Prognostic implications of changes in cardiac troponin I levels in patients with non-ST elevation acute coronary syndrome

Abstract

Objective: Information is limited on the prognostic implications of cardiac troponin I (cTnI) changes during the first days of non-ST elevation acute coronary syndrome (NSTE-ACS).

Methods: High-sensitivity cTnI levels were measured at study inclusion and after 48?h in 1615 conservatively managed NSTE-ACS patients from the Global Use of Strategies To Open Occluded Coronary Arteries (GUSTO) IV trial.

Results: Patients with moderately increased cTnI levels and without a relevant decrease over time had a significantly raised mortality at 30 days and 1 year. No relevant associations between cTnI changes and recurrent myocardial infarction were seen.

Conclusion: The cTnI change is predictive for subsequent mortality in selected conservatively managed NSTE-ACS patients.     

The aetiology of myocardial injury after non-cardiac surgery

Recognition of myocardial injury after non-cardiac surgery is difficult, since strong analgesics (e.g. opioids) can mask anginal symptoms, and ECG abnormalities are subtle or transient. Thorough knowledge of the pathophysiological mechanisms is therefore essential. These mechanisms can be subdivided into four groups: type I myocardial infraction (MI), type II MI, non-ischaemic cardiac pathology, and non-cardiac pathology. The incidence of type I MI in patients with a clinical suspicion of perioperative acute coronary syndrome (ACS) is 45–57 %. This percentage is higher in patients with a high likelihood of MI such as patients with ST-elevation ACS. Of note, the generalisability of this statement is limited due to significant study limitations. Non-ischaemic cardiac pathology and non-cardiac pathology should not be overlooked as a cause of perioperative myocardial injury (PMI). Especially pulmonary embolism and dysrhythmias are a common phenomenon, and may convey important prognostic value. Implementation of routine postoperative troponin assessment and accessible use of minimally invasive imaging should be considered to provide adequate individualised therapy. Also, addition of preoperative imaging may improve the stratification of high-risk patients who may benefit from preoperative or perioperative interventions.     

Conventional and novel diagnostic biomarkers of acute myocardial infarction: a promising role for circulating microRNAs

Abstract

Biomarkers play a critical role in the diagnosis of acute myocardial infarction (AMI), especially in patients with atypical clinical and/or electrocardiographic presentation or co-morbidities, like the elderly. High-sensitivity assays based on specific biomarkers (e.g. cardiac troponins) enabling earlier AMI diagnosis have recently become available in clinical practice. Although no single biomarker of myocardial necrosis is ever likely to afford AMI diagnosis, a combination including different biomarkers for necrosis and ischemia, like new circulating molecules (microRNAs), could enhance diagnostic specificity. We review the recent literature on conventional and novel AMI biomarkers, with special emphasis on circulating microRNAs.     

Diagnostic re-classification and prognostic risk stratification of patients with acute chest pain

Unstable angina and myocardial infarction are prevalent manifestations of acute coronary artery disease, combined in the term ‘acute coronary syndromes’. The introduction of sensitive markers for myocardial necrosis has led to confusion regarding the distinction between small myocardial infarctions and ‘true’ unstable angina, and the application of ever more sensitive markers has accelerated the pace at which patients with unstable angina are being re-classified to non-ST-segment elevation myocardial infarction. But in how many patients with acute chest pain is myocardial ischaemia really the cause of their symptoms? Numerous studies have shown that most have <5 ng/l high-sensitivity cardiac troponin, and that their prognosis is excellent (event rate <0.5% per year), incompatible with ‘impending infarction’. This marginalisation of patients with unstable angina pectoris should lead to the demise of this diagnosis. Without unstable angina, the usefulness of the term acute coronary syndromes may be questioned next. It is better to abandon the term altogether and revert to the original diagnosis of thrombus-related acute coronary artery disease, myocardial infarction. A national register should be the next logical step to monitor and guide the application of effective therapeutic measures and clinical outcomes in patients with myocardial infarction.

     

High sensitivity cardiac troponin T in patients not having an acute coronary syndrome: results from the TRAPID-AMI study

Purpose: To describe the baseline, 1?hr and delta high sensitivity cardiac troponin (hs-cTnT) values in patients with suspected acute myocardial infarction (AMI) but without a final acute coronary syndrome (ACS) diagnosis.

Materials and methods: hs-cTnT assay for RAPID rule out of acute myocardial infarction (TRAPID-AMI) was a prospective diagnostic trial that enrolled emergency department (ED) patients with suspected AMI. Final patient diagnoses were adjudicated by a clinical events committee and subjects placed in different clinical groups: AMI, unstable angina, non-ACS cardiac, non-cardiac and unknown origin. The baseline, 1?hr and delta hs-cTnT values were analysed in the 902 non-ACS patients.

Results: Amongst the 1282 studied the patient groups were 213 (17%) AMI, 167 (13%) unstable angina, 113 (9%) non-ACS cardiac, 288 (22%) non-cardiac and 501 (39%) unknown origin. The hs-cTnT values in the non-cardiac and unknown origin groups were combined. The median hs-cTnT values (ng/L) were higher (p?<?0.001) in the non-ACS cardiac compared to the non-cardiac/unknown origin group at baseline (11.8,?<5) and 1?hr (12.3,?<5). Their negative predictive values were 0.955 (baseline) and 0.954 (1?hr) for predicting non-ACS cardiac versus non-cardiac/unknown origin diagnoses.

Conclusions: Hs-cTnT may help predict whether non-ACS ED patients have a final non-ACS cardiac or non-cardiac/unknown origin diagnoses.     

Characteristics of a nickel–albumin binding assay for assessment of myocardial ischaemia

Background: The aim of this study was to describe a method to measure ischaemia-induced alterations of the binding capacity of serum albumin to exogenous nickel.

Methods: We measured the levels of cardiac troponin I (cTnI), serum albumin, ischaemia-modified albumin (IMA) measured by a cobalt–albumin binding assay (CABA), and a nickel–albumin binding assay (NABA) in the following groups: myocardial infarction (n?=?32) and non-ischaemic chest pain (n?=?64).

Results: IMA, cTnI and NABA levels were higher in the myocardial infarction group. NABA presented a higher ability to discriminate myocardial ischaemia than CABA.

Conclusions: Patients with myocardial infarction have reduced nickel binding to human serum albumin, and NABA may have an important role as an early marker of myocardial ischaemia.     

Oxidative stress in myocardial ischaemia reperfusion injury: a renewed focus on a long-standing area of heart research

Advances in the treatment of coronary artery disease have seen a significant drop in mortality and morbidity particularly amongst patients with acute myocardial infarction (MI). In particular, percutaneous trans-luminal balloon angioplasty (PTCA) with stenting to re-open atherosclerotic coronary arteries has yielded marked improvement in clinical outcome for patients with acute MI. Furthermore, with the advent of drug-eluting stents occurrence rates for coronary artery restenosis, one common clinical problem associated with angioplasty and stent deployment, have declined markedly. However, coronary restenosis in diabetic patients remains an on-going problem. The success of drug-eluting stents has seen a renewed focus on myocardial ischaemia reperfusion (IR) injury as this represents one area of research where many questions remain unanswered. In particular, the relationship between myocardial IR injury and decreased myocardial micro-vasculature re-flow post PTCA (that ultimately leads to poor clinical outcome and myocardial damage/dysfunction) is one area of research with the potential to decrease current complication rates further in patients suffering myocardial IR injury sustained during MI. This review discusses the role for oxidative stress, oxidant source(s) and both gene regulation and stem-cell therapy as potential strategic targets in the ischaemic myocardium, with the ultimate aim of providing significant cardioprotection in the setting of acute MI.     

Plasma low-molecular-weight thiol/disulphide homeostasis as an early indicator of global and focal cerebral ischaemia

Objective: Recent studies have shown that cerebral ischaemia causes not only local, but also systemic oxidative stress. This leads to oxidation of thiol-containing compounds, including low-molecular-weight thiols (cysteine, glutathione, homocysteine and others). Therefore, the aim of this work was to verify the hypothesis that the thiol/disulphide homeostasis of low-molecular-weight thiols is disturbed in the early stages of cerebral ischaemia.

Methods: Two experimental rat models of ischaemia were used: a global model of vascular ischaemia (clamping the common carotid arteries?+?haemorrhage) and focal ischaemia (middle cerebral artery occlusion). The total levels of thiols and their reduced forms were measured before surgery and after 40 minutes of reperfusion (global) or 3?hours (focal) ischaemia.

Results: The global ischaemia model caused a marked (2.5–4 times, P?P?Discussion: These results suggest that plasma low-molecular-weight thiols are actively involved in oxidation reactions at early stages of cerebral ischaemia; therefore, their reduced forms or redox state may serve as a sensitive indicator of acute cerebrovascular insufficiency.     

CK-MBmass, hs-cTnT及CK-MB与急性心肌梗死的相关性及其联合诊断价值

摘要 目的：研究肌酸激酶同工酶质量（CK-MBmass)、肌酸激酶同工酶（CK-MB）和高敏心肌肌钙蛋白T（hs-cTnT）在急性心肌梗死患者（AMI）血清中的含量,并探讨三者联合对AMIDE诊断价值。方法：选择2018年1月到2021年10月我院收治的AMI患者90例作为研究组,并选择同期在我院体检健康志愿者40例作为对照组,比较两组AMI患者血清CK-MBmass,hs-cTnT和CK-MB。根据Killp分级法将不同心力衰竭将AMI患者分为II、III和IV级,并根据心肌梗死范围将AMI患者分为轻度、中度和重度心肌梗死组。比较不同AMI患者血清CK-MBmass,hs-cTnT和CK-MB。通过受试者工作曲线计算血清CK-MBmass,hs-cTnT和CK-MB联合诊断AMI的阳性预测值、阴性预测值、敏感度和特异度。结果：（1）AMI患者血清CK-MBmass,hs-cTnT和CK-MB均显著高于健康志愿者（P<0.05）;（2）AMI患者血清CK-MBmass,hs-cTnT和CK-MB随Killp分级或心肌梗死范围升高而升高（P<0.05）;（3）AMI患者血清CK-MBmass,hs-cTnT,CK-MB与急性心肌梗死患者左室射血分数（LVEF）呈负相关（P<0.05）,与左室舒张末期容积（LVEDd）和梗死范围呈正相关（P<0.05）;（4）血清CK-MBmass,hs-cTnT和CK-MB联合检测急性心肌梗死的阳性预测值、阴性预测值、敏感度和特异度均高于单独诊断。结论：血清CK-MBmass,hs-cTnT和CK-MB在AMI患者含量升高,并且与患者心功能和心肌梗死范围有关,适用于AMI的联合诊断。     

Acute hyperglycaemia enhances oxidative stress and aggravates myocardial ischaemia/reperfusion injury: role of thioredoxin‐interacting protein

Hyperglycaemia during acute myocardial infarction is common and associated with increased mortality. Thioredoxin‐interacting protein (Txnip) is a modulator of cellular redox state and contributes to cell apoptosis. This study aimed to investigate whether or not hyperglycaemia enhances Txnip expression in myocardial ischaemia/reperfusion (MI/R) and consequently exacerbates MI/R injury. Rats were subjected to 30 min. of left coronary artery ligation followed by 4 hrs of reperfusion and treated with saline or high glucose (HG, 500 g/l, 4 ml/kg/h intravenously). In vitro study was performed on cultured rat cardiomyocytes subjected to simulated ischaemia/reperfusion (SI/R) and incubated with HG (25 mM) or normal glucose (5.6 mM) medium. In vivo HG infusion during MI/R significantly impaired cardiac function, aggravated myocardial injury and increased cardiac oxidative stress. Meanwhile, Txnip expression was enhanced whereas thioredoxin activity was inhibited following HG treatment in ischaemia/reperfusion (I/R) hearts. In addition, HG activated p38 MAPK and inhibited Akt in I/R hearts. In cultured cardiomyocytes subjected to SI/R, HG incubation stimulated Txnip expression and reduced thioredoxin activity. Overexpression of Txnip enhanced HG‐induced superoxide generation and aggravated cardiomyocyte apoptosis, whereas Txnip RNAi significantly blunted the deleterious effects of HG. Moreover, inhibition of p38 MAPK or activation of Akt markedly blocked HG‐induced Txnip expression in I/R cardiomyocytes. Most importantly, intramyocardial injection of Txnip siRNA markedly decreased Txnip expression and alleviated MI/R injury in HG‐treated rats. Hyperglycaemia enhances myocardial Txnip expression, possibly through reciprocally modulating p38 MAPK and Akt activation, leading to aggravated oxidative stress and subsequently, amplification of cardiac injury following MI/R.     

Thioredoxin-1 is required for the cardioprotecive effect of sildenafil against ischaemia/reperfusion injury and mitochondrial dysfunction in mice

Abstract

Sildenafil is a phosphodiesterase type 5 inhibitor which confers cardioprotection against myocardial ischaemia/reperfusion (I/R) injury. The aim of this study was to determine if Trx1 participates in cardioprotection exerted by sildenafil in an acute model of I/R, and to evaluate mitochondrial bioenergetics and cellular redox status. Langendorff-perfused hearts from wild type (WT) mice and a dominant negative (DN-Trx1) mutant of Trx1 were assigned to placebo or sildenafil (0.7?mg/kg i.p.) and subjected to 30?min of ischaemia followed by 120?min of reperfusion. WT?+?S showed a significant reduction of infarct size (51.2?±?3.0% vs. 30?±?3.0%, p < .001), an effect not observed in DN-Trx. After I/R, sildenafil preserved state 3 oxygen consumption from WT, but had a milder effect in DN-Trx1 only partially protecting state 3 values. Treatment restored respiratory control (RC) after I/R, which resulted 8% (WT) and 24% (DN-Trx1) lower than in basal conditions. After I/R, a significant increase in H₂O₂ production was observed both for WT and DN-Trx (WT: 1.17?±?0.13?nmol/mg protein and DN-Trx: 1.38?±?0.12?nmol/min mg protein). With sildenafil, values were 21% lower only in WT I/R. Treatment decreased GSSG levels both in WT and DN-Trx1. In addition, GSSG/GSH² ratio was partially restored by sildenafil. Also, an increase in p-eNOS/eNOS even before the myocardial ischaemia was observed with sildenafil, both in WT (14%, p > .05) and in DN-Trx (35%, p < .05). Active Trx1 is required for the onset of the cardioprotective effects of sildenafil on I/R injury, together with the preservation of cellular redox balance and mitochondrial function.     

Glycogen phosphorylase isoenzyme BB in diagnosis of myocardial ischaemic injury and infarction

This review deals with glycogen phosphorylase (GP) and its isoenzyme BB in the diagnosis of ischaemic myocardial injury. Early identification and confirmation of acute myocardial infarction is essential for correct patient care and disposition decision in the emergency department. In this respect, glycogen phosphorylase isoenzyme BB (GPBB) based on its metabolic function is an enzyme for early laboratory detection of ischaemia. In the aerobic heart muscle GPBB together with glycogen is tightly associated with the vesicles of the sarcoplasmic reticulum. Release of GPBB, the main isoform in the human myocardium, essentially depends on the degradation of glycogen, which is catalyzed by GP. Ischaemia is known to favour the conversion of bound GP in the b form into GP a, thereby accelerating glycogen breakdown, which is the ultimate prerequisite for getting GP into a soluble form being able to move freely in the cytosol. The efflux of GPBB into the extracellular fluid follows if ischaemia-induced structural alterations in the cell membrane become manifest. The clinical application of GPBB as a marker of ischaemic myocardial injury is a very promising tool for extending our knowledge of the severity of myocardial ischaemic events in the various coronary syndromes. The rational roots of this development were originated from Albert Wollenberger's research work on the biochemistry of cardiac ischaemia and the transient acceleration of glycogenolysis mainly brought about by GP activation.     

Unbound free fatty acid concentrations are increased in cardiac ischemia

Monitoring increased plasma unbound free fatty acid (FFA_u) concentrations has been proposed as a biomarker for myocardial ischemia. In the current study, 30 acute coronary syndrome (ACS) patients presenting in the emergency department, with chest pain within 12 h of onset, were clinically evaluated along with serial cardiac troponin I (cTnI) and FFA_u measurements. Increased FFA_u were found in 28 of 30 (93%) of ACS patients, ranging from 2.0 to 430 nM. For the nine ACS patients with myocardial infarction (MI), FFA_u levels were increased at presentation for all (100%). In contrast, cTnI was increased in only 9 of 30 (30%) patients, mean 0.7 μg/L, and in only 2 of 9 (22%) MI patients, mean 1.3 μg/L. During the 24 h following admission, cTnI increased in all 9 MI patients. FFA_u concentrations increased in every sample in which cTnI increased. Our findings suggest that FFA_u is increased in ischemia regardless of the presence or absence of myocardial necrosis, as reflected by increased or normal cTnI, respectively.     

Spontaneous and granulocyte–colony-stimulating factor-enhanced marrow response and progenitor cell mobilization in mice after myocardial infarction

Background aimsHematopoietic (HPC), mesenchymal (MPC) and/or endothelial (EPC) progenitor cells are being studied to repair the myocardium after acute or chronic ischemia. We examined marrow response to myocardial infarction (MI) and the ability of granulocyte–colony-stimulating factor (G-CSF) to enhance mobilization of HPC, MPC and EPC in peripheral blood (PB) and bone marrow (BM) of MI mice.MethodsWe induced MI in C57Bl/6 mice, while sham-operated (SO) animals were similarly operated on but without coronary artery ligation. Animals were treated with either saline or G-CSF, from day ?5 to day +5 after MI or from day 0 to day +5. Progenitor cell numbers in PB and BM were evaluated by fluorescence-activated cell sorting (FACS) analysis and cell culture.ResultsWhite blood cells (WBC) decreased in BM and increased in PB after MI; G-CSF amplified this effect in BM but not in PB. HPC numbers decreased in BM after MI, while HPC and granulocyte–macrophage colony-forming units (GM-CFU) increased in PB only after G-CSF treatment, and more prominently so in MI than in SO mice. MPC and fibroblast–colony-forming units (F-CFU) as well as EPC were mobilized into the PB after MI and further after G-CSF treatment. Plasma troponin T concentrations decreased after G-CSF treatment.ConclusionsBM is globally affected by acute MI, but not simple body injury, with intense mobilization of marrow MPC and EPC into the PB but inhibition of HPC. Progenitor cell entry into the PB may be paralleled by depletion of their BM pools. G-CSF is required for HPC mobilization and enhances MPC and EPC entry into the PB.     

Soluble fms-like tyrosine kinase-1 (sFLT-1) predicts post-percutaneous coronary intervention (PCI) myocardial infarction (MI type 4a)

Context: Acute myocardial infarction (AMI) related to percutaneous coronary intervention (PCI) (MI type 4a) occurs in up to 26% of elective patients.

Objective: To evaluate if sFLT-1 helps to predict MI type 4a in troponin negative patients with elective PCI.

Materials and methods: We enrolled 135 patients, 106 had a PCI. sFLT-1 levels were assessed at five time points before and after PCI.

Results: MI type 4a occurred in 22.1% of patients. sFLT-1 levels at admission above 251 pg/mL indicated a significant relative risk for MI type 4a of 2.83.

Conclusion and discussion: Increased sFLT-1 levels at baseline might indicate unstable atherosclerosis and risk for microembolization and thus be predictive of MI type 4a.     

Mammalian target of rapamycin inhibition attenuates myocardial ischaemia–reperfusion injury in hypertrophic heart

Pathological cardiac hypertrophy aggravated myocardial infarction and is causally related to autophagy dysfunction and increased oxidative stress. Rapamycin is an inhibitor of serine/threonine kinase mammalian target of rapamycin (mTOR) involved in the regulation of autophagy as well as oxidative/nitrative stress. Here, we demonstrated that rapamycin ameliorates myocardial ischaemia reperfusion injury by rescuing the defective cytoprotective mechanisms in hypertrophic heart. Our results showed that chronic rapamycin treatment markedly reduced the phosphorylated mTOR and ribosomal protein S6 expression, but not Akt in both normal and aortic‐banded mice. Moreover, chronic rapamycin treatment significantly mitigated TAC‐induced autophagy dysfunction demonstrated by prompted Beclin‐1 activation, elevated LC3‐II/LC3‐I ratio and increased autophagosome abundance. Most importantly, we found that MI/R‐induced myocardial injury was markedly reduced by rapamycin treatment manifested by the inhibition of myocardial apoptosis, the reduction of myocardial infarct size and the improvement of cardiac function in hypertrophic heart. Mechanically, rapamycin reduced the MI/R‐induced iNOS/gp91^phox protein expression and decreased the generation of NO and superoxide, as well as the cytotoxic peroxynitrite. Moreover, rapamycin significantly mitigated MI/R‐induced endoplasmic reticulum stress and mitochondrial impairment demonstrated by reduced Caspase‐12 activity, inhibited CHOP activation, decreased cytoplasmic Cyto‐C release and preserved intact mitochondria. In addition, inhibition of mTOR also enhanced the phosphorylated ERK and eNOS, and inactivated GSK3β, a pivotal downstream target of Akt and ERK signallings. Taken together, these results suggest that mTOR signalling protects against MI/R injury through autophagy induction and ERK‐mediated antioxidative and anti‐nitrative stress in mice with hypertrophic myocardium.     

Acute Myocardial Infarction Attributable to Adrenergic Crises in a Patient with Pheochromocytoma and Neurofibromatosis 1

ObjectiveTo describe a rare case of acute myocardial infarction in a patient with neurofibromatosis 1 and pheochromocytoma and to review the literature on the coexistence of these 2 diseases, the causes of myocardial injury in patients with pheochromocytoma, and the utility of genetic testing and pheochromocytoma screening for those patients and their families.MethodsWe present a case report, including the detailed clinical, laboratory, and radiographic data, results of adrenal mass pathology, and results of coronary angiography. We also survey other relevant reports available in the literature.ResultsA 43-year-old woman with a history of longstanding hypertension, neurofibromatosis 1, headaches, sweating, and palpitations presented to the hospital with chest pain and shortness of breath. She was found to have an acute myocardial infarction and pulmonary edema, as well as a right adrenal mass. A pheochromocytoma was suspected, and phenoxybenzamine was added to her treatment regimen. Cardiac catheterization showed nonobstructive coronary disease. The levels of plasma catecholamine metabolites were extremely high. The patient underwent uncomplicated laparoscopic right adrenalectomy 2 weeks after this admission. Surgical pathology confirmed the diagnosis of pheochromocytoma.ConclusionAdrenergic crisis attributable to pheochromocytoma can result in acute myocardial infarction even in the absence of obstructive coronary disease. Inclusion of pheochromocytoma in the differential diagnosis of hypertension in patients with neurofibromatosis is very important and helps avoid mistakes in the management of such patients. (Endocr Pract. 2007;13:269-273)     

Implications of troponin testing in clinical medicine

During the past decade considerable research has been conducted into the use of cardiac troponins, their diagnostic capability and their potential to allow risk stratification in patients with acute chest pain. Determination of risk in patients with suspected myocardial ischaemia is known to be as important as retrospective confirmation of a diagnosis of myocardial infarction (MI). Therefore, creatine kinase (CK)-MB - the former 'gold standard' in detecting myocardial necrosis - has been supplanted by new, more accurate biomarkers.Measurement of cardiac troponin levels constitute a substantial determinant in assessment of ischaemic heart disease, the presentations of which range from silent ischaemia to acute MI. Under these conditions, troponin release is regarded as surrogate marker of thrombus formation and peripheral embolization, and therefore new therapeutic strategies are focusing on potent antithrombotic regimens to improve long-term outcomes. Although elevated troponin levels are highly sensitive and specific indicators of myocardial damage, they are not always reflective of acute ischaemic coronary artery disease; other processes have been identified that cause elevations in these biomarkers. However, because prognosis appears to be related to the presence of troponins regardless of the mechanism of myocardial damage, clinicians increasingly rely on troponin assays when formulating individual therapeutic plans.     

急性心肌梗死患者血浆BNP、NT-proBNP、MYO及cTnI水平的表达及临床意义

目的:探讨急性心肌梗死患者血浆B型利钠肽(BNP)、N-末端B型利钠肽原(NT-proBNP)、肌红蛋白(MYO)及心肌肌钙蛋白I(cTnI)的表达及临床意义。方法:选择2015年8月至2016年8月我院收治的162例急性心肌梗死患者记为观察组,另选择162例同期于我院健康体检志愿者为对照组进行对比研究。应用免疫分离法检测两组血浆BNP、NT-proBNP、MYO及cTnI水平。对比两组血浆BNP、NT-proBNP、MYO及cTnI的表达水平,以及BNP、NT-proBNP、MYO、cTnI单独检测和联合检测在急性心肌梗死诊断中的灵敏度及特异性,并分析各指标之间的相关性。结果:观察组血浆BNP、NT-proBNP、MYO及cTnI水平均高于对照组,差异有统计学意义(P0.05)。四项联合检测的灵敏度分别高于血浆BNP、NT-proBNP、MYO及cTnI单独检测,特异性分别高于血浆NT-proBNP、MYO单独检测,差异有统计学意义(P0.05),四项联合检测的特异性分别高于血浆BNP、cTnI单独检测,但差异无统计学意义(P0.05)。通过Spearman相关性分析显示,观察组血浆BNP、NT-proBNP、MYO及cTnI各指标水平之间呈正相关(P0.05)。结论:血浆BNP、NT-proBNP、MYO及cTnI在急性心肌梗死中具有明显高表达,且四项联合检测的灵敏度及特异性较高,各指标之间存在正相关关系,可为急性心肌梗死早期诊断提供科学的依据,值得临床推广。