【摘要】 目的:探討不穩(wěn)定型心絞痛(UAP)患者發(fā)生急性心肌梗死(AMI)的影響因素,以及N末端腦鈉肽前體(NT-proBNP)對AMI發(fā)生風(fēng)險的預(yù)測價值。方法:選擇2021年2月—2023年2月上饒市人民醫(yī)院收治的120例UAP患者作為研究對象。所有患者均檢測NT-proBNP水平,并比較不同嚴(yán)重程度UAP患者NT-proBNP水平。隨訪1年,記錄UAP患者AMI的發(fā)生情況,并根據(jù)是否發(fā)生AMI將其分為兩組:發(fā)生組(n=23)和未發(fā)生組(n=97)。對發(fā)生AMI的UAP患者進(jìn)行多因素logistic回歸分析。繪制受試者操作特征(ROC)曲線,以曲線下面積(AUC)評估NT-proBNP對UAP患者AMI發(fā)生風(fēng)險的預(yù)測效能。結(jié)果:不同嚴(yán)重程度UAP患者NT-proBNP對比,差異有統(tǒng)計學(xué)意義(Plt;0.05);重度組NT-proBNP高于輕度組和中度組,中度組NT-proBNP高于輕度組,差異均有統(tǒng)計學(xué)意義(Plt;0.05)。120例UAP患者中有23例(19.17%)發(fā)生AMI。發(fā)生組重度UAP占比、NT-proBNP均高于未發(fā)生組,差異均有統(tǒng)計學(xué)意義(Plt;0.05)。多因素logistic回歸分析顯示,重度UAP[OR=3.550,95%CI(1.213,10.387)]、NT-proBNP[OR=3.991,95%CI(1.364,11.676)]均是UAP患者發(fā)生AMI的獨(dú)立危險因素(Plt;0.05)。ROC曲線分析結(jié)果顯示,NT-proBNP預(yù)測UAP患者AMI發(fā)生的敏感度為69.57%,特異度為79.81%,AUC為0.721[95%CI(0.635,0.797)]。結(jié)論:UAP嚴(yán)重程度及NT-proBNP水平均是UAP患者發(fā)生AMI的影響因素,NT-proBNP對UAP患者AMI發(fā)生有一定的預(yù)測價值。
【關(guān)鍵詞】 不穩(wěn)定型心絞痛 N末端腦鈉肽前體 急性心肌梗死
Analysis of the Influencing Factors of AMI in Patients with Unstable Angina Pectoris and the Predictive Value of NT-proBNP for AMI/HE Qian, HUANG Ting, LIU Shanhu, LIU Yuzhong. //Medical Innovation of China, 2024, 21(33): -170
[Abstract] Objective: To investigate the influencing factors of acute myocardial infarction (AMI) in patients with unstable angina pectoris (UAP) and the predictive value of N-terminal pro-brain natriuretic peptide (NT-proBNP) on the occurrence risk of AMI. Method: A total of 120 patients with UAP admitted to Shangrao People's Hospital from February 2021 to February 2023 were selected as the study objects. The level of NT-proBNP was detected in all patients, and the level of NT-proBNP in patients with UAP with different severity was compared. Followed up for 1 year, the occurrence of AMI in patients with UAP was recorded, and they were divided into two groups according to whether AMI occurred: occurrence group (n=23) and non-occurrence group (n=97). Multivariate logistic regression analysis was performed for UAP patients with AMI. The receiver operator characteristic (ROC) curve was drawn, and the area under the curve (AUC) was used to evaluate the predictive efficacy of NT-proBNP on the occurrence risk of AMI in patients with UAP. Result: The difference of NT-proBNP in patients with UAP with different severity was statistically significant (Plt;0.05). NT-proBNP in severe group was higher than that in mild group and moderate group, and NT-proBNP in moderate group was higher than that in mild group, the differences were statistically significant (Plt;0.05). Among 120 patients with UAP, 23 cases (19.17%) occurred AMI. The proportion of severe UAP and NT-proBNP in the occurrence group were higher than those in the non-occurrence group, the differences were statistically significant (Plt;0.05). Multivariate logistic regression analysis showed that severe UAP [OR=3.550, 95%CI (1.213, 10.387)] and NT-proBNP [OR=3.991, 95%CI (1.364, 11.676)] were all independent risk factors of the occurrence of AMI in patients with UAP (Plt;0.05). ROC curve analysis results showed that the sensitivity of NT-proBNP in predicting AMI occurrence in patients with UAP was 69.57%, and the specificity was 79.81%, the AUC was 0.721[95%CI (0.635, 0.797)]. Conclusion: The severity of UAP and NT-proBNP are all influencing factors of the occurrence of AMI in patients with UAP, and NT-proBNP has certain predictive value for the occurrence of AMI in patients with UAP.
[Key words] Unstable angina pectoris N-terminal pro-brain natriuretic peptide Acute myocardial infarction
First-author's address: Department of Cardiology, Shangrao People's Hospital, Shangrao 334000, China
doi:10.3969/j.issn.1674-4985.2024.33.040
不穩(wěn)定型心絞痛(unstable angina pectoris,UAP)是一種嚴(yán)重的心血管疾病,其特點(diǎn)是病情進(jìn)展迅速且有較高轉(zhuǎn)變?yōu)榧毙孕募」K溃╝cute myocardial infarction, AMI)的風(fēng)險[1-2]。AMI是導(dǎo)致患者心力衰竭、再發(fā)心肌梗死及死亡的重要原因。因此,對于UAP患者而言,早期識別并預(yù)測AMI的發(fā)生至關(guān)重要。已有研究表明,UAP處于穩(wěn)定型心絞痛(stable angina pectoris,SAP)與AMI的一個過渡階段[3-4]。然而,目前臨床上仍然缺乏有效的生物標(biāo)志物來準(zhǔn)確預(yù)測UAP患者發(fā)展為AMI的風(fēng)險。N末端腦鈉肽前體(N-terminal pro-brain natriuretic peptide, NT-proBNP)作為一種潛在的生物標(biāo)志物受到關(guān)注。NT-proBNP能夠反映心臟的功能狀態(tài),并與心肌損傷密切相關(guān)[5]。其有較長的半衰期、良好的穩(wěn)定性和較低的外部因素干擾,這使得它成為一項較理想的檢測指標(biāo)。因此,本研究旨在通過收集并分析UAP患者的NT-proBNP水平,并評估其對AMI發(fā)生的預(yù)測能力。
1 資料與方法
1.1 一般資料
本研究回顧性選擇2021年2月—2023年2月上饒市人民醫(yī)院收治的120例UAP患者作為研究對象。納入標(biāo)準(zhǔn):符合UAP診斷標(biāo)準(zhǔn)[6];無其他心血管疾病如心肌炎、心臟瓣膜疾病等。排除標(biāo)準(zhǔn):重要器官(如肝、腎)功能嚴(yán)重受損;合并惡性腫瘤;精神障礙;有冠狀動脈相關(guān)手術(shù)史;近3個月接受過手術(shù)。本研究已通過本院醫(yī)學(xué)倫理委員會審批。
1.2 方法
1.2.1 NT-proBNP檢測方法 患者入院2 h內(nèi)采集2 mL靜脈血,高速離心機(jī)離心后,以化學(xué)發(fā)光法檢測血清NT-proBNP水平。NT-proBNP≥300 ng/L定義為高水平。
1.2.2 UAP嚴(yán)重程度 參考Braunwald分級和危險分層確定UAP的嚴(yán)重程度,輕度:首次發(fā)生,無靜息疼痛,或近2周新發(fā)但無長時間靜息性胸痛,肌鈣蛋白T(cTnT)水平正常;中度:近30 d內(nèi)發(fā)生過心絞痛,但48 h內(nèi)無發(fā)作,cTnT水平升高(gt;0.01 μg/L但lt;0.1 μg/L);重度:48 h內(nèi)有發(fā)作,靜息性胸痛持續(xù)時間(gt;20 min),cTnT水平顯著升高(≥0.1 μg/L)[7]。
1.2.3 AMI發(fā)生判斷 隨訪1年,參照文獻(xiàn)[8]《急性心肌梗死診斷和治療指南》中的相關(guān)診斷標(biāo)準(zhǔn),根據(jù)患者發(fā)生AMI的情況將其分為發(fā)生組和未發(fā)生組。
1.2.4 臨床資料收集 收集患者的臨床資料,包括性別、年齡、體重指數(shù)(BMI)、合并基礎(chǔ)疾病、吸煙史、飲酒史、血常規(guī)指標(biāo)等。
1.3 統(tǒng)計學(xué)處理
用SPSS 22.0進(jìn)行數(shù)據(jù)處理。以(x±s)、率(%)分別對計量資料和計數(shù)資料進(jìn)行描述,兩組間比較分別采用t檢驗、字2檢驗;多組間的計量資料比較采用方差分析,兩兩比較采用LSD-t檢驗;UAP患者發(fā)生AMI的獨(dú)立影響因素采用多因素logistic回歸分析;繪制受試者操作特征(ROC)曲線,計算ROC曲線下面積(AUC),評估預(yù)測模型的準(zhǔn)確性。Plt;0.05為差異有統(tǒng)計學(xué)意義。
2 結(jié)果
2.1 不同嚴(yán)重程度UAP患者NT-proBNP水平比較
不同嚴(yán)重程度UAP患者NT-proBNP對比,差異有統(tǒng)計學(xué)意義(Plt;0.05);重度組NT-proBNP高于輕度組和中度組,差異均有統(tǒng)計學(xué)意義(Plt;0.05);中度組NT-proBNP高于輕度組,差異有統(tǒng)計學(xué)意義(Plt;0.05)。見表1。
2.2 UAP患者AMI發(fā)生情況
120例UAP患者,發(fā)生AMI有23例,AMI發(fā)生率為19.17%。
2.3 發(fā)生組和未發(fā)生組臨床資料比較
兩組性別、年齡、體重指數(shù)(BMI)、合并基礎(chǔ)疾病、吸煙史、飲酒史、白細(xì)胞計數(shù)、血小板計數(shù)、血紅蛋白比較,差異均無統(tǒng)計學(xué)意義(Pgt;0.05);發(fā)生組重度UAP占比、NT-proBNP均高于未發(fā)生組,差異均有統(tǒng)計學(xué)意義(Plt;0.05)。見表2。
2.4 UAP患者發(fā)生AMI的影響因素
以UAP嚴(yán)重程度(重度=1,輕、中度=0)、NT-proBNP(取原始數(shù)據(jù))為自變量,UAP患者是否發(fā)生AMI為應(yīng)變量(發(fā)生=1,未發(fā)生=0),進(jìn)行多因素logistic回歸分析。結(jié)果顯示,重度UAP、NT-proBNP均為UAP患者發(fā)生AMI的危險因素(Plt;0.05)。見表3。
2.5 NT-proBNP對UAP患者AMI發(fā)生的預(yù)測效能
ROC曲線結(jié)果顯示,NT-proBNP對UAP患者AMI發(fā)生預(yù)測的敏感度為69.57%,特異度為79.81%,AUC為0.721[95%CI(0.635,0.797)],見圖1。
3 討論
UAP是一種嚴(yán)重的心肌缺血性疾病,每年因UAP住院的人數(shù)在100萬以上,其死亡率可高達(dá)8%,嚴(yán)重威脅患者的生命健康[9-11]。有關(guān)研究報道,UAP患者易惡化為AMI、心律失常,進(jìn)而導(dǎo)致患者死亡[12]。目前臨床中缺乏有效且特異性高的指標(biāo)來預(yù)測UAP患者發(fā)展為AMI的風(fēng)險。鑒于此,本研究旨在探討UAP患者發(fā)生AMI的影響因素,以及NT-proBNP水平對AMI發(fā)生的預(yù)測價值。
本研究結(jié)果顯示,不同嚴(yán)重程度UAP患者NT-proBNP比較有統(tǒng)計學(xué)意義,重度組高于中度組和輕度組,中度組高于輕度組,隨著病情加重,NT-proBNP逐漸升高,提示UAP患者疾病嚴(yán)重程度與NT-proBNP之間可能存在聯(lián)系。本研究結(jié)果顯示,發(fā)生組重度UAP占比、NT-proBNP均高于未發(fā)生組,經(jīng)多因素logistic分析結(jié)果顯示,重度UAP、NT-proBNP均為UAP患者發(fā)生AMI的危險因素。重度UAP患者的病情本身較為危急,血液流動受阻,心肌供血不足的情況更為突出,這種持續(xù)的缺血狀態(tài)會加劇心肌細(xì)胞的損傷和壞死,從而直接增加AMI的發(fā)生概率[13-14]。NT-proBNP作為一種由心房細(xì)胞在壓力或損傷時釋放的糖蛋白,其血清濃度與UAP嚴(yán)重程度密切相關(guān),NT-proBNP的異常升高可能反映了心臟負(fù)荷的增加和心室功能的受損,其同樣是增加AMI發(fā)生風(fēng)險的一個重要因素[15-16]。ROC曲線結(jié)果顯示,NT-proBNP對UAP患者AMI發(fā)生預(yù)測的敏感度為69.57%,特異度為79.81%,AUC為0.721,提示NT-proBNP對UAP患者AMI發(fā)生有一定的預(yù)測價值。分析NT-proBNP可對AMI發(fā)病進(jìn)行預(yù)測的可能機(jī)制為,NT-proBNP是心室在承受壓力或牽張時,由心室肌細(xì)胞自然產(chǎn)生并釋放的一種生物活性多肽,它不僅在調(diào)節(jié)體液平衡、促進(jìn)利尿及舒張血管等方面發(fā)揮重要作用,更是心肌健康狀態(tài)的一個敏感指示器,與心肌損傷的起始、進(jìn)展及結(jié)局緊密相關(guān)。UAP發(fā)作的情況下,冠狀動脈的狹窄或痙攣導(dǎo)致心肌血流急劇減少,引發(fā)心肌缺血。這種缺血狀態(tài)會直接影響心室的功能,造成心室肌細(xì)胞受損,心室壁的順應(yīng)性下降,進(jìn)而觸發(fā)心室肌細(xì)胞合成并釋放更多的NT-proBNP到血液中[17-18]。因此,隨著UAP的發(fā)作和心肌缺血的加劇,血清中NT-proBNP的水平會相應(yīng)升高。
綜上所述,重度UAP、NT-proBNP是UAP患者發(fā)生AMI的危險因素,且NT-proBNP對UAP患者AMI發(fā)生有一定的預(yù)測價值。
參考文獻(xiàn)
[1] JIA R F,LI L,LI H,et al.Meta-analysis of C-reactive protein and risk of angina pectoris[J].Am J Cardiol,2020,125(7):1039-1045.
[2]李玉香.瑞舒伐他汀結(jié)合氯吡格雷治療冠心病不穩(wěn)定型心絞痛患者的臨床價值分析[J].中外醫(yī)療,2024,43(11):94-97.
[3] LI P,XIN Q,HUI J,et al.Efficacy and safety of Tongxinluo Capsule as adjunctive treatment for unstable angina pectoris: a systematic review and meta-analysis of randomized controlled trials[J]. Front Pharmacol, 2021, 12(24):978-982.
[4] KRISTENSEN A,PAREEK M,KRAGHOLM K H,et al.
Unstable angina as a component of primary composite endpoints in clinical cardiovascular trials: pros and cons[J].Cardiology,2022,36(27):81-86.
[5] EDWARDS K D,TIGHE M P.How to use N-terminal pro-brain natriuretic peptide (NT-proBNP) in assessing disease severity in bronchiolitis[J].Arch Dis Child Educ Pract Ed,2020,105(5):282-288.
[6]雷玲.美國“不穩(wěn)定型心絞痛和非ST段抬高心肌梗死治療指南”更新[J].世界臨床藥物,2012,33(8):511.
[7]章武戰(zhàn),周亮良,劉生華,等.血漿N末端腦鈉肽前體水平與不穩(wěn)定型心絞痛Braunwald分級及心血管不良事件的關(guān)系[J].心腦血管病防治,2018(4):298-300.
[8]中華醫(yī)學(xué)會心血管病學(xué)分會,中華心血管病雜志編輯委員會,《中國循環(huán)雜志》編輯委員會.急性心肌梗死診斷和治療指南[J].中國循環(huán)雜志,2001,16(6):407-422.
[9] WANG T,MEHTA O H,LIAO Y B,et al.Meta-analysis of bleeding scores performance for acute coronary syndrome[J].Heart Lung Circ,2020,29(12):1749-1757.
[10] CASTIGLIONE V,AIMO A,VERGARO G,et al.Biomarkers for the diagnosis and management of heart failure[J].Heart Fail Rev,2022,27(2):625-643.
[11]李丹,吳敏.基于網(wǎng)狀Meta分析對8個經(jīng)典名方治療不穩(wěn)定型心絞痛的臨床療效評價[J].世界中醫(yī)藥,2024,19(4):492-504.
[12] BHATT D L,LOPES R D,HARRINGTON R A.Diagnosis and treatment of acute coronary syndromes: a review[J].JAMA,2022,27(7):662-675.
[13] ABEL A,CLARK A L.Long-term pharmacological management of reduced ejection fraction following acute myocardial infarction: current status and future prospects[J].Int J Gen Med,2021,14(26):7797-7805.
[14]曹學(xué)民,張穎.血清ApoB/ApoA1、LTBP-2、VASP對不穩(wěn)定型心絞痛進(jìn)展至急性心肌梗死的預(yù)測效能[J].河北醫(yī)藥,2023,45(11):1637-1640.
[15] SCHWINGER R.Pathophysiology of heart failure[J].Cardiovasc Diagn Ther,2021,11(1):263-276.
[16] SBOLLI M,DEFILIPPI C.BNP and NT-proBNP interpretation in the neprilysin inhibitor era[J].Curr Cardiol Rep,2020,22(11):150-153.
[17] CAI R P,XU Y L,SU Q.Dapagliflozin in patients with chronic heart failure: a systematic review and meta-analysis[J].Cardiol Res Pract,2021,43(9):80-83.
[18] DEMIRAY A,AFSAR B,COVIC A,et al.The role of uric acid in the acute myocardial infarction: a narrative review[J].Angiology,2022,73(1):9-17.
(收稿日期:2024-08-19) (本文編輯:陳韻)