Journal of Geriatric Cardiology(2013)10:102109 2013JGC All rights rerved;
潮目
Review Open Access High-nsitive cardiac troponin T
Ru-Yi Xu1,Xiao-Fa Zhu1,Ye Yang1,Ping Ye2
1Dep artment of Geriatric Cardiolo gy,Nav y General Hospital,No.6,Fucheng R oad,B eijing100048,China
2Dep artment of Geriatric Cardiolo gy,Chine PL A General Hospital,No.28,Fux ing Road,Beijin g100853,China
Abstract
Cardiac troponin is the preferred biomarker for the diagnosis of acute myocardial infarction(AMI).The recent development of a high-nsitive cardiac troponin T(hs-cTnT)assay permits detection of very l
ow levels of cTnT.Using the hs-cTnT assay improves the over-all diagnostic accuracy in patients with suspected AMI,while a negative result also has a high negative predictive value.The gain in nsitiv-ity may be particularly important in patients with a short duration from symptom ont to admission.Measurement of cardiac troponin T with the hs-cTnT assay may provide strong prognostic information in patients with acute coronary syndromes,stable coronary artery dia, heart failure and even in the general population;however,incread nsitivity comes at a cost of decread specificity.Serial testing,as well as clinical context and co-existing dias,are likely to become increasingly important for the interpretation of hs-cTnT assay results.
J Geriatr Cardiol2013;10:102109.doi:10.3969/j.issn.1671-5411.2013.01.015
mistressKeywords:Troponin T;Acute myocardial infarction;Risk stratification
1Introduction
The troponin complex regulates the contraction of stri-ated muscles and consists of three subunits(troponin C, troponin T,and troponin I).Troponin C is a18ku protein that binds to calcium ions.Troponin T is a37ku protein that binds to tropomyosin,thereby attaching the troponin complex to the thin filament.Troponin I is a24ku protein that binds to actin and decreas troponin C affinity for c
al-cium,thus inhibiting actin–myosin interactions.[1] Troponin T and troponin I are prent in cardiac and skeletal muscles,but are encoded by different genes in the two types of muscle,yielding proteins that are immu-nologically distinct.[1]Assays that are bad on high-affinity antibodies and are specific for cardiac troponin T(cTnT) and cardiac troponin I(cTnI)are available.Becau the amino acid quence of cardiac troponin C and skeletal tro-ponin C is identical,no such assays have been developed for the troponin C component.
The majority of cardiac troponin(cTn)is bound to myo-filaments,and the remainder is free in the cytosol which
Correspond ence to:Ping Ye,PhD,Department of Geriatric Cardiology, Chine PL A General Hospital,No.28,Fuxin g Road,Beijing100853, China.E-mail:yep in
Telephone:+86-10-66876369Fax:+86-10-66876349
Received:November10,2012Revid:January31,2013 Accepted:February26,2013Pub lished online:March28,2013accounts for3%–8%of the total amount.[2]After disruption of the sarcolemmal membrane of the cardiomyocyte,tro-ponin from the cytoplasmic pool is initially relead,fol-lowed by a more protracted relea from quantities bound to deteriorating myofilaments.[1]In peripheral blood,
cTnT begins to ri within three to four hours after the ont of myocardial injury and remains incread for10–14days.[3] 2Cardiac troponin assays
There are a number of cTnI assays on the market.The cTnI assays are not standardized at this time and studies have documented substantial differences across methods.[4] Apart from the lack of commutable reference material,other factors contributing to quantitative differences between the cTnI methods include the variable antibody immunoreactiv-ity to different circulating cTnI forms and varying calibra-tors ud in different cTnI assays.[4]The proper way to achieve complete standardization for cTnI assays would be to u antibodies with similar epitope specificities and a rum-bad common reference material for calibration.[4] However,that is a complicated process and the progress has been slow.[5]
In contrast to cTnI,there is only one manufacturer for the cTnT assay and the above shortcomings could be avoided. The first-generation assay for cTnT ud bovine cTnT as the reference material and exhibited non-specific binding to human skeletal muscle troponin,[6]but this problem was
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overcome by refinement of the detection antibody in the cond-generation assay and the u of rec
ombinant human cTnT for standardization in the third-generation assay.[7,]8 The fourth-generation cTnT assay us fragment anti-gen-binding(FAB)of two cTnT-specific mou mono-clonal antibodies in a sandwich format.The antibodies rec-ognize epitopes located in the central part of the cTnT molecule(amino acid positions125–131and135–147). Detection of cTnT is bad on an electrochemiluminescence immunoassay using a Tris(bipyridyl)-ruthenium(II)com-plex as a label.[9]The fourth-generation cTnT assay has a limit of detection(LoD)of0.01ng/mL,a99th percentile cut-off point of0.01ng/mL,and a10%coefficient of varia-tion(CV)of0.03ng/mL.[10]For the diagnosis of acute myocardial infarction(AMI),the fourth-generation cTnT assay is considered the standard assay.In addition,samples in which there is an increas of cTn in the blood exceeding the99t h percentile of the normal reference population,the guidelines suggest that the CV of the ideal cTn assay ud is ≤10%at the99th percentile concentration.[11,]12Clearly,the fourth-generation cTnT assay lacks adequate precision.
The new high-nsitive cTnT(hs-cTnT)assay is a modi-fication of the fourth-generation cTnT assay.[9]The bio-tinylated capture antibody was not changed.The detection antibody was genetically re-engineered,replacing the con-stant C1region in the monoclonal mou FAB fragment with a human IgG C1region,leading to a mou-human chimeric detection antibody.[9]The rationale for this re-plac
ement was to further reduce the susceptibility to inter-ference by heterophilic antibodies.The variable region of the detection antibody is identical to that of the fourth-gene-ration assay.The analytical nsitivity was improved by increasing the sample volume from15L to50L,in-creasing the ruthenium concentration of the detection anti-body,and lowering the background signal via buffer opti-mization.As a result of the modifications,the analytic performance of the hs-cTnT assay was significantly im-proved;specifically,the LoD was0.003ng/mL(3ng/L),the 99t h percentile cut-off point was0.014ng/mL(14ng/L),and the CV was10%at0.013ng/mL(13ng/L).[9]Due to a lower LoD and a incread precision,the hs-cTnT assay is able to detect more subtle elevations indicative of cardiac injury
3Ear ly diagnosis of myocardial infar ction The early identification of individuals at high or interme-diate risk for myocardial ischemia is crucial becau pa-tients benefit the most from early and aggressive treat-ment.[13]The rapid and reliable diagnosis of AMI is a major unmet clinical need.[14]Myocardial necrosis is accompanied by the relea of structural proteins and other intracellular macromolecules into the cardiac interstitium,such as cTn, creatine kina,and myoglobin.[3]The preferred biomarker for myocardial necrosis is cTn,which has nearly absolute myocardial tissue specificity as well as high clinical nsi-tivity,thereby reflecting even microscopic zones of myo-cardi
al necrosis.[15]According to international connsus and task force definitions of myocardial infarction(MI),the diagnosis of MI is bad mainly on evidence of myocardial ischemia,together with an elevated cTn level exceeding the 99t h percentile and demonstrating an increa or decrea over time.[11]The universal definition recommends the u of a more nsitive troponin assay with a CV of10%at the diagnostic cut-off concentration reprenting the99th per-centile of a reference population.[12]The recently developed hs-cTnT assay which has a lower CV satisfies this crite-rion,[9]together with a lower LoD.
In unlected emergency department(ED)patients with symptoms suggestive of an AMI,the hs-cTnT assay sig-nificantly improved the early diagnosis of AMI compar-ed with the standard troponin T assay(fourth-generation cTnT).[16]According to the diagnostic criterion for an AMI, a hs-cTnT level>the99th percentile(0.014ng/mL),had a nsitivity,specificity,negative predictive value,and posi-tive predictive value(95%confidence interval[CI])of95% (90%–98%),80%(77%–83%),99%(97%–100%),and 50%(43%–56%),respectively.[16]Bad on a standard tro-ponin T assay>10%CV(0.035ng/mL),the nsitivity, specificity,negative predictive value,and positive predic-tive value(95%CI)for diagnosis of AMI was72%(64%–80%),97%(96%–98%),94%(92%–96%),and85%(76%–91%),respectively.The diagnostic accuracy for AMI,as quantified by the area un
der the receiver-operating-cha-racteristic curve(AUC),was significantly higher with the hs-cTnT assay than the standard assay(AUC for hs-cTnT, 0.96,95%CI,0.94–0.98vs.AUC for the standard assay, 0.90;95%CI,0.86–0.94).[16]The superiority of the hs-cTnT assay was most pronounced among patients with a recent ont of chest pain.Among patients who prented within three hours after the ont of chest pain,the AUC was sig-nificantly higher with the hs-cTnT assay than the standard assay(AUC for hs-cTnT,0.92,95%CI,0.87–0.97vs.AUC for the standard assay,0.76,95%CI,0.64–0.88).[16]The diagnostic performance of the hs-cTnT assay was similar in patients with non-ST gment elevation MI(NSTEMI)and ST gment elevation MI.[16]The hs-cTnI assay also im-proved the diagnostic ability in patients with AMIs.[16] Aldous et al.[17]reported that in patients with chest pain who did not have ST gment elevation,the hs-cTn assay at a
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cut-off point of99t h percentile(0.014ng/mL)was highly nsitive for the diagnosis of MI two hours after pren-tation compared with the standard assay.Improvement in the early diagnosis of AMIs in such patients is of paramount importance,becau of the opportunity to extend early treatment options to all patients with AMIs.[16]More rapid diagnosis of AMI may reduce more complications by fa-cilitating an earlier revascularization,earlier transfer to the coronary care unit,and earlier initiation
of evidence-bad treatment for AMIs.[14,]16
In patients with symptoms suggestive of acute coronary syndrome(ACS)and an initially negative cTnT concentra-tion(<0.03ng/mL with the standard cTnT assay),[18]the criterion for the hs-cTnT assay(hs-cTnT≥0.014ng/mL) enables earlier detection of evolving NSTEMI compared to the criterion of the standard cTnT assay(cTnT≥0.03 ng/mL).[18]On admission,61.5%of the patients with ACS had hs-cTnT concentrations≥0.014ng/mL,and incread gradually to100%of patients within six hours,and the overall number of MI diagnos incread by34.6%.[18] In elderly patients(>70years of age)prenting with symptoms suggestive of AMI,the AUC was significantly greater for the hs-cTnT assay compared to the standard cTnT assay(AUC for the hs-cTnT assay,0.94vs.AUC for the standard cTnT assay,0.90).[19]Becau51%of the eld-erly patients with a final diagnosis other than an AMI had elevated baline hs-cTnT levels(≥0.014ng/mL),the best cut-off value to detect an AMI for the hs-cTnT assay bad on the AUC in elderly patients differed clearly from tho in younger patients(0.054ng/mL for elderly patients vs.0.017 ng/mL for younger patients).[19]
In patients with pre-existing coronary artery dia (CAD)prenting with symptoms suggestive of an AMI, the diagnostic accuracy at prentation was significantly greater for the hs-cTn assay compared with the standard assay(AUC for the hs-cTnT assay,0.92vs.AUC for the standard cTnT as
say,0.87).[20]The optimal cut-off levels tend to be higher in patients with pre-existing CAD than in patients without a history of CAD(0.030ng/mL for patients with pre-existing CAD vs.0.020ng/mL for patients without a history of CAD).[20]
For rial changes in the hs-cTnT assay within two hours after prenting with symptoms of a MI in patients with suspected ACS,Aldous et al.[21]reported that the diagnostic specificity of hs-cTnT improved with the u of relative change(δ)≥20%in patients with concentrations≥99th percentile at a cost of a reduction in nsitivity,while the diagnostic nsitivity improved with the u of aδ≥20%in patients within0–2hours at concentrations<99th percentile. However,Reichlin et al.[22]showed that the absolute changes in hs-cTnT levels have a significantly higher diagnostic accuracy for AMI than relative changes,and the optimal criterion of absolute change was0.007ng/mL for two hours.
九年级英语视频In addition to diagnosing a MI,precily and promptly ruling out a MI is important in an overcrowded ED.[23]With the previous cTn assay in most patients,blood should be obtained for testing upon prentation to the hospital and at 6–9h after prentation to provide adequate clinical nsi-tivity for detecting a MI.[3]The diagnostic performance of the hs-cTnT assay was excellent,even in patients within two hours after the ont of chest pain.[16]The nsitivity for MI approaches100%by including a cond sample within three hours of prentation.[18,]24With the hs-cTnT assay,the negative pred
ictive value for MI with a single test on admis-sion is95%,and thereby at least as high as achieved with previous assays using rial measurements.[25]Body et al.[26] reported that undetectable hs-cTnT(<0.003ng/mL)at prentation had a high negative predictive value for pa-tients with chest pain at ED.An initially undetectable hs-cTnT has a nsitivity of99.8%(95%CI,99.1%–100.0%) and a negative predictive value of99.4%(95%CI, 96.6%–100.0%)for ruling out an AMI.[26]Pending further validation,this strategy may reduce the need for rial test-ing and empirical treatment,enabling earlier reassurance for patients with chest pain and fewer unnecessary evaluations and hospital admissions.[26]
4The prognostic value of hs-cTnT
4.1In patient s with C AD or diabet es mellitus
The cTn level is an important marker for risk stratifica-tion in patients with ACS.In patients with a suspected AMI, compared with the standard cTnT assay,the prognostic ac-curacy of hs-cTnT for death was significantly higher(AUC, 0.79;95%CI,0.74–0.84)than cTnT(AUC,0.69;95%CI, 0.62–0.76).After adjustment for the Thrombolysis in Myo-cardial Infarction(TIMI)risk score that included the stan-dard cTnT assay result,hs-cTnT>the99th percentile(0.014 ng/mL)was associated with a haz
ard ratio(HR)for death of 2.60(95%CI,1.42–4.74).Addition of hs-cTnT to the TIMI risk score improved the reclassification of patients(net re-classification improvement,0.91;95%CI,0.67–1.14).Sub-group analys showed that this effect resulted from the better classification of patients without an AMI at the time of testing.[27]In patients with pre-existing CAD and symp-toms suggestive of an AMI,elevated levels of hs-cTnT pre-dicted mortality independent of pre-existing CAD,age, gender,and cardiovascular risk factors.[20]In patients with chest pain who did not have ST gment elevation,the hs-cTnT assay was superior to the standard assay in pre-
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dicting death(HR,5.4;95%CI,2.7–10.7)and heart failure ([HF];HR,27.8;95%CI,6.6–116.4)at one year.[17]The hs-cTnT levels(≥0.001ng/mL)were detected in97.7%of patients with a mean age of63.6years,stable CAD,and prerved left ventricular function;>99th percentile of ap-parently healthy subjects(0.0133ng/mL)reprented11.1% among this population.[28]During a median follow-up period of5.2years,after adjustment for other independent prog-nostic indicators,the hs-cTnT levels were significantly as-sociated with the incidence of cardiovascular death(ad-justed hazard ratio[aHR]per unit increa in the natural logarithm of the troponin T level,2.09;95%CI,1.60–2.74) and HF(Ahr,2.20,95%CI,1.66–2.90)but not with MI.[28] An incread risk associated with higher level
s of hs-cTnT was evident well below the LoD(0.01ng/mL)of standard cTnT assays and below the99th percentile of values in a healthy population.[28]In the convalescence pha after an ACS,the levels of hs-cTnT continued to have prognostic value.A high ven week hs-cTnT(>0.014ng/mL)pre-dicted adver clinical outcomes independent of conven-tional risk factors,left ventricular dysfunction and left ven-tricular hypertrophy on echocardiography(aHR,2.69,95% CI,1.45–5.00).Patients with persistent hs-cTnT elevation at ven weeks were also at an incread risk of cardiovascular events compared with patients who had an initial high hs-TnT which then normalized.[29]In female patients with diabetes mellitus(DM),the hs-cTnT levels were detectable in45.5%of participants.[30]After adjustment for traditional risk factors and hemoglobin A1c,detectable hs-cTnT was associated with subquent total cardiovascular dia and cardiovascular dia-related deaths.[30]
4.2In patient s with HF傲慢与偏见下载
Among patients with chronic HF,the cTnT was detect-able in92.0%of the patients using the hs-cTnT assay(LoD ≥0.001ng/mL)compared to10.4%using the standard cTnT assay(LoD≥0.01ng/mL).[31]After a median follow-up of 24months,mortality was7.8%in the lowest quartile of hs-cTnT levels and35.6%in the highest quartile of hs-cTnT levels.The risk of death and hospitalization for HF in-cread significantly with an increa in the hs-cTnT level. Levels of hs-cTnT>median(0.012ng/mL)w
ere associated with more vere HF and wor outcomes.[31]Levels of hs-cTnT<the LoD using the standard cTnT assay retained prognostic value.[31]In patients with chronic HF recruited in multicenter clinical trials,the prevalence of elevated hs-cTnT(≥0.0135ng/mL)at baline was64.0%in GISSI-HF and47.1%in Val-HeFT.[32]Increas in the hs-cTnT levels over time were associated with age,DM, worning of renal function,and increas in N-terminal pro-brain natriuretic peptide(NT-proBNP)concentrations.[32] Changes in hs-cTnT concentrations were associated with all-cau mortality and worning HF.Serial measurement of hs-cTnT levels had robust prognostic value beyond that of a single measurement.[32]In patients with acute decom-pensated HF,a positive cTn test is associated with higher in-hospital mortality independent of other predictive vari-ables.[33]
4.3In patient s with acute pulmonary embolism
Acute pulmonary embolism(PE)is a relatively common cardiovascular emergency,but it can lead to acute life-threatening,and potentially reversible right ventricular fail-ure.An acute PE should be suspected in all patients who prent with new or worning dyspnea,chest pain,or sus-tained hypotension without an alternative obvious cau.[34] Early risk stratification of patients with acute PE is also important.In normo-tensive patients with confirmed PEs, the median value of hs-cTnT was0.0272ng/mL and64%of patients had a hs-cTnT level≥0.014ng/mL.[35]The baline hs-cTnT lev
els were higher in patients with adver30-day outcomes.A hs-cTnT cut-off value of0.014ng/mL showed excellent prognostic nsitivity and negative predictive value(both100%).[35]In comparison,as many as50%of patients with adver early outcome would have been mis-classified as low risk if a standard cTnT assay(cut-off0.03 ng/mL)was ud.Logistic regression indicated a two-fold increa in the risk of an adver outcome for each increa in hs-cTnT by one standard deviation of the natural loga-rithm.Patients with elevated hs-cTnT levels had a reduced probability of long term survival.[35]Lankeit et al.[36] showed that the hs-cTnT assay can improve risk stratifica-tion in patients with acute PEs.In526normo-tensive pa-tients with acute PEs,a hs-cTnT level>0.014ng/mL pre-dicted early death and a decread probability of6-month survival.[36]Like the simplified Pulmonary Embolism Se-verity Index(sPESI)score,the hs-cTnT predicts risk for short-term adver outcomes in normo-tensive patients with acute PEs.A hs-cTnT level of0.014ng/mL and a sPESI score of one had similar nsitivity(94%vs.87%),specific-ity(40%vs.42%),and an AUC(0.67vs.0.73)in predicting 30-day adver outcomes.[37]
4.4In patient s with pulmonar y arterial hypertension
Right ventricular failure is a leading cau of death in pa-tients with pulmonary arterial hypertension(PAH).In PAH patients with a mean pulmonary artery pressure of45±18 mmHg,the level
s of cTnT were detectable in90.9%of the participants using the hs-cTnT assay compared to30.9% using the standard assay.[38]Concentrations>the99th per-decent是什么意思
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centile were obrved in27.3%of the participants using the hs-cTnT assay compared to10.9%using the standard as-say.[38]The levels of hs-cTnT were related to systolic right ventricular dysfunction and an impaired6-min walk dis-tance,and predicted death at least as effectively as heart-type fatty-acid-binding protein(hFABP)or NT-proBNP. Moreover,the levels of hs-cTnT above predicted the World Health Organization functional II class better than NT-proBNP or hFABP.[38]
4.5In the general population
In community-dwelling adults>65years of age without prior HF,a cTnT level was detectable(≥0.003ng/mL)by hs-cTnT in the majority of participants(66.2%).[39]In this cohort of older adults without known HF,the baline hs-cTnT levels and the changes in hs-cTnT levels were sig-nificantly associated with a risk of new-ont HF and car-diovascular death.[39]For participants with the highest hs-cTnT concentrations(>0.0129ng/mL),there was an incidence of6.4per100person-years for HF(aHR,2.48; 95%CI,2.04–3.00)and4.8per100person-years for car-diovascular death(aHR,
2.91;95%CI,2.37–3.58)com-pared to participants with undetectable hs-cTnT levels(in-cidence,1.6per100person-years for HF and1.1per100 person-years for cardiovascular death).[39]For individuals with an initially detectable hs-cTnT,a subquent increa of>50%was associated with a greater risk for HF(aHR, 1.61;95%CI,1.32–1.97)and cardiovascular death(aHR, 1.65;95%CI,1.35–2.03)and a decrea of>50%was as-sociated with a lower risk for HF(aHR,0.73;95%CI, 0.54–0.97)and cardiovascular death(aHR,0.71;95%CI, 0.52–0.97)compared to participants with a<50% change.[39]
In the general population aged30–65years,the hs-cTnT levels were associated with structural heart dia and subquent risk for all-cau mortality.[40]The prevalence of detectable cTnT(≥0.003ng/mL)was25.0%using the hs-cTnT assay compared to0.7%using the standard assay.[40]The prevalence of left ventricular hypertrophy incread from7.5%in the lowest hs-cTnT category(< 0.003ng/mL)to48.1%in the highest hs-cTnT category(≥0.014ng/mL);the prevalence of left ventricular systolic dysfunction and chronic kidney dia(CKD)also in-cread across categories.[40]During a median follow-up of 6.4years,all-cau mortality incread from1.9%to28.4% across higher hs-cTnT categories.[40]After adjustment for traditional risk factors,C-reactive protein level,CKD,and NT-proBNP level,the hs-cTnT category remained indepen-dently associated with all-cau mortality.[40]
In the general population aged54–74years of age free from CAD and stroke at baline,the hs-cTnT levels(≥0.003ng/mL)were detected in66.5%of the participants.[41] The prevalence of detectable hs-cTnT in this population was similar to another study(66.2%),including participants>65 years of age without prior HF.[39]At the10-year follow-up in fully adjusted models,compared to participants with un-detectable levels of hs-cTnT(<0.003ng/mL),tho par-ticipants with hs-cTnT levels in the highest category(≥0.014ng/mL)had a significantly incread risk for CAD (HR,2.29;95%CI,1.81–2.89),fatal CAD(HR,7.59;95% CI, 3.78–5.25),total mortality(HR, 3.96;95%CI,
3.21–绝望主妇第三季
4.88),and new-ont HF(HR,
5.95;95%CI,
4.47–7.92).Even a minimally elevated hs-cTnT level(≥0.003ng/mL)was associated with an incread risk for mortality and new-ont HF.For patients with stable CAD and individuals free from CAD and stroke at baline,the hs-cTnT levels has stronger prognostic value for new-ont HF and total mortality,with the exception of MI.[28,]41
5The mechanism of hs-cTnT elevation in patients not having an AMI
Despite the nearly absolute specificity of cTn for myo-cardial tissue,the greater nsitivity of the cTnT assay was confusing.[42]For the standard cTnT assay,the prevalence of detectable cTnT(≥0.01ng/mL)is rare(0.7%)in the general population.[43]For the hs-cTnT assay,in the general popula-tion54–74years of age free from CAD,stroke and HF at baline,a hs-cTnT concentrations>0.014ng/mL was de-tected in7.4%of individuals.[41]A similar prevalence was reported in another study.[39]In adults>65years of age without prior HF,a hs-cTnT concentrations>12.94ng/L was detected in16.6%of individuals.[39]
In patients with stable CAD,a stronger correlation ex-isted between the hs-TnT level and the total non-calcified plaque burden(r=0.79).[44]Moreover,patients with re-modeled non-calcified plaque had even higher hs-TnT val-ues than all other groups,suggesting that the chronic,clini-cally silent rupture of non-calcified plaque with subquent microembolisation may be a potential source of hs-cTnT elevation.[44]
变化无常英语In patients with HF,the prevalence of detectable troponin is high.Using the hs-TnT assay(LoD<0.001ng/mL,92% of patients had a detectable value.[31]In addition to CAD, others mechanisms of cardiomyocyte damage could contri-bute to the cTn relea in patients with HF,such as inflam-matory cytokines,oxidative stress,hibernating myocardium, and apoptosis.[45,]46In patient
s with end-stage renal dia (ESRD),the prevalence of elevated hs-cTnT concentrations is100%,and the elevated hs-cTnT concentrations are highly
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