Levosimendan in septic shock in patients with biochemical evidence of cardiac dysfunction: a subgroup analysis of the LeoPARDS randomised trial

Myocardial dysfunction is common in sepsis but optimal treatment strategies are unclear. The inodilator, levosimendan was suggested as a possible therapy; however, the levosimendan to prevent acute organ dysfunction in Sepsis (LeoPARDS) trial found it to have no benefit in reducing organ dysfunction in septic shock. In this study we evaluated the effects of levosimendan in patients with and without biochemical cardiac dysfunction and examined its non-inotropic effects. Two cardiac biomarkers, troponin I (cTnI) and N-terminal prohormone of brain natriuretic peptide (NT-proBNP), and five inflammatory mediators were measured in plasma from patients recruited to the LeoPARDS trial at baseline and over the first 6 days. Mean total Sequential Organ Failure Assessment (SOFA) score and 28-day mortality were compared between patients with normal and raised cTnI and NT-proBNP values, and between patients above and below median values. Levosimendan produced no benefit in SOFA score or 28-day mortality in patients with cardiac dysfunction. There was a statistically significant treatment by subgroup interaction (p = 0.04) in patients with NT-proBNP above or below the median value. Those with NT-proBNP values above the median receiving levosimendan had higher SOFA scores than those receiving placebo (mean daily total SOFA score 7.64 (4.41) vs 6.09 (3.88), mean difference 1.55, 95% CI 0.43–2.68). Levosimendan had no effect on the rate of decline of inflammatory biomarkers. Adding levosimendan to standard care in septic shock was not associated with less severe organ dysfunction nor lower mortality in patients with biochemical evidence of cardiac dysfunction.     

Multi-biomarker risk stratification of N-terminal pro-B-type natriuretic peptide, high-sensitivity C-reactive protein, and cardiac troponin T and I in end-stage renal disease for all-cause death

BACKGROUND: In patients with end-stage renal disease (ESRD), the ability of single and multiple biomarker monitoring to predict adverse outcomes has not been well established. This study determined the prognostic value of multiple biomarkers for all-cause death over 2 years in 399 ESRD patients. METHODS: The risk of all-cause death was determined by use of multiple biomarkers based on concentrations for a reference population (normal) and cutoffs based on tertile distributions in the ESRD group. Biomarkers studied included N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity C-reactive protein (hsCRP; Dade Behring and Roche assays), and cardiac troponin T (cTnT; Roche) and I (cTnI; Dade Behring and Beckman Coulter assays). Relative risks of death were estimated and survival curves computed. RESULTS: A total of 101 deaths occurred during 594 patient-years of follow-up. Increased NT-proBNP concentrations were not predictive of death on the basis of the normal cutoffs. However, tertile analysis of NT-proBNP was significantly predictive of death and had a ROC area under the curve equivalent to or better than any of the other biomarkers. Biomarkers independently predictive of survival were hsCRP (P <0.001, either assay), cTnT (P <0.05), and cTnI (Dade, P <0.05). Two-year mortality rates were 6% (n = 45) with normal hsCRP, cTnI, and cTnT concentrations; 19% (n = 173) with increased hsCRP or cTnT and normal cTnI; 44% (n = 160) with both hsCRP and cTnT increased and normal cTnI; 61% (n = 21) with increased cTnI (Dade) or 47% (n = 74) with increased cTnI (Beckman) regardless of hsCRP or cTnT concentrations. Defined by the normal cutoffs, increased concentrations of biomarkers were present in various proportions of the 399 patients with ESRD: NT-proBNP, 99%; hsCRP, 46% (both Roche and Dade assays); cTnT, 85%; cTnI, 19% (Beckman assay) and 5% (Dade assay). CONCLUSIONS: Although mechanisms likely vary for causation, increased plasma hsCRP, cTnT, and cTnI above the cutoffs for our reference (normal) population were all independently predictive of subsequent death in ESRD patients. Tertile analysis for NT-proBNP also demonstrated prognostic value.     

Usefulness of myocardial performance index and biochemical markers for early detection of anthracycline-induced cardiotoxicity in adults

BACKGROUND: Anthracycline therapy is limited by cardiotoxicity. Currently no diagnostic parameter is available allowing ubiquitous and reliable detection of preclinical anthracycline cardiomyopathy and prediction of prognosis. PATIENTS AND METHODS: In 100 consecutive patients receiving anthracycline-based chemotherapy serial measurements of left ventricular systolic and diastolic function, Tei index (a Doppler echocardiographic parameter of global ventricular function), cardiac troponin T (cTnT) and NT-probrain natriuretic peptides (BNP) at baseline and during 1-year follow-up were performed. RESULTS: Mean ejection fraction (LVEF) significantly decreased immediately after completion of anthracycline therapy (mean dose 226.1 +/- 8.3 mg/m(2)) und further declined during follow-up (65.9 +/- 0.6% Vs. 61.6 +/- 0.7%; P < 0.001), while mean E/A ratio decreased after 6 months (P = 0.05). No patient presented with cardiac symptoms. The Tei index increased after therapy in the majority of patients (78.8%) compared with pre-therapy values indicating myocardial alteration in more patients than previously recognized. cTnT levels did not exceed the upper limit of the normal range in any patient. Seven patients had low-level elevations of cTnT. Only one of these patients developed a concomitant decrease in LVEF. Mean N-terminal-pro-BNP (NT-proBNP) levels did not significantly change after anthracycline administration. However, in 13 patients (15.3%) a marked, transient increase of NT-proBNP was obtained after the first anthracycline cycle without cardiac dysfunction presumably due to altered cardiac loading conditions during chemotherapy. CONCLUSION: Low to moderate doses of anthracyclines resulted in subclinical myocardial alteration in more patients than so far noticed. Clinical implications of increased Tei index remain to be determined in long-term. Our results do not support that assessment of cTnT or BNP levels may safely replace serial echocardiographic evaluation of systolic and diastolic function for the monitoring of anthracycline cardiotoxicity.     

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction

BACKGROUND: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). METHODS: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36 h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI) > 125 g/m for males and > 110 g/m for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). RESULTS: Median cTnT was 0.012 (< 0.010-0.032) microg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT >or= 0.010 micro/L. cTnT was positively correlated with CKMB (rho = 0.40, p = 0.04) and BNP (rho = 0.43, p = 0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (rho = -0.58, p = 0.007), and there was a positive correlation between cTnT and LVMI (rho = 0.44, p = 0.03). No other analyte was correlated to LVMI. CONCLUSIONS: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.     

Cardiac troponins and renal function in nondialysis patients with chronic kidney disease

BACKGROUND: Serum cardiac troponin concentrations are commonly increased in end-stage renal disease (ESRD) in the absence of an acute coronary syndrome (ACS). The data on cardiac troponin I (cTnI) are more variable than those for cardiac troponin T (cTnT). There is little information on cardiac troponin concentrations in patients with chronic kidney disease (CKD) who have not commenced dialysis. METHODS: We studied 222 patients: 56 had stage 3 (moderate CKD); 70 stage 4 (severe CKD); and 96 stage 5 (kidney failure). Patients underwent echocardiography and were followed prospectively for a median of 19 months; all-cause mortality was recorded. RESULTS: Overall, serum cTnT was increased above the 99th percentile reference limit in 43% of all CKD patients studied, compared with 18% for cTnI. Serum cTnT and cTnI concentrations were more commonly increased in the presence of more severe CKD (11 and 6 patients in stage 3, 27 and 8 in stage 4, and 57 and 24 in stage 5 (P < 0.0001 and <0.02, respectively). Among 38 patients with detectable cTnI, 32 had detectable cTnT (r(s) = 0.67; P < 0.0001). There was evidence that decreasing estimated glomerular filtration rate increased the odds of having detectable cTnT (P < 0.001) but not cTnI (P = 0.128). There was no evidence to support an adjusted association of detectable cardiac troponins with increasing left ventricular mass index. Increased cTnT (P = 0.0097), but not cTnI, was associated with decreased survival. CONCLUSIONS: Increased cTnT and cTnI concentrations are relatively common in predialysis CKD patients, in the absence of an ACS, including among those with stage 3 disease. The presence of left ventricular hypertrophy alone does not explain these data. Detectable cTnT was a marker of decreased survival.     

Serum cardiac troponin T in patients hospitalized with heart failure is associated with left ventricular hypertrophy and systolic dysfunction

Background: Cardiac troponin T (cTnT) is a highly sensitive and specific marker of acute myocardial infarction. Serum cTnT is also slightly elevated in patients with severe heart failure and is associated with left ventricular hypertrophy (LVH) in patients treated with haemodialysis. In this study serum cTnT concentrations and echocardiographic findings were investigated in heart failure patients without acute coronary syndrome. cTnT was also compared with other cardiac markers and plasma levels of brain natriuretic peptide (BNP). Methods: Twenty-six patients hospitalized with heart failure were included in the study. Echocardiographic measurements and blood sampling were carried out 12-36?h after admission. Serum cTnT (3rd generation assay), cardiac troponin I (cTnI), creatine kinase MB (CKMB) and CK were measured. Plasma BNP was analysed using the Shionoria assay. LVH was defined as left ventricular mass index (LVMI)&;gt;125?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for males and&;gt;110?g/m&;lt;formula&;gt;²&;lt;/formula&;gt; for females. Left ventricular systolic function was estimated from the mitral annulus motion (AV-mean LV). Results: Median cTnT was 0.012 (&;lt;0.010-0.032)?μg/L. Sixty-two percent of the patients (16 of 26) had elevated serum cTnT≥0.010?μg/L. cTnT was positively correlated with CKMB (ρ=0.40, p=0.04) and BNP (ρ=0.43, p=0.03), but not with cTnI and CK. A negative correlation was found between cTnT and AV-mean LV (ρ=?0.58, p=0.007), and there was a positive correlation between cTnT and LVMI (ρ=0.44, p=0.03). No other analyte was correlated to LVMI. Conclusions: Serum cTnT but not cTnI was associated with left ventricular dysfunction and LVH in patients hospitalized with heart failure. This explains why cTnT tends to be slightly elevated in patients with heart failure without symptoms of acute myocardial ischaemia.     

Is a pattern of increasing biomarker concentrations important for long-term risk stratification in acute coronary syndrome patients presenting early after the onset of symptoms?

BACKGROUND: Guidelines for treatment of acute coronary syndrome (ACS) recommend observing a rise or fall in cardiac troponin (cTn) concentrations for assessing acute injury. It is unknown whether a rising pattern presages a more adverse long-term prognosis than elevations that do not change. The present study assessed whether a rising pattern of cardiac biomarkers was more prognostic than simple elevations. METHODS: We measured N-terminal pro-brain natriuretic peptide (NT-proBNP) (Roche), cTnT (Roche) and cTnI (Beckman Coulter) in 212 ACS patients. These biomarkers were measured in coincident EDTA and heparin plasma samples available from at least 2 different time points, an early first specimen obtained a median of 2 hours after onset of symptoms, interquartile range (IQR) 2-4 hours, and a later second specimen obtained at 9 hours, IQR 9-9 hours. The cTn concentration in the second specimen was used to classify myocardial necrosis (cTnI >0.04 ug/L; cTnT >0.01 ug/L). Outcomes [death, myocardial infarction (MI), heart failure (HF)] were obtained >8 years after the initial presentation. For patients with myocardial necrosis and a cTn concentration ratio (second/first measured concentrations) > or =1.00, the concentration ratios and the absolute concentrations in the second specimen were used to assess prognosis after 4 years. RESULTS: In myocardial necrosis, the relative change (cTn2/cTn1) was greater for cTnI than for cTnT (P <0.01), whereas the relative change in NT-proBNP was the same regardless of which troponin was used to classify necrosis (P = 0.71). The concentration ratio for cTnI, cTnT, and NT-proBNP was not useful for risk stratification (i.e., death/MI/HF; P > or =0.15). CONCLUSIONS: A rise in cardiac troponin or NT-proBNP concentration in ACS patients presenting early after onset of pain is not helpful for long-term prognosis.     

Maternal cardiac function in early pregnancies with high uterine artery resistance.

OBJECTIVE: To compare the maternal cardiac function and serum concentration of cardiac troponin T (cTnT) and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in first-trimester patients, according to uterine artery Doppler velocimetry (UADV). METHODS: This cross-sectional study included singleton pregnancies with normal UADV (n=17) and abnormal UADV (n=19). Maternal echocardiography was performed and blood samples were taken at 11-14 weeks. Echocardiographic parameters included: (a) left ventricular (LV) long axis velocities; (b) atrial size; (c) LV filling pressure; (d) the ratio of peak mitral flow velocity in early diastole and early mitral annular diastolic velocity (E/Ea ratio); and (e) the E/flow propagation velocity ratio. The maternal serum concentrations of cTnT and NT-proBNP were determined by sensitive and specific immunoassays. RESULTS: Patients with abnormal UADV had higher estimated left ventricular filling pressure (P=0.004), higher E/Ea ratio (P=0.03), higher E/flow propagation ratio (P=0.02), and lower LV long axis velocity (P=0.02) than those with normal UADV. There were no significant differences in the maternal serum concentration of cTnT or NT-proBNP. CONCLUSIONS: Patients with abnormal UADV in the first trimester have higher left ventricular filling pressure and may have left ventricular systolic dysfunction.     

Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock

BACKGROUND: Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock. METHODS: Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography. RESULTS: Increased plasma concentrations of cTnI (>/=0.4 microgram/L) and cTnT (>/=0.1 microgram/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001). CONCLUSIONS: These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.     

Improved assay of cardiac troponin I is more sensitive than other assays of necrosis markers

OBJECTIVE: Highly sensitive and specific assays of cardiac troponins I and T are the preferred biomarkers in diagnosing myocardial infarction (MI). Assays of cardiac troponin I (cTnI) have been improved with the addition of antibodies against the cTnI molecule and may have increased sensitivity. We hypothesized that a cTnI assay with modern antibody configuration will exhibit equal or better sensitivity in the setting of acute MI compared to cTnT and other markers of myocardial necrosis. MATERIAL AND METHODS: We investigated release kinetics of cTnI (Abbott ADV, Abbott Diagnostics), cTnT (Roche Diagnostics), CKMBmass, myoglobin and heart fatty acid binding protein (H-FABP) in 23 patients admitted with acute ST-segment elevation MI undergoing primary percutaneous coronary intervention. Calibrators for the Abbott ADV cTnI assay are traceable to the United States National Institute of Standards and Technology (NIST) reference material for cTnI. Eleven blood samples were drawn from each patient in the period from admission to 24 h. Biomarkers of necrosis showed marked increases in relative concentrations, especially within the first 2 h after admission. RESULTS: From 30 min after admission onwards, cTnI exhibited significantly higher relative concentrations compared to cTnT, CKMBmass, Myoglobin and H-FABP (p<0.05). CONCLUSIONS: The NIST standardized Abbott TnI ADV assay appears to be more sensitive than cTnT and other biomarkers in the early phase of MI.     

氨基末端脑利钠肽前体对无症状性心功能不全诊断价值的研究

【目的】探讨无症状性心功能不全患者氨基末端脑利钠肽前体（NT-proBNP）血浆浓度的变化规律,为早期诊断心功能不全提供依据。【方法】选择在本院住院无心功能不全症状的高危者120例作为研究对象,检测其NT—proBNP浓度,依据NT-proBNP水平将120例受试者分为NT—proBNP升高组（试验组）和NT-proBNP正常组（对照组）,并进行心脏彩色多普勒超声检查,测定其左室射血分数（LVEF）、舒张早期心室最大充盈速度／舒张晚期心室最大充盈速度（E／A）、左室舒张末期内径（LVEDD）、室间隔厚度（IVST）、左室后壁厚度（LVPWT）、左室短轴缩短分数（FS）,对两组样本各项心功能指标进行比较分析,并对NT—proB—NP水平和各项心功能指标进行相关性分析。【结果】试验组左室收缩功能和舒张功能各指标均较对照组差（P〈0．05）,提示存在心功能不全。【结论】无症状人群血浆NT—proBNP浓度升高提示心功能不全,NT—proBNP可作为心功能不全的早期诊断依据之一,其升高程度与心功能受损程度呈正相关。     

充血性心力衰竭患者血清肌钙蛋白T、肌钙蛋白Ⅰ检测及临床分析

目的研究充血性心力衰竭患者血清肌钙蛋白T(cTnT)和肌钙蛋白Ⅰ(cTnI)水平与心功能的关系及其对预后的判断。方法检测110例不同病因、不同心功能分级的充血性心力衰竭患者的cTnT、cTnI及左室射血分数(LVEF),并与40名健康对照组的结果进行比较。结果心功能Ⅱ级组cTnT为(78.56±25.65)pg/mL,cTnI为(0.85±0.57)ng/mL,LVEF值为57.46%±4.42%;心功能Ⅲ级分别为(249.25±76.21)pg/mL、(3.75±1.83)ng/mL、44.27%±10.13%;心功能Ⅳ级组分别为(375.62±81.29)pg/mL、(8.57±2.56)ng/mL、36.75%±5.66%,与健康对照组[分别为(3.65±0.96)pg/mL、(0.02±0.01)ng/mL、65.52%±8.01%]比较,差异有统计学意义(P<0.01),且心功能越差,cTnT、cTnI浓度越高;cTnT、cTnI与LVEF值均呈负相关,r分别为-0.487、-0.360,差异有统计学意义(P<0.01)。结论检测cTnT、cTnI对于判断充血性心力衰竭患者病情严重程度及预后具有重要的临床价值,是早期评估患者风险的重要方法。     

血清游离脂肪酸与急性心力衰竭患者心功能的相关性

目的探究血清游离脂肪酸(FFA)与急性心力衰竭(AHF)患者心功能的相关性。方法将163例AHF患者依左心室射血分数(LVEF)分为LVEF<40%组及LVEF≥50%组。检测患者入院时FFA、N末端前体脑利钠肽(NT-proBNP)、心肌肌钙蛋白I(cTnI)等相关指标,行心脏彩色超声检查监测LVEF、左心室短轴缩短率(FS)、左心室舒张末内径(LVEDD)以及左心室收缩末内径(LVESD)、心肌做功指数(TEi指数)等指标。结果LVEF<40%组FFA、NT-proBNP、cTnI明显高于LVEF≥50%组(P<0.05)。FFA、NT-proBNP、cTnI是AHF患者LVEF<40%发生的危险因素。FFA、NT-proBNP预测AHF患者LVEF<40%发生的AUC分别为0.856、0.810。在AHF患者中高FFA组较低FFA组患者的心功能明显降低(P<0.05)。结论FFA、NT-proBNP、cTnI是AHF患者LVEF<40%发生的危险因素,其中FFA对于患者心功能的恶化具有一定的预测价值。     

Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology

BACKGROUND: Spurious increases in serum troponins, especially troponin T, have been reported in patients with and without acute myocardial syndromes. METHODS: We studied 78 autopsied patients without clinical myocardial infarction (MI) and correlated histologic cardiac findings with antemortem serum creatine kinase (CK), its MB isoenzyme (CK-MB), cardiac troponin I (cTnI), and cardiac troponin T (cTnT). RESULTS: There was no significant myocardial pathology in 15 patients. Cardiac pathologies were in five groups: scarring from previous MI or patchy ventricular fibrosis (n = 9), recent MI (n = 27), healing MI (n = 7), degenerative myocyte changes consistent with congestive heart failure (CHF; n = 12), and other cardiac pathologies (n = 8). The median concentrations in the five groups were not significantly different for either CK or CK-MB. Compared with the no-pathology group, only the MI group was significantly different for cTnI, and the MI and other pathology groups were significantly different for cTnT. For patients with MI, 22%, 19%, 48%, and 65% had increased CK, CK-MB, cTnI, and cTnT, respectively; for CHF and other cardiac pathologies combined, the percentages were 28%, 17%, 22%, and 50%. For patients with increased cTnI, 72% and 28% had MI and other myocardial pathologies, respectively; patients with increased cTnT had 64% and 36%, respectively. Patients without myocardial pathology had no increases in CK-MB, cTnI, or cTnT. CONCLUSIONS: All patients with increased serum CK-MB, cTnI, and cTnT had significant cardiac histologic changes. The second-generation cTnT assay appears to be a more sensitive indicator of MI and other myocardial pathologies than the cTnI assay used in this study.     

Minor troponin T elevation in patients 6 months after acute myocardial infarction: an observational study

Background  Troponin elevation in patients with stable coronary heart disease is associated with adverse outcome and prognosis. However, the mechanism is not yet clearly understood. Our objectives were to examine the prevalence and range of cardiac troponin T (cTnT) in stable patients, 6 months after acute myocardial infarction (AMI) using a new high sensitive cTnT assay and to investigate the association of minor cTnT elevation in these patients to clinical variables, NT-proBNP and cardiac MRI-findings. Study design and methods  cTnT was measured in 98 patients 6 months after AMI with a precommercial assay by electrochemiluminescence methods (Roche Diagnostics, Mannheim, Germany). cTnT values were correlated with clinical and angiographic variables, NT-proBNP concentrations and with cardiac MRI-findings. Results  Minor cTnT concentrations were detectable in 90% of the entire cohort, of whom 16% had cTnT values above the 99th percentile (>12 ng/L). These patients were also significantly older, suffered more frequently from hypertension, had a higher New York Heart Association class and received more often diuretics at follow up. Patients with cTnT elevation had a more impaired left ventricular ejection fraction (P = 0.02) but did not have an increased infarct size (P = 0.73). Conclusions  Elevated minor cTnT levels are frequently detectable in patients 6 months after AMI. Increased cTnT level were associated with clinical parameter for heart failure, impaired ejection fraction and higher NT-proBNP levels suggesting that myocardial dysfunction is a main cause for cTnT elevation in these patient group.     

血清NT-proBNP联合cTnI检测对ACOP心肌损伤的临床价值

目的：探讨血清N末端B型脑钠肽原（NT-proBNP）联合肌钙蛋白I（cTnI）检测对急性一氧化碳中毒（ACOP）患者心肌损伤的临床价值。方法：选取201210-2014—03在我科住院的ACOP患者68例,按照中毒程度分为轻、中、重3组。取同一时期30例健康志愿者作为对照组。患者入院后立即抽取静脉血测定血清NT-proBNP和cTnI,比较它们与对照组以及轻、中、重度CO中毒组间的差异。结果：和对照组相比较,CO中毒各组NT-proBNP和cTnI水平显著升高,P〈0．01。轻中重3组组间比较,重度组及中度高于轻度组,重度组高于中度组,有显著性意义（P〈0．01）。NT-proBNP和cTnI之间正相关（r=0．957,P〈0．05）。结论：CO中毒后NT-proBNP和cTnI显著升高,联合检测NT-proBNP和cTnI可提高对ACOP后心肌损伤诊断的灵敏度和特异性评估,对诊断ACOP后心肌损伤有着重要意义。     

Improved assay of cardiac troponin I is more sensitive than other assays of necrosis markers

Objective. Highly sensitive and specific assays of cardiac troponins I and T are the preferred biomarkers in diagnosing myocardial infarction (MI). Assays of cardiac troponin I (cTnI) have been improved with the addition of antibodies against the cTnI molecule and may have increased sensitivity. We hypothesized that a cTnI assay with modern antibody configuration will exhibit equal or better sensitivity in the setting of acute MI compared to cTnT and other markers of myocardial necrosis. Material and methods. We investigated release kinetics of cTnI (Abbott ADV, Abbott Diagnostics), cTnT (Roche Diagnostics), CKMBmass, myoglobin and heart fatty acid binding protein (H‐FABP) in 23 patients admitted with acute ST‐segment elevation MI undergoing primary percutaneous coronary intervention. Calibrators for the Abbott ADV cTnI assay are traceable to the United States National Institute of Standards and Technology (NIST) reference material for cTnI. Eleven blood samples were drawn from each patient in the period from admission to 24?h. Biomarkers of necrosis showed marked increases in relative concentrations, especially within the first 2?h after admission. Results. From 30?min after admission onwards, cTnI exhibited significantly higher relative concentrations compared to cTnT, CKMBmass, Myoglobin and H‐FABP (p<0.05). Conclusions. The NIST standardized Abbott TnI ADV assay appears to be more sensitive than cTnT and other biomarkers in the early phase of MI.     

Cardiac markers (BNP, NT-pro-BNP, Troponin I, Troponin T, in female amateur runners before and up until three days after a marathon

PURPOSE: Transient cardiac ventricular dysfunction or sudden cardiac deaths have been reported for male athletes participating in marathon racing. Less is known about the myocardial response in females. We examined natriuretic peptides and cardiac troponins in female athletes after a marathon. METHODS: At the 31st real,- Berlin Marathon plasma levels of NT-pro-BNP, BNP, cTnI and cTnT were measured in 15 women (age 35+/-6 years; finishing times between 3:22 h and 5:21 h) at four different time points (before, immediately after, day one and day three). RESULTS: An increase in [NT-pro-BNP] was observed immediately after the marathon (median [NT-pro-BNP] before: 39.6 pg ml(-1), after: 138.6 pg ml(-1), p=0.003) with a further increase on day one. [BNP] did not increase immediately after the marathon but increased on day one (median [BNP] before: 15 pg ml(-1), day one: 27.35 pg ml(-1), p=0.006). On day three, [NT-pro-BNP] and [BNP] returned to initial values. [cTnI] was under the detection limit prior to the marathon in all runners. [cTnT] was under the detection limit before the marathon except in one runner who presented a concentration of 0.03 ng ml(-1). Cardiac troponins (median [cTnl] after: 0.098 ng ml(-1), p=0.028; median [cTnT] after: 0.032 ng ml(-1), p=0.012) increased immediately after the marathon and returned to initial values on day one [cTnT] and three [cTnI]. DISCUSSION: Parameters representing cardiac stress increased in females after a marathon. Different kinetics of natriuretic peptides BNP and NT-pro-BNP post-marathon could be due to their different half-lives and dependence on renal function. The increase of cTnI and cTnT may result from minor myocardial lesions.     

心肌标志物检测在慢性阻塞性肺疾病患者低氧血症中的意义

目的　探讨心肌标志物检测在慢性阻塞性肺疾病 (COPD)患者低氧血症中的临床意义。方法　对10 5例COPD急性发作期患者同时测定动脉血氧分压 (PaO2 )及血清肌钙蛋白I(cTnI)、肌钙蛋白T(cTnT)和肌酸激酶同工酶质量 (CK MBmass)水平。结果　COPD患者伴不同程度低氧血症 ,血清cTnI、cTnT和CK MBmass水平均明显高于正常对照组 (P <0 .0 1) ,且重度低氧血症组患者血清中 3项心肌标志物浓度均明显高于中度低氧血症组和轻度低氧血症组 ,相互比较差异有显著性 (P <0 .0 1) ;各患者组PaO2 水平与相对应的血清cT nI、cTnT和CK MBmass水平间呈负相关 (分别为r =- 0 .812、P <0 .0 1;r =- 0 .790、P <0 .0 1和r =- 0 .70 5、P <0 .0 5 ) ;血清cTnI、cTnT和CK MBmass检测的阳性率分别为 6 5 .7%、5 8.1%、4 1.9% ,以cTnI的阳性率最高 ,与cTnT和CK MBmass比较差异有显著性 (分别为P <0 .0 5、P <0 .0 1)。结论　COPD患者低氧血症可导致血清中心肌标志物浓度增高 ,且与PaO2 水平呈负相关 ,常规检测血清中心肌标志物浓度 ,尤其是cTnI ,对及时了解COPD患者心肌损害程度、改善疗效有重要意义。     

Multiple biomarker use for detection of adverse events in patients presenting with symptoms suggestive of acute coronary syndrome

BACKGROUND: We investigated multiple biomarkers of various pathophysiologic pathways to determine their relationships with adverse outcomes in patients presenting with symptoms of acute coronary syndrome. METHODS: We obtained plasma specimens from 457 patients on admission and measured 7 biomarkers: myeloperoxidase (MPO), soluble CD40 ligand (CD40L), placental growth factor (PlGF), metalloproteinase-9 (MMP-9), high-sensitivity C-reactive protein (hsCRP), cardiac troponin I (cTnI), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). We used the Modification of Diet in Renal Disease formula to calculate the estimated glomerular filtration rate (eGFR). Endpoints were cardiac events (myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft, cardiac death) and all-cause mortality. We estimated cumulative event rates over a 4-month period with the Kaplan-Meier method and relative risk (RR) with the Cox proportional hazards model. RESULTS: Patients with increased PlGF, NT-proBNP, hsCRP, or cTnI or decreased eGFR had 11% to 20% higher all-cause mortality rates than patients with concentrations within reference intervals: 20.4% (eGFR), 16.0% (PlGF), 15.8% (hsCRP), 12.7% (NT-proBNP), and 11.3% (cTnI; all P < or = 0.03). No differences in mortality rates were observed between those with increased vs normal concentrations of MPO, CD40L, or MMP-9. Decreased eGFR (RR 3.4, P = 0.004) and increased NT-proBNP (RR 7.9, P = 0.04) were independently predictive of mortality, and PlGF (RR 2.0, P = 0.08) approached significance. Patients with increased NT-proBNP (12.3%) or cTnI (33.8%) had higher cardiac event rates (each P <0.02), with increased MPO (11.1%) showing a trend (P = 0.09). Patients in whom both cTnI and MPO were increased had a cardiac event rate of 43%. CONCLUSION: Multiple biomarkers that are likely indicative of different underlying pathophysiologic mechanisms are independently predictive of increased risk for adverse events in patients with acute coronary syndrome.