【摘要】心血管疾?。–VD)是引起全球發(fā)病率和死亡率持續(xù)升高的慢性非傳染性疾病,吸煙、肥胖和血脂異常等多因素共同參與其發(fā)病過(guò)程,對(duì)公共衛(wèi)生構(gòu)成了嚴(yán)重的威脅和挑戰(zhàn)。因此,亟需探索新的有效風(fēng)險(xiǎn)預(yù)測(cè)因子及干預(yù)措施,準(zhǔn)確識(shí)別高?;颊?,“前移”預(yù)防窗口,控制致病危險(xiǎn)因素,延緩病程進(jìn)展,這己成為防治CVD的根本。甘油三酯葡萄糖指數(shù)通過(guò)代謝及炎癥反應(yīng)等途徑驅(qū)動(dòng)動(dòng)脈粥樣硬化的形成,從而加劇向冠心病的演變過(guò)程;在血管內(nèi)皮功能、血管緊張素原的異位合成、腎素-血管緊張素-醛固酮系統(tǒng)、交感神經(jīng)系統(tǒng)及鹽吸收中發(fā)揮作用,從而影響血壓的變化;此外,隨著胰島素抵抗程度的增加,心臟脂肪酸利用率下降、AMPK/PGC-1信號(hào)轉(zhuǎn)導(dǎo)通路損害及活性氧水平增加,從而導(dǎo)致心力衰竭。血小板與淋巴細(xì)胞比值是一種炎癥標(biāo)志物,通過(guò)血小板和淋巴細(xì)胞的變化在CVD中發(fā)揮作用?,F(xiàn)結(jié)合最新研究對(duì)以上兩個(gè)指標(biāo)預(yù)測(cè)CVD的潛在價(jià)值進(jìn)行綜述。
【關(guān)鍵詞】心血管疾病;臨床指標(biāo);甘油三酯葡萄糖指數(shù);血小板與淋巴細(xì)胞比值
【DOI】10.16806/j.cnki.issn.1004-3934.2024.11.014
Triglyceride-Glucose Index and Platelet-to-Lymphocyte Ratio in Cardiovascular Diseases
XIONG Xing1,WANG Zhimei1,ZHANG Ning1,WEN Xia2
(1.Inner Mongolia Clinical Medical College,Inner Mongolia Medical University,Hohhot 010020,Inner Mongolia,China;2.Department of Emergency,Inner Mongolia Autonomous Region People’s Hospital,Hohhot 010020,Inner Mongolia,China)
【Abstract】Cardiovascular disease (CVD) is a chronic non-infectious disease that causes the global incidence rate and mortality to continue to rise.Smoking,obesity,dyslipidemia and other factors participate in its pathogenesis,posing a serious threat and challenge to public health.Therefore,it is urgent to explore new effective risk prediction factors and intervention measures,accurately identify high-risk patients,move forward the prevention window,control pathogenic risk factors and delay disease progression,which have become the fundamental measures for preventing and treating CVD.Triglyceride-glucose index drives the formation of atherosclerosis through metabolic and inflammatory pathways,thus exacerbating the evolution to coronary heart disease.It also plays a role in vascular endothelial function,ectopic synthesis of angiotensinogen,renin-angiotensin-aldosterone system,sympathetic nervous system and salt absorption,thus affecting blood pressure changes.In addition,with the increase of insulin resistance,the utilization of cardiac fatty acids decreased,AMPK/PGC-1 signal transduction pathway impaired,and reactive oxygen species levels increased,leading to heart failure.The platelet-to-lymphocyte ratio is an inflammatory marker that plays a role in CVD through changes in platelets and lymphocytes.Based on the latest research,this article reviews the potential value of the above two indicators in predicting CVD.
【Keywords】Cardiovascular disease;Clinical indicators;Triglyceride-glucose index;Platelet-to-lymphocyte ratio
心血管疾?。╟ardiovascular disease,CVD)仍是世界上疾病負(fù)擔(dān)的主要原因[1],一項(xiàng)來(lái)自美國(guó)心臟協(xié)會(huì)的統(tǒng)計(jì)報(bào)告[2]顯示:2020年全球CVD死亡人數(shù)比2010年增加了18.71%,是全球的主要死亡原因。因此,CVD的早發(fā)現(xiàn)、早診斷、早預(yù)防迫在眉睫。其中,探索各種簡(jiǎn)單和廣泛可用的臨床指標(biāo)來(lái)預(yù)測(cè)其與CVD風(fēng)險(xiǎn)的相關(guān)性必不可少。目前,已有許多臨床指標(biāo)被發(fā)現(xiàn)與CVD密切相關(guān),但大多數(shù)是建立在對(duì)疾病診斷的基礎(chǔ)上,期望探索出更多高靈敏度及特異性的指標(biāo)以評(píng)估CVD發(fā)生的風(fēng)險(xiǎn),甚至在一定程度上能替代一些有創(chuàng)的檢查,從而及早干預(yù)疾病發(fā)展。如甘油三酯葡萄糖指數(shù)(triglyceride-glucose index,TyG指數(shù))和血小板與淋巴細(xì)胞比值(platelet-to-lymphocyte ratio,PLR)被證明與CVD間存在相關(guān)性,且其數(shù)值越高,CVD風(fēng)險(xiǎn)越大[3-4]。此外,TyG指數(shù)和PLR的測(cè)定在臨床中具有低成本、簡(jiǎn)便、創(chuàng)傷小等優(yōu)勢(shì),易于開(kāi)展。接下來(lái)分別從以上兩個(gè)指標(biāo)與CVD的關(guān)系展開(kāi)綜述。
1"TyG指數(shù)
胰島素抵抗(insulin resistance,IR)是代謝綜合征和2型糖尿病的主要病理生理學(xué)機(jī)制[5],是一種胰島素敏感性受損的臨床狀態(tài)[6]。在臨床實(shí)踐中,甘油三酯和血糖是心臟代謝風(fēng)險(xiǎn)的經(jīng)典標(biāo)志物,這些標(biāo)志物水平的改變與IR、動(dòng)脈粥樣硬化的進(jìn)展和CVD的發(fā)生直接相關(guān)。研究[7]表明,IR是動(dòng)脈粥樣硬化和CVD的危險(xiǎn)因素。高胰島素-正常血糖鉗夾術(shù)和靜脈葡萄糖耐量試驗(yàn)是評(píng)估IR的金標(biāo)準(zhǔn),由于檢測(cè)方式繁瑣,因此主要用于科學(xué)研究,在臨床實(shí)踐中難以推廣。穩(wěn)態(tài)模型評(píng)估IR指數(shù)是目前廣泛應(yīng)用的一種檢測(cè)β細(xì)胞功能和IR的方法,但對(duì)于接受胰島素治療或β細(xì)胞功能不全的受試者應(yīng)用價(jià)值有限[8]。為解決這些缺陷,有意義的臨床替代指標(biāo)不斷被挖掘。近年來(lái),由甘油三酯和空腹血糖得出的TyG指數(shù)已被證實(shí)是IR的可靠替代標(biāo)志物[9]。該指數(shù)計(jì)算公式為:TyG指數(shù)= ln [空腹甘油三酯(mg/dL)×空腹血糖(mg/dL)/2],ln為自然對(duì)數(shù),TyG指數(shù)是由空腹甘油三酯和空腹葡萄糖水平組成的復(fù)合指標(biāo)。值得注意的是,在一項(xiàng)中位隨訪25年的研究[10]中發(fā)現(xiàn):TyG指數(shù)每增加一個(gè)單位,CVD風(fēng)險(xiǎn)增加96%(HR=1.96,95%CI 1.44~2.66),全因死亡風(fēng)險(xiǎn)增加85% (HR=1.85,95%CI 1.45~2.36)。
1.1"TyG指數(shù)與動(dòng)脈粥樣硬化
動(dòng)脈粥樣硬化是血管的一種慢性炎癥狀態(tài),它是通過(guò)富含脂質(zhì)病變的生長(zhǎng)、單核細(xì)胞和巨噬細(xì)胞在血管壁內(nèi)層積聚并釋放促炎介質(zhì)而發(fā)生的,從而導(dǎo)致動(dòng)脈粥樣硬化的形成[11]。慢性炎癥在動(dòng)脈粥樣硬化中起關(guān)鍵作用,脂蛋白膽固醇積累和IR促進(jìn)炎癥和動(dòng)脈粥樣硬化斑塊的形成[12](如圖1)。動(dòng)脈粥樣硬化的特點(diǎn)是受累動(dòng)脈的病變從內(nèi)膜開(kāi)始,先后有脂質(zhì)積聚、纖維組織增生和鈣質(zhì)沉著,并有動(dòng)脈中層的逐漸退變和鈣化,在此基礎(chǔ)上繼發(fā)斑塊內(nèi)出血、斑塊破裂及局部血栓形成。
IR是驅(qū)動(dòng)動(dòng)脈粥樣硬化CVD的主要潛在異常因素[13]。IR導(dǎo)致動(dòng)脈硬化的部分原因是相關(guān)的慢性高胰島素血癥,慢性高胰島素血癥增加極低密度脂蛋白膽固醇的合成、血管平滑肌細(xì)胞的生長(zhǎng)和增殖、低密度脂蛋白膽固醇運(yùn)輸?shù)絼?dòng)脈平滑肌細(xì)胞,以及激活參與炎癥的基因[12](如圖2)。此外,TyG指數(shù)作為一種簡(jiǎn)單、快速的IR生物標(biāo)志物,與致動(dòng)脈粥樣硬化的小而密低密度脂蛋白膽固醇顆粒水平的優(yōu)勢(shì)相關(guān)[14]。目前,已有研究[15]發(fā)現(xiàn)TyG指數(shù)與各種臨床條件下的動(dòng)脈粥樣硬化以及心血管事件風(fēng)險(xiǎn)較高的患者之間存在顯著的相關(guān)性。Li等[16]的研究也證實(shí)了無(wú)論常規(guī)影響因素如何,TyG指數(shù)與動(dòng)脈粥樣硬化呈正相關(guān)。
1.2"TyG指數(shù)與冠心病
冠心?。╟oronary heart disease,CHD)是指冠狀動(dòng)脈發(fā)生粥樣硬化引起管腔狹窄或閉塞,導(dǎo)致心肌缺血缺氧或壞死而引起的心臟病。在CHD的演變過(guò)程中,動(dòng)脈粥樣硬化斑塊的形成和發(fā)展在CHD的病理生理過(guò)程中發(fā)揮重要作用,可能的機(jī)制包括內(nèi)皮細(xì)胞損傷、炎癥、氧化應(yīng)激、糖脂代謝紊亂和血栓等[17]。IR在CHD的發(fā)生發(fā)展過(guò)程中發(fā)揮了重要作用。如IR可引起血管炎癥[18],血管炎癥是斑塊形成的驅(qū)動(dòng)力,是斑塊破裂的典型特征,可導(dǎo)致急性冠脈綜合征[19]。TyG指數(shù)作為IR的可靠替代指標(biāo),在CHD各階段均有潛在作用,影響動(dòng)脈粥樣硬化斑塊的形成,與冠狀動(dòng)脈鈣化、硬化有關(guān),可預(yù)測(cè)冠狀動(dòng)脈狹窄程度[20]。Thai等[21]發(fā)現(xiàn),TyG指數(shù)≥10與狹窄血管數(shù)量增加和狹窄的嚴(yán)重程度顯著相關(guān)。冠狀動(dòng)脈造影作為診斷CHD的金標(biāo)準(zhǔn),可直觀地明確冠狀動(dòng)脈狹窄的數(shù)量和程度,若TyG指數(shù)在一定程度上能反映冠狀動(dòng)脈病變的嚴(yán)重程度,對(duì)于基層臨床醫(yī)務(wù)者及患者都將是一大福音。此外,Park等[22]證實(shí),TyG指數(shù)在預(yù)測(cè)無(wú)傳統(tǒng)心血管危險(xiǎn)因素的亞臨床冠狀動(dòng)脈疾?。╟oronary artery disease,CAD)中具有顯著的價(jià)值,就特定的冠狀動(dòng)脈斑塊亞型而言,TyG指數(shù)與該人群中非鈣化或混合性冠狀動(dòng)脈斑塊風(fēng)險(xiǎn)增加獨(dú)立相關(guān)。Mahdavi-Roshan等[23]發(fā)現(xiàn),確診CAD的患者與對(duì)照組相比,較高的甘油三酯、總膽固醇和空腹血糖水平以及較低的高密度脂蛋白膽固醇水平與CHD風(fēng)險(xiǎn)升高相關(guān),而血清低密度脂蛋白膽固醇水平與CHD風(fēng)險(xiǎn)之間的直接關(guān)聯(lián)僅在排除糖尿病患者和他汀類藥物使用者后才變得明顯,然而,與上述傳統(tǒng)評(píng)估指標(biāo)相比,TyG指數(shù)升高和CHD風(fēng)險(xiǎn)升高更顯著。因此,CVD患者常規(guī)監(jiān)測(cè)TyG指數(shù)可能具有較大獲益。
1.3"TyG指數(shù)與高血壓
高血壓作為CVD的危險(xiǎn)因素之一,嚴(yán)重影響人類健康。目前,全球約31.1%的成年人患有高血壓,隨著人口老齡化,這一數(shù)字在全球范圍內(nèi)激增[24]。因此,及早發(fā)現(xiàn)高危人群,制定有效的一級(jí)預(yù)防策略,對(duì)于扭轉(zhuǎn)高血壓快速上升的趨勢(shì)十分重要。研究[25]發(fā)現(xiàn),脂蛋白代謝紊亂,特別是甘油三酯、空腹血糖升高都是CVD的既定危險(xiǎn)因素,尤其是高血壓。IR和高血壓的相關(guān)性可通過(guò)至少以下幾種機(jī)制來(lái)解釋:炎癥性內(nèi)皮功能障礙,血管緊張素原的異位合成[26],以及高胰島素血癥刺激腎素-血管緊張素-醛固酮系統(tǒng)和交感神經(jīng)系統(tǒng),促進(jìn)血管平滑肌細(xì)胞和內(nèi)皮細(xì)胞肥大,導(dǎo)致外周血管阻力增加和高血壓[27]。此外,IR促進(jìn)鹽吸收并間接導(dǎo)致水鈉潴留,導(dǎo)致高血壓[28]。因此,TyG指數(shù)或IR與血壓之間的緊密聯(lián)系具有較強(qiáng)的生理學(xué)依據(jù)。一項(xiàng)橫斷面研究[29]表明,較高的TyG指數(shù)與健康個(gè)體血壓升高的風(fēng)險(xiǎn)顯著相關(guān)。同樣,在Wang等[28]的logistic回歸分析中也顯示,TyG指數(shù)與高血壓前期及高血壓密切相關(guān),同時(shí)還發(fā)現(xiàn)TyG指數(shù)對(duì)高血壓的預(yù)測(cè)能力優(yōu)于甘油三酯或高密度脂蛋白膽固醇。TyG指數(shù)優(yōu)于甘油三酯或高密度脂蛋白膽固醇的關(guān)鍵機(jī)制可能是糖毒性和脂毒性調(diào)節(jié)IR所致[30]。由于TyG指數(shù)的優(yōu)越性,以及甘油三酯和空腹血糖的檢測(cè)簡(jiǎn)單易行,在正常人群中大規(guī)模篩查TyG指數(shù)對(duì)高血壓的一級(jí)預(yù)防具有重要意義。
1.4"TyG指數(shù)與心力衰竭
心力衰竭(heart failure,HF)是由多種CVD引起的一種復(fù)雜的臨床綜合征,在全世界范圍內(nèi)具有高發(fā)病率和高死亡率的特點(diǎn)[31]。據(jù)估計(jì),發(fā)達(dá)國(guó)家HF患病率為1%~2%,預(yù)計(jì)到2060年將翻一番[32]。研究[33]表明,隨著IR程度的增加,心臟利用脂肪酸的能力下降,導(dǎo)致脂質(zhì)堆積和增加,最后引起心臟肥大和收縮功能障礙,加劇左心室重塑,導(dǎo)致HF。IR還會(huì)損害AMPK/PGC-1信號(hào)轉(zhuǎn)導(dǎo)通路,從而降低線粒體膜電位和ATP合成,導(dǎo)致心臟重構(gòu)[34];線粒體功能障礙會(huì)刺激活性氧水平增加,反過(guò)來(lái),活性氧水平的增加降低了脂肪酸氧化的能力,進(jìn)一步驅(qū)動(dòng)線粒體功能障礙和細(xì)胞凋亡,導(dǎo)致脂質(zhì)堆積、心肌纖維化和HF[35]。TyG指數(shù)作為IR的有效替代指標(biāo),在臨床研究[36]中發(fā)現(xiàn),TyG指數(shù)與HF患者較差的預(yù)后呈正相關(guān)。同樣,Yang等[37]也證實(shí),較高的TyG指數(shù)與HF患者較差的預(yù)后顯著相關(guān);且TyG指數(shù)可作為HF患者心肌纖維化的新型生物標(biāo)志物。Zhou等[38]發(fā)現(xiàn),與TyG指數(shù)最低三分位數(shù)的患者相比,最高三分位數(shù)的患者表現(xiàn)出最易發(fā)生全因死亡(HR=1.53,95%CI 1.19~1.98)和心血管死亡(HR=1.52,95%CI 1.19~1.96);且TyG指數(shù)與HF再住院之間存在顯著關(guān)聯(lián)(HR=1.31,95%CI 1.07~1.61)。此外,Zhang等[31]基于2007—2018年國(guó)家健康和營(yíng)養(yǎng)檢查調(diào)查的數(shù)據(jù)發(fā)現(xiàn),當(dāng)TyG指數(shù)>8.91時(shí),HF的風(fēng)險(xiǎn)隨著TyG指數(shù)的增加而迅速增加,提示TyG指數(shù)可能有助于識(shí)別HF高危人群。
TyG指數(shù)在上述CVD中的相關(guān)臨床研究見(jiàn)表1。
2"PLR
PLR是一種新型炎癥標(biāo)志物,可應(yīng)用于多種疾病,用于預(yù)測(cè)炎癥和死亡率[40],最初被認(rèn)為是腫瘤預(yù)后的預(yù)測(cè)因子,并與腫瘤患者的炎癥有關(guān)[41]。隨著研究不斷深入,逐漸發(fā)現(xiàn)PLR與CVD事件獨(dú)立相關(guān)[4]。研究[42]發(fā)現(xiàn)外周血小板計(jì)數(shù)升高與心血管事件風(fēng)險(xiǎn)增加相關(guān),因?yàn)檠“逵?jì)數(shù)的增加被認(rèn)為是過(guò)度炎癥狀態(tài)和血栓形成活動(dòng)的反映,這二者都被認(rèn)為是動(dòng)脈粥樣硬化CVD的關(guān)鍵病理生理因素。此外,淋巴細(xì)胞計(jì)數(shù)是生理應(yīng)激的指標(biāo),它與炎癥呈負(fù)相關(guān),淋巴細(xì)胞計(jì)數(shù)越低,心血管風(fēng)險(xiǎn)和死亡率越高[43]。淋巴細(xì)胞減少癥是炎癥過(guò)程的一個(gè)常見(jiàn)特征,主要是由于淋巴細(xì)胞凋亡增加及其在淋巴系統(tǒng)內(nèi)的重新分布所致,淋巴細(xì)胞減少反映了免疫抑制的普遍狀態(tài)[44]。
2.1"PLR與動(dòng)脈粥樣硬化
研究[40]表明,PLR是CVD患者一個(gè)強(qiáng)有力的預(yù)后因素。然而,PLR在CVD中的意義不僅與預(yù)后相關(guān),在其發(fā)生發(fā)展過(guò)程中也同樣發(fā)揮著關(guān)鍵的作用。如慢性炎癥反應(yīng)是動(dòng)脈粥樣硬化發(fā)病機(jī)制的關(guān)鍵因素,與血小板和淋巴細(xì)胞的數(shù)量及功能相關(guān)[45]。一方面,血小板釋放免疫調(diào)節(jié)介質(zhì),如前列腺素E2、血小板激活因子,這些介質(zhì)會(huì)導(dǎo)致炎癥狀態(tài)[46]。正常數(shù)量的血小板是凝血過(guò)程所必需的,然而過(guò)量的血小板會(huì)對(duì)血管壁產(chǎn)生反應(yīng),并導(dǎo)致動(dòng)脈血栓形成。此外,過(guò)多的血小板會(huì)促進(jìn)炎癥并增加動(dòng)脈粥樣硬化的風(fēng)險(xiǎn)[4]。活化的血小板參與血栓形成,響應(yīng)動(dòng)脈粥樣硬化斑塊破裂或內(nèi)皮細(xì)胞侵蝕,從而促進(jìn)動(dòng)脈粥樣硬化性血栓性疾病或不良心血管事件的發(fā)展[43]。另一方面,在涉及斑塊生長(zhǎng)、脂質(zhì)核心發(fā)育、斑塊破裂和血栓形成的動(dòng)脈粥樣硬化病變中觀察到淋巴細(xì)胞凋亡[47]。而且,在動(dòng)脈粥樣硬化不穩(wěn)定斑塊中觀察到淋巴細(xì)胞的比例明顯低于穩(wěn)定斑塊[48]。
2.2"PLR與CHD
PLR可能被認(rèn)為是全身炎癥的生物標(biāo)志物,并與各種CVD(包括急性冠脈綜合征)的不良臨床結(jié)果相關(guān)[49],而且高水平的PLR可能與急性冠脈綜合征患者非肇事病變的易損斑塊特征有關(guān)[50]。急性心肌梗死時(shí),淋巴細(xì)胞浸潤(rùn)到缺血和再灌注心肌并表達(dá)各種白細(xì)胞介素,這些白細(xì)胞介素在單核細(xì)胞的遷移中發(fā)揮重要作用,并誘導(dǎo)金屬蛋白酶組織抑制劑的表達(dá)[43]。Larmann等[51]發(fā)現(xiàn),PLR>204.4時(shí),與CHD患者圍手術(shù)期30 d主要不良心腦血管事件相關(guān)。同樣,Azab等[52]也發(fā)現(xiàn),PLR與非ST段抬高型心肌梗死后患者的長(zhǎng)期死亡率相關(guān)。此外,Zhou等[45]觀察到ST段抬高型心肌梗死且PLR>171組患者與PLR較低組相比,在5年隨訪期間表現(xiàn)出更嚴(yán)重的冠狀動(dòng)脈狹窄和更差的預(yù)后,以及更高的主要不良心血管事件發(fā)生率;而且在進(jìn)行冠狀動(dòng)脈造影后發(fā)現(xiàn),與PLR<101組的患者相比,PLR>171組的患者發(fā)生3支CAD的風(fēng)險(xiǎn)明顯增加。
2.3"PLR與高血壓
目前,原發(fā)性高血壓被認(rèn)為是一種低度炎癥狀態(tài)[53],而且亞臨床炎癥的程度可用促炎細(xì)胞因子的濃度來(lái)衡量,也可用全血細(xì)胞計(jì)數(shù)衍生的標(biāo)志物來(lái)衡量,如PLR[54]。在成人中,發(fā)現(xiàn)高血壓患者PLR升高,而且被認(rèn)為是死亡風(fēng)險(xiǎn)增加的標(biāo)志[43]。當(dāng)血小板被激活時(shí),會(huì)分泌多種促炎可溶性因子,血小板因子4是由活化的血小板分泌的最豐富的因子,并在內(nèi)皮細(xì)胞中積累;同樣,受刺激的血小板也會(huì)分泌并儲(chǔ)存白細(xì)胞介素-1β、P選擇素和可溶性CD40L,從而導(dǎo)致全身炎癥、脈管系統(tǒng)炎癥[55]。Barhoumi等[56]的動(dòng)物研究證明,調(diào)節(jié)性T淋巴細(xì)胞可抑制血管緊張素Ⅱ介導(dǎo)的血壓升高和血管損傷。因此,淋巴細(xì)胞降低可能導(dǎo)致高血壓的發(fā)生,這可能是低淋巴細(xì)胞計(jì)數(shù)與高血壓之間關(guān)聯(lián)的解釋。此外,根據(jù)血壓的晝夜變化,與白天相比,睡眠期間的收縮壓和舒張壓預(yù)計(jì)會(huì)降低10%以上,這種情況發(fā)生在杓型高血壓患者身上;在非杓型高血壓患者中,這種變異不會(huì)發(fā)生[57]。有研究[58]報(bào)告,PLR升高可預(yù)測(cè)非杓型晝夜節(jié)律模式的高血壓患者。因此,PLR可作為高血壓風(fēng)險(xiǎn)的間接預(yù)測(cè)因子,有助于優(yōu)化預(yù)防策略。
2.4"PLR與HF
在HF等應(yīng)激狀態(tài)下,下丘腦-垂體-腎上腺軸會(huì)分泌大量皮質(zhì)醇和兒茶酚胺,導(dǎo)致淋巴細(xì)胞重新分布到淋巴器官,從而減少淋巴細(xì)胞數(shù)量,最終導(dǎo)致HF患者的存活率下降[59]。此外,HF患者的冠狀動(dòng)脈血流量較低,而較高的血小板可能導(dǎo)致血栓形成,使預(yù)后惡化[60]。在HF患者中還發(fā)現(xiàn)血小板和淋巴細(xì)胞分泌高水平的趨化因子C-C,趨化因子與疾病嚴(yán)重程度成正比[61]。一項(xiàng)納入1 299例HF患者的研究[62]發(fā)現(xiàn),較高的PLR三分位數(shù)與入院時(shí)呼吸困難嚴(yán)重程度、左室射血分?jǐn)?shù)降低、N末端腦鈉肽前體和肌鈣蛋白水平升高成正比。此外,Delcea等[61]發(fā)現(xiàn),大多數(shù)評(píng)估5年隨訪的長(zhǎng)期HF死亡率的研究證實(shí),PLR是HF病死率的獨(dú)立預(yù)測(cè)因子,其臨界值為150.00~194.97。
PLR指數(shù)在上述CVD中的相關(guān)臨床研究見(jiàn)表2。
3"展望
未來(lái)的研究仍需大樣本、多中心、高質(zhì)量的研究來(lái)進(jìn)一步確定TyG指數(shù)和PLR二者聯(lián)合預(yù)測(cè)CVD的敏感度、特異度及最佳截?cái)嘀?。此外,可?dòng)態(tài)監(jiān)測(cè)其在各類CVD中的變化趨勢(shì),探討不同階段TyG指數(shù)和PLR水平的變化對(duì)CVD發(fā)生、發(fā)展及預(yù)后的判斷價(jià)值,全面了解其在CVD中的意義,將有利于更精確地發(fā)現(xiàn)存在潛在危險(xiǎn)因素的人群,優(yōu)化疾病篩查方案,及早干預(yù)疾病的發(fā)展進(jìn)程,從而提高患者的生存質(zhì)量,有助于患者從二級(jí)預(yù)防中獲益。
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收稿日期:2024-04-30