左主干病變或三支冠脈病變發(fā)生率:D組顯著高于A組(χ2=78.9973,P=0.0000)、B組(χ2=13.8091,P=0.0002)及C組(χ2=44.7846,P=0.0000);B組顯著高于A組(χ2=19.7072,P=0.000)及C組(χ2=10.8407,P=0.0009);A組與C組間無統(tǒng)計學(xué)差異(χ2=0.0173,P=0.8952)。(2)不良心血管事件的發(fā)生率:D組顯著高于A組(χ2=89.4940,P=0.0003)、B組(χ2=11.0878,P=0.0009)及C組(χ2=38.5719,P=0.0005);B組顯著高于A組(χ2=29.8000,P=0.0005)及C組(χ2=9.5431,P=0.0020);A組與C組間無統(tǒng)計學(xué)差異(χ2=2.0582,P=0.1514)。 結(jié)論 聯(lián)合心電圖aVR導(dǎo)聯(lián)ST段抬高和肌鈣蛋白I陽性對預(yù)測NSTE-ACS患者的預(yù)后有重要的臨床價值,值得心血管臨床給予其更高程度的關(guān)注。
aVR導(dǎo)聯(lián)ST段抬高;肌鈣蛋白I;非ST段抬高型急性冠狀動脈綜合征;預(yù)后
非ST段抬高型急性冠狀動脈綜合征(non-ST-segment elevation acute coronary syndrome,NSTEACS)是由不穩(wěn)定性動脈粥樣硬化斑塊不完全阻塞相關(guān)冠狀動脈導(dǎo)致的急性心臟疾病,且以血小板為主的“白血栓”,是臨床上最常見的冠心病類型之一。NSTE-ACS患者的冠狀動脈粥樣硬化斑塊具有不穩(wěn)定性,臨床上不良心血管事件發(fā)生的危險較高。早期識別此類患者,有助于準(zhǔn)確判斷預(yù)后,在臨床治療方案的制定,減低致殘率、致死率方面意義重大。據(jù)報道,在判斷NSTE-ACS患者的預(yù)后方面,相對于其余導(dǎo)聯(lián)ST段壓低而言,aVR導(dǎo)聯(lián)ST段抬高有更高的預(yù)測價值[1-2],另有文獻(xiàn)顯示,不管NSTE-ACS患者的近期或遠(yuǎn)期預(yù)后,肌鈣蛋白I都與之密切相關(guān)[3-4],但目前少有研究聯(lián)合二者用于NSTE-ACS患者早期危險分層,本研究旨在探討二者的結(jié)合在預(yù)測NSTE-ACS患者預(yù)后中的價值。
1.1一般資料
本院自2014年1月~2015年1月收集的205例NSTE-ACS患者,對所有患者均測定cTnI,測量心電圖aVR導(dǎo)聯(lián)ST段抬高程度并行冠脈造影,并根據(jù)結(jié)果分別行冠脈介入治療或藥物保守治療,出院后隨訪6個月。其中男134例,女71例,平均年齡(66.0±10.0)歲。診斷均符合中華醫(yī)學(xué)會心血管病學(xué)分會關(guān)于NSTE-ACS診斷標(biāo)準(zhǔn)。入選標(biāo)準(zhǔn):(1)急性非ST段抬高型心肌梗死;(2)不穩(wěn)定性心絞痛,包括初發(fā)型、惡化勞累型、靜息型及梗死后心絞痛。排除標(biāo)準(zhǔn):(1)變異型心絞痛;(2)近6個月內(nèi)行PCI治療者;(3)曾行冠脈旁路移植術(shù);(4)腎功能衰竭患者;(5)腫瘤患者;(6)血液病患者;(7)膿毒血癥和感染性休克等其他非冠脈疾病。
1.2實驗室檢測與心電圖描記
所有患者采血化驗cTnI,參考值0~0.4ng/mL,排除檢查標(biāo)本所致肌鈣蛋白假陽性,以指標(biāo)高于參考值者為陽性。所有患者記錄標(biāo)準(zhǔn)12導(dǎo)聯(lián)心電圖,測量ST段的方法:以TP段位為基線,把QRS波群起點當(dāng)作基點,將J點后80ms作為ST段測量點,進(jìn)行測量,以任何心電圖導(dǎo)聯(lián)ST段偏離基線≥0.5mm認(rèn)為出現(xiàn)ST段變化,連續(xù)測量6個ST段,取其平均值作為測量數(shù)據(jù),記錄aVR導(dǎo)聯(lián)ST段抬高值。
1.3治療與隨訪
所有患者住院期間給予雙重抗血小板、低分子肝素鈣及他汀類藥物,根據(jù)病情給予控制心率、擴(kuò)張冠脈、改善心功能等藥物。均行選擇性冠狀動脈造影術(shù),冠脈造影結(jié)果確定分組,左冠狀動脈主干狹窄程度≥50%者為左主干病變,右冠狀動脈、左冠狀動脈前降支、左冠狀動脈回旋支狹窄程度均≥50%者為三支病變。隨訪6個月,觀察患者非致死性心肌梗死(包括再梗)、心力衰竭、心血管死亡以及血運重建等不良心血管事件的發(fā)生率。
1.4統(tǒng)計學(xué)方法
應(yīng)用SPSS17.0軟件進(jìn)行數(shù)據(jù)分析,計數(shù)資料以頻數(shù)或率表示,計量資料以表示,計量資料采用t檢驗;計數(shù)資料采用χ2檢驗。P<0.05為差異有統(tǒng)計學(xué)意義。
2.1aVR-ST不抬高組和aVR-ST抬高組兩組間比較
兩組的性別、年齡、陳舊心梗、既往PCI、高血壓及糖尿病構(gòu)成無統(tǒng)計學(xué)差異。aVR-ST抬高組患者的cTnI陽性率、左主干或三支冠脈病變率及6個月內(nèi)不良心血管事件發(fā)生率均高于aVR-ST不抬高組。差異有統(tǒng)計學(xué)意義(P<0.05)。見表1。
2.2cTnI陰性組和cTnI陽性組臨床資料比較
以cTnI是否升高分為cTnI陰性組(cTnI<0.4ng/mL)與cTnI陽性組(cTnI>0.4ng/mL)。兩組的性別、年齡、陳舊心梗、既往PCI、高血壓及糖尿病構(gòu)成無統(tǒng)計學(xué)差異。cTnI陽性組患者的aVR導(dǎo)聯(lián)ST段抬高率、左主干或三支冠脈病變率以及6個月內(nèi)不良心血管事件發(fā)生率均高于cTnI陰性組,差異有統(tǒng)計學(xué)意義。見表2。
2.3aVR導(dǎo)聯(lián)ST段變化與cTn I結(jié)合,各組不良心血管事件發(fā)生比較
將aVR導(dǎo)聯(lián)ST段變化與cTnI結(jié)合,將患者分為4組。A組:aVR-ST不抬高與cTnI陰性,B組:aVRST抬高與cTnI陰性,C組:aVR-ST不抬高與cTnI陽性,D組:aVR-ST抬高與cTnI陽性。①兩兩比較 四組患者的左主干或三支冠脈病變率,以P<0.05為差異有統(tǒng)計學(xué)意義。A組與B組比較,χ2=19.7072,P=0.000;A組與C組比較,χ2=0.0173,P=0.8952;B組 與 C組 比 較,χ2=10.8407,P=0.0009;D組與A組比較,χ2=78.9973,P=0.0000;D組與B組比較,χ2=13.8091,P=0.0002;D組與C組比較,χ2=44.7846,P=0.0000。結(jié)果提示D組患者的左主干或三支冠脈病變率最高,B組次之,A組與C組間差異無統(tǒng)計學(xué)意義。②兩兩比較 4組患者6個月內(nèi)不良心血管事件發(fā)生率,以P<0.0071為差異有統(tǒng)計學(xué)意義。A組與B組比較,χ2=29.80000,P=0.0005;A組與C組比較,χ2=2.0582,P=0.1514;B組與C組比較,χ2=9.5431,P=0.0020;D組與A組 比 較,χ2=89.4940,P=0.0003;D組 與 B組比較,χ2=11.0878,P=0.0009;D組與C組比較,χ2=38.5719,P=0.0005。結(jié)果提示A組與C組間差異無統(tǒng)計學(xué)意義,D組不良心血管事件的發(fā)生率高于其他三組。見表3。
表1 aVR-ST不抬高組和aVR-ST抬高組臨床資料
表2 cTnI陰性組和cTnI陽性組臨床資料比較
NSTE-ACS包括不穩(wěn)定性心絞痛和非ST段抬高型心肌梗死(NSTEMI),并發(fā)癥多、病死率高,為指導(dǎo)臨床早期干預(yù),Braunwald等[5]主張對NSTEACS患者進(jìn)行危險分層。NSTE-ACS時,冠脈常常存在不完全阻塞,多數(shù)患者常有短暫性ST段壓低或T波低平、倒置,但部分患者雖有嚴(yán)重狹窄,也可無心電圖改變。盡管如此,體表心電圖檢查還是早期診斷NSTE-ACS簡單有效的非創(chuàng)傷性檢查。Barrabes等[1]研究發(fā)現(xiàn),ST段上抬≥0.5mm時,aVR導(dǎo)聯(lián)ST段抬高的程度與患者的臨床預(yù)后有顯著相關(guān)性。Filip等[6,12-13]研究證實aVR導(dǎo)聯(lián)ST段抬高及其程度可以作為NSTE-ACS患者30天死亡率的獨立預(yù)測因素。Kosuge等[7-8]認(rèn)為aVR導(dǎo)聯(lián)ST段抬高是對NSTE-ACS患者是否存在三支或左主干病變及其短期預(yù)后的判斷的有效指標(biāo)。已有研究證實,多支冠脈病變以及左主干病變患者的aVR導(dǎo)聯(lián)ST段抬高的發(fā)生率明顯高于不抬高組,并且在患者血運重建治療情況上統(tǒng)計學(xué)差異,這都提示aVR導(dǎo)聯(lián)ST段的抬高對預(yù)測NSTE-ACS患者的預(yù)后有重要價值。
表3 aVR導(dǎo)聯(lián)ST段變化與cTn I結(jié)合,各組不良心血管事件比較[n(%)]
肌鈣蛋白(troponin,Tn)是橫紋肌收縮的重要調(diào)解蛋白,由TnI、TnT和TnC三個亞單位組成,TnI又分為心肌亞型(cTnI)、快骨骼肌亞型(fTnI)和慢骨骼肌亞型(sTnI)3種亞型。cTnI在基因上有特異的氨基酸排列,僅存在于心肌內(nèi),但在個體發(fā)育的各個階段都不在骨骼肌中表達(dá)[9],因而具有高度的心肌特異性。cTnI的特異性及時間窗較肌紅蛋白或CK-MB都短,對30d以內(nèi)的短期預(yù)后及1年以內(nèi)的長期預(yù)后有預(yù)測價值。NSTE-ACS患者CK-MB正常但cTnI增高的,其死亡風(fēng)險增高。而且隨著cTnI值增高, NSTE-ACS患者死亡風(fēng)險增大。Apple等[10,14]指出cTnI升高可作為獨立指標(biāo)用以預(yù)報NSTE-ACS患者心臟事件的危險性,可以用于判斷NSTE-ACS患者的預(yù)后。Merrill等[11]研究也證實,cTnI水平的測定可作為ACS患者危險分層中的重要指標(biāo)。本研究顯示cTnI陽性的NSTE-ACS患者其左主干或三支冠脈病變率以及6個月內(nèi)不良心血管事件發(fā)生率均明顯高于cTnI陰性組,提示cTnI水平的測定可用于NSTEACS患者危險分層,這與上述其他研究結(jié)果一致。
而且本研究對NSTE-ACS患者的心電圖aVR導(dǎo)聯(lián)ST段的偏移情況及cTnI水平進(jìn)行不同組合,隨訪6個月后,結(jié)果顯示,aVR導(dǎo)聯(lián)ST段抬高合并cTnI陽性時,不管左主干病變、三支冠狀動脈血管病變的發(fā)生率,還是不良心血管事件(包括心肌梗死、再梗塞、死亡、行血運重建等)的發(fā)生率均明顯高于其他組合。綜上所述,cTnI陽性及aVR導(dǎo)聯(lián)ST段抬高聯(lián)合判斷對預(yù)測NSTE-ACS患者的風(fēng)險及預(yù)后有重要的臨床價值,值得我們重視。
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aVR lead ST segment elevation combined with cardiac troponin I in prediction of prognosis of patients with Non-ST-segment elevation acute coronary syndrome
ZHANG XiaohuiZENG Wei
Electrocardiographic Room,Affiliated Hospital ofTaishan Medical College,Tai'an 271000,China
Objective To investigate the value of electrocardiogram aVR lead ST segment elevation combined with cardiac troponin I in prediction of prognosis of patients with Non-ST-segment elevation acute coronary syndrome. Methods 205 cases of patients with Non-ST-segment elevation acute coronary syndrome from January 2014 to January 2015 in our hospital were included in our study.All patients were detected cTnl,detected ST segment elevation of aVR lead in electrocardiogram,and carried on coronary angiography.According to the results,all of them were followed up for 6 months after discharge.They were divided into 4 groups:group A that was cTnl negative combined with AVR-ST non- elevation group (100 cases),group B that was cTnl negative combined with AVRST elevation group(31 cases),group C that was cTnl positive combined with AVR-ST non- elevation group (43 cases),group D that was cTnl positive combined with AVR-ST elevation group (31 cases).Incidence of left main lesion or three coronary artery disease and incidence of adverse cardiovascular events (including death, myocardial infarction,reinfarction,revascularization) of the four groups were observed.There were statistical significance (P<0.05). Results (1)Incidence of left main lesion or three coronary artery disease:group D was significantly higher than group A (χ2=78.9973,P=0.0000),group B (χ2=13.8091,P=0.0002) and group C (χ2=44.7846,P=0.0000).Group B was significantly higher than group A (χ2=19.7072,P=0.000) and goup C (χ2=10.8407,P=0.0009).There was no statistical significance between group A and group C (χ2=0.0173,P=0.8952).(2)Incidence of adverse cardiovascular events:group D was significantly higher than group A (χ2=89.4940,P=0.0003),group B (χ2=11.0878,P=0.0009) and group C(χ2=38.5719,P=0.0005).Group B was sinificantly higher than group A (χ2=29.8000,P=0.0005) and group C (χ2=9.5431,P=0.0020).There was no statistical significance between group A and group C (χ2=2.0582,P=0.1514). Conclusion The value of electrocardiogram aVR lead ST segment elevation combined with cardiac troponin I inprediction of prognosis of patients with Non-ST-segment elevation acute coronary syndrome is great.It deserves a higher degree of attention to cardiovascular clinical.
aVR lead ST segment elevation;Troponin I;Non-ST-segment elevation acute coronary syndrome;Prognosis
R541.4
A
2095-0616(2016)18-11-05
(2016-07-22)