Marker For Acute Myocardial Infarction Research Articles

Highly sensitive immunoassay for the diagnosis of acute myocardial infarction using silica spheres encapsulating a quantum dot layer.

Commercial ELISA kits for substance P (SubP), which are helpful for the clinical diagnosis of acute myocardial infarction, are limited in efficacy because of low sensitivity. A highly sensitive immunoassay was developed using silica spheres encapsulating a quantum dot-layer (SQS) and labeling antibodies, on a Parylene A-modified plate. The high sensitivity was possible by taking advantage of the enhanced photoluminescence of the SQS and dense immobilization of SubP on a Parylene A-modified plate. Glutaraldehyde was used for cross-linking of SQS to the anti-SubP antibody and SubP to the Parylene A coating. The SQS-linked immunosorbent assay (SQSLISA) was optimized and validated. The dynamic range for the assay was 1-10000 pg/mL with a linear correlation factor of 0.9992 when the competitive SQSLISA was employed. The intra- and interday accuracies were 93-100% and 87-122%, respectively. The reproducibility was lower than 11%. The developed method was applied to clinical samples collected from healthy controls (n = 30) and acute myocardial infarction (n = 16) and it displayed a high correlation with the commercial ELISA kit, with a limit of detection that was 30-fold lower. Clinical sample analysis confirmed that SubP is a promising diagnostic marker for acute myocardial infarction. The SQSLISA is expected to be a practical and useful assay tool.

Troponin T immunosensor based on liquid crystal and silsesquioxane-supported gold nanoparticles.

A nanostructured immunosensor based on the liquid crystal (E)-1-decyl-4-[(4-decyloxyphenyl)diazenyl]pyridinium bromide (Br-Py) and gold nanoparticles supported by the water-soluble hybrid material 3-n-propyl-4-picolinium silsesquioxane chloride (AuNP-Si4Pic(+)Cl(-)) was built for the detection of troponin T (cTnT), a cardiac marker for acute myocardial infarction (AMI). The functionalized nanostructured surface was used to bind anti-cTnT monoclonal antibodies through electrostatic interaction. The immunosensor (ab-cTnT/AuNP-Si4Pic(+)Cl(-)/Br-Py/GCE) surface was characterized by microscopy techniques. The electrochemical behavior of the immunosensor was studied by cyclic voltammetry and electrochemical impedance spectroscopy. A calibration curve was obtained by square-wave voltammetry. The immnunosensor provided a limit of detection of 0.076 ng mL(-1) and a linear range between 0.1 and 0.9 ng mL(-1) (appropriate for AMI diagnosis).

Uric acid as a predictor of in-hospital mortality in acute myocardial infarction: a meta-analysis.

Uric acid (UA) is generalized as a byproduct the terminal steps of purine catabolism, which are catalyzed by xanthine oxidoreductase. Xanthine oxidase activity and uric acid synthesis are reported to be increased under tissue ischemia. Therefore, elevated uric acid may act as a prognostic marker of acute myocardial infarction (AMI). A few studies have showed that UA is associated with therapeutic outcomes in patients with acute myocardial infarction. The purpose of this meta-analysis is to evaluate the prognostic significance of the UA as a predictor of in-hospital mortality. We performed a systematic review and included studies that used both UA and in-hospital mortality from Embase and PubMed. Six studies have been included in this review with totally 5,686 patients. During the follow-up, high UA level was found to be associated with an increased risk of in-hospital mortality [risk ratios (RR) 2.10 (1.03-4.26), number needed to harm (NNH) 37], MACE [RR 3.44 (2.33-5.08), NNH 17]. High UA level has the potential to be an important prognostic marker for in-hospital mortality in individuals with AMI.

Robust myocardial T2 and T2 * mapping at 3T using image-based shimming.

Intramyocardial hemorrhage and area at risk are both prognostic markers in acute myocardial infarction (AMI). Myocardial T2 and T2 * mapping have been used to detect such tissue changes at 1.5T but these techniques are challenging at 3.0T due to additional susceptibility variation. We studied T2 and T2 * myocardial mapping techniques at 3.0T on a system employing B1 shimming and compared two different methods of B0 shimming. Fifteen volunteers and six AMI patients were scanned on a 3T system. Volume and image-based (IB) B0 shimming techniques were implemented. Single breath-hold, multiecho gradient, and spin echo sequences were employed from which T2 * and T2 maps were calculated. In volunteers, there was no significant difference in mean values obtained with volume or IB shimming for T2 mapping (39.1 ± 6.0 msec vs. 39.4 ± 6.1 msec; P > 0.05) or for T2 * mapping (24.2 ± 6.7 msec vs. 24.1 ± 5.2 msec; P > 0.05). There were no significant regional differences in mean T2 values between septal, anterior, and posterior segments with either shimming technique (all P > 0.05); but there were significant regional differences in mean T2 * values using volume shimming (27.8 ± 5.2 msec vs. 28.4 ± 5.8 msec vs. 15.9 ± 8.3 msec; P < 0.05)-but not with IB shimming (25.7 ± 5.4 msec vs. 25.3 ± 5.9 msec vs. 18.7 ± 4.6 msec; P > 0.05). At 3.0T, cardiac T2 mapping is robust. Although T2 * mapping is prone to more regional heterogeneity this can be reduced by using IB instead of conventional volume B0 shimming.

Liquid crystal and gold nanoparticles applied to electrochemical immunosensor for cardiac biomarker

A label-free electrochemical immunosensor based on the ionic liquid crystal (E)-1-decyl-4-[(4-decyloxyphenyl)diazenyl]pyridinium bromide (Br–Py) coated on a glassy carbon electrode (GCE) for the quantitative detection of myoglobin (Mb), a cardiac marker for acute myocardial infarction, is reported herein for the first time. The monoclonal anti-myoglobin antibody (ab-Mb) was covalently immobilized using glyoxal on a film of polyethyleneimine-coated gold nanoparticles (AuNP-PEI). The proposed method for Mb detection is based on voltammetric suppression of the Br–Py signal when the immunosensor was incubated with Mb antigen. The electrochemical performance of the Mb immunosensor was studied by electrochemical impedance spectroscopy, and cyclic and square-wave voltammetry. Under the optimal conditions, the proposed immunosensor shows a good linear relationship between the electrochemical inhibition response and the concentration of Mb over the range of 9.96–72.8ngmL−1 with a detection limit of 6.29ngmL−1. The results obtained indicate that the proposed immunosensor provides good sensitivity and simple operation for detecting acute myocardial infarction with Mb as a biomarker.

Biochemical markers of acute myocardial infarction

Introduction: A number of biomarkers have been used to aid in the diagnosis of acute myocardial infarction (AMI), in the risk stratification of patients and for predicting events after acute coronary syndrome (ACS). Some of these biomarkers are widely used in clinical practice while others still have no scientific evidence to support their clinical use. Objectives: To analyze the clinical significance of the various biochemical markers for AMI, alone or in combined use, seeking a description according to the source, behavior in the evolution of the disease, including validation, diagnostic limitations, and clinical significance in different contexts. Methods: We performed a literature review using the PubMed database, including original articles and reviews on the use of biomarkers for AMI. The search was limited to articles written in English, published in the last five years. Results: 90 articles were accessed, 57 of which were excluded. Of the 32 selected studies, 14 were randomized and controlled. After judicious analysis, several biomarkers were described: troponin, creatine kinase-MB fraction, myoglobin, H-FABP, BNP and its inactive N-terminal fragment, ANP, copeptin, growth/differentiation factor-15, interleu

A carbon nanotube screen-printed electrode for label-free detection of the human cardiac troponin T

Label-free immunosensor based on amine-functionalized carbon nanotubes screen-printed electrode is described for detection of the cardiac troponin T, an important marker of acute myocardial infarction. The disposable sensor was fabricated by tightly squeezing an adhesive carbon ink containing carbon nanotubes onto a polyethylene terephthalate substrate forming a thin film. The use of carbon nanotubes increased the reproducibility and stability of the sensor, and the amine groups permitted nonrandom immobilization of antibodies against cardiac troponin T. Amperometric responses were obtained by differential pulse voltammetry in presence of a ferrocyanide/ferricyanide redox probe after troponin T incubation. The calibration curve indicated a linear response of troponin T between 0.0025 ng mL(-1) and 0.5 ng mL(-1), with a good correlation coefficient (r=0.995; p<0.0001, n=7). The limit of detection (0.0035 ng mL(-1) cardiac troponin T) was lower than any previously described by immunosensors and was comparable with conventional analytical methods. The high reproducibility and clinical range obtained using this immunosensor support its utility as a potential tool for point-of-care acute myocardial infarction diagnostic testing.

CXCR4+ and FLK-1+ Identify Circulating Cells Associated with Improved Cardiac Function in Patients Following Myocardial Infarction

The biomarkers CXCR4/FLK-1 select cardiac progenitors from a stem cell pool in experimental models. However, the translational value of these cells in human ischemic heart disease is unknown. Here, flow-cytometry identified CD45(-)/CXCR4(+)/FLK-1(+) cells in 30 individuals without ischemic heart disease and 33 first-time acute myocardial infarction (AMI) patients. AMI patients had higher CD45(-)/CXCR4(+)/FLK-1(+) cell-load at 48-h and 3- and 6-months post-AMI (p = 0.003,0.04,0.04, respectively) than controls. Cardiovascular risk factors and left ventricular (LV) ejection fraction were not associated with cell-load. 2D-speckle-tracking strain echocardiography assessment of LV systolic function showed improvement in longitudinal strain and dyssynchrony during follow-up associated with longitudinal increases in and higher 48-h post-AMI CD45(-)/CXCR4(+)/FLK-1(+) cell-load (r = -0.525, p = 0.025; r = -0.457, p = 0.029, respectively). In conclusion, CD45(-)/CXCR4(+)/FLK-1(+) cells are present in adult human circulation, increased in AMI and associated with improved LV systolic function. Thus, CD45(-)/CXCR4(+)/FLK-1(+) cells may provide a diagnostic tool to follow cardiac regenerative capacity and potentially serve as a prognostic marker in AMI.

ST segment elevations: Always a marker of acute myocardial infarction?

Chest pain is one of the chief presenting complaints among patients attending Emergency department. The diagnosis of acute myocardial infarction may be a challenge. Various tools such as anamnesis, blood sample (with evaluation of markers of myocardial necrosis), ultrasound techniques and coronary computed tomography could be useful. However, the interpretation of electrocardiograms of these patients may be a real concern. The earliest manifestations of myocardial ischemia typically interest T waves and ST segment. Despite the high sensitivity, ST segment deviation has however poor specificity since it may be observed in many other cardiac and non-cardiac conditions. Therefore, when ST-T abnormalities are detected the physicians should take into account many other parameters (such as risk factors, symptoms and anamnesis) and all the other differential diagnoses. The aim of our review is to overview of the main conditions that may mimic a ST segment Elevation Myocardial Infarction (STEMI).

ASSA13-11-11 Should the D-Dimer Be Acted as a Useful Marker For Acute Myocardial Infarction?

<h3>Objective</h3> D-dimer is a primary degradation product of thrombus. Whether it will be increased in myocardial infarction is still controversial. To study the change of D-dimer in coronary artery disease, this study investigated the level of plasma D-dimer in different type AMI patients at different stage. <h3>Methods</h3> The study group consisted of 200 patients suffered with acute coronary syndrome (ACS) from Jan 2011 to Jun 2012. 100 of the patients were diagnosed as STEMI; the rest was NSTEMI. And 100 patients excluded organic disease were enrolled as the contrast group. Blood was drawn at the time of admission, 12h and 24 hours after that. The samples were measured for cTnI, BNP, hs-CRP and fibrin D-dimer. All ACS patients were underwent active PCI strategy. <h3>Results</h3> Mean age of these patients was 65.6 years. Female is about 41.2% and male about 58.8%. In patients with STEMI, the level of cTnI, BNP and hs-CRP was significantly higher than that in patients without organic disease at the time of admission, 12h and 24h after that. While the level of D-dimer was not significantly different among the three groups at any time. The data is 103.4 ± 13.3ug/l, 108.2 ± 9.4ug/l and 98.5 ± 12.6ug/l in STEMI patients at the time of admission, 12h and 24h after that, respectively. The level of D-dimer is 103.1 ± 11.3ug/l, 97.8 ± 8.6ug/l and 98.6 ± 11.6ug/l in NSTEMI patients at the time of admission, 12h and 24h after hat, respectively. The contrast patients data is 96.4 ± 9.3ug/l, 98.3 ± 8.6ug/l and 95.5 ± 10.2ug/l at the time of admission, 12h and 24h after that, respectively. <h3>Conclusions</h3> Early level of circulating cTnI, BNP and hs-CRP was significantly higher in ACS, while there was no dynamic change of D-dimer level in patients with ACS, whatever STEMI or NSTEMI.

Detection and Validation of Circulating Endothelial Cells, a Blood-based Diagnostic Marker of Acute Myocardial Infarction

BackgroundCirculating endothelial cells (CECs) are markers of vascular damage that have clinical relevance in many diseases, including acute myocardial infarction (AMI), and may be predictors of treatment responses. Herein, we investigated the diagnostic and prognostic value of CEC monitoring in AMI patients and a murine model.Methodology/Principal FindingsCECs were defined as Hoechst 33342+/CD45−/CD31+/CD146+/CD133− in human blood samples and Hoechst 33342+/CD45−/CD31+/KDR+/CD117− in murine samples. To evaluate the validity and variability of our CEC detection system, peripheral blood samples of vascular endothelial growth factor-treated athymic nude mice and AMI patients were collected and subjected to intra-assay analysis. CEC detection by flow cytometry and real-time PCR were compared. Blood samples were obtained from 61 AMI patients, 45 healthy volunteers and 19 samples of the original AMI patients accepted one month treatment, via flow cytometry and expressed as a percentage of peripheral blood mononuclear cells.ResultsOur CEC detection method was validated and had limited variability. CEC concentrations were higher in AMI patients compared to healthy controls. One month post-treatment, CECs levels decreased significantly.Conclusions/SignificanceCEC levels may be useful as a diagnostic and prognostic biomarker in AMI patients.

Diagnosis and Treatment of Erectile Dysfunction for Reduction of Cardiovascular Risk

We established erectile dysfunction as an often neglected but valuable marker of cardiovascular risk, particularly in younger men and men with diabetes. We also reviewed evidence that lifestyle change, combined with informed prescribing of pharmacotherapies used to mitigate cardiovascular risk, can improve overall vascular health and sexual functioning in men with erectile dysfunction. We performed a PubMed® search for articles and guidelines pertinent to relationships between erectile dysfunction and cardiovascular disease, cardiovascular and all cause mortality, and pharmacotherapies for dyslipidemia and hypertension. The clinical guidance presented incorporates the current literature and the expertise of the multispecialty investigator group. Numerous cardiovascular risk assessment tools exist but risk stratification remains challenging, particularly in patients at low or intermediate short-term risk. Erectile dysfunction has a predictive value for cardiovascular events that is comparable to or better than that of traditional risk factors. Interventional studies support lifestyle changes as a means of improving overall vascular health as well as sexual functioning. Statins, diuretics, β-blockers and renin-angiotensin system modifiers may positively or negatively affect erectile function. Furthermore, the phosphodiesterase type 5 inhibitors used to treat erectile dysfunction may have systemic vascular benefits. Erectile dysfunction treatment should be considered secondary to decreasing cardiovascular risk. However, informed prescribing may prevent worsening sexual function in men receiving pharmacotherapy for dyslipidemia and hypertension. As the first point of medical contact for men with erectile dysfunction symptoms, the primary care physician or urologist has a unique opportunity to identify those who require early intervention to prevent cardiovascular disease.

English

BACKGROUND AND OBJECTIVE: At very early stages of acute myocardial infarction (AMI), highly sensitive biomarkers are still lacking. Human heart-type fatty acid- binding protein (H-FABP) has a high potential as an early marker for acute myocardial infarction (AMI) being more sensitive than current routine cardiac markers. The objective of this study is to determine the efficacy of a newly developed qualitative test to measure H eart- type fatty acid-binding protein (H-FABP) levels in the blood for the early diagnosis of acute myocardial infarction (AMI) in patients with chest pain and compared with cardiac Troponin T. DESIGN: Prospective study. METHODS: Fifty patients with acute ischemic-type chest pain were prospectively enrolled and classified according to the American Heart Association/American College of Cardiology guidelines. An initial blood sample was obtained for H-FABP, cTnT, and CK-MB (first 4 hours of symptoms). After 4 hours (4 - 12 hours), repeat samples of H-FABP, cTnT, and CK-MB were obtained. RESULTS: Fifty patients presenting to hospital with a median symptom onset of 3.3 hrs (IQR 2-6 h) were enrolled in this study and 38 (76%) had AMI. At presentation, H-FABP gave the highest sensitivity of 77% (95% CI: 60.7-88.9) and specificity of 91% (95% CI: 58.7-99.8) and troponin T (cTnT) gave the highest specificity of 100% (95% CI: 69.2-100). This study demonstrated that H-FABP immunotest gave a better diagnostic classification at the early stage. Also, AMI was identified significantly earlier by H-FABP than cTnT (29 vs. 8 patients, p<0.05). CONCLUSIONS: Assessment of Heart-type fatty acid-binding protein (H-FABP) within the first 4 h of symptoms is superior to cTnT for detection of AMI, and is a useful additional biomarker for patients with acute ischemic chest pain.

Plasma Free Fatty Acid Concentrations as a Marker for Acute Myocardial Infarction

Acute myocardial infarction carries a high mortality among cardiac patients.The discovery of the fact that certain enzymes like CPK, LDH liberated into circulation following necrosis of the myocardial cells came as boon for physicians and patients. There has been a constant search of different parameters for the diagnosis and management of CoronaryArtery Diseases (CAD). The present study was undertaken to investigate a possible relation between the changes in plasma free fatty acid (FFA) concentration and acute myocardial infarction. Fifty cases (25 males and 25 females) of acute myocardial infarction were selected for the present study. All the patients were in the age group of 40-70 years. For the control group fifty (25 male and 25 female) subjects of same age group were selected from patient's relatives and friends. Plasma free fatty acid concentration was estimated by Titrametric method of Trout et al., (1960), a modified version of Dole (1956). The statistical analysis of the data of the present study was done by using SPSS, version 14.0.1 was used. Our study showed a significant increase in plasma FFA in the first 24 hours of acute myocardial infarction with subsequent normalisation on the 7th day.The difference between the first and the seventh day was statistically significant. The FFA were found raised in cases of acute myocardial infarction.On the basis of present study, it is worth to say that estimation of serum free fatty acid should be done routinely at the earliest opportunity in all cases of acute myocardial infarction.

Telomere Length Variation in Juvenile Acute Myocardial Infarction

Leukocyte telomere length (LTL) provides a potential marker of biological age, closely related to the endothelial dysfunction and consequently to the atherosclerotic process. To investigate the relationship between the LTL and the risk of premature acute myocardial infarction and to evaluate the predictive value of LTL on the onset of major cardiovascular events, 199 patients from 18 to 48 years old with first diagnosis of acute myocardial infarction were enrolled and were matched with 190 controls for sex and age (±1 year). Clinical data and coronary artery disease were evaluated at enrollment and at follow up. LTL was measured at enrollment using a quantitative PCR-based method. No significant differences were observed in LTL between cases and controls (p = 0.20) and with the presence of coronary artery disease in patients (p = 0.47). Hypercholesterolemic cases presented LTL significantly longer than cases without hypercholesterolemia (t/s: 0.82±0.16 p = 0.79 and t/s norm: 0.79±0.19 p = 0.01), as confirmed in multivariate regression analysis (p = 0.005, β = 0.09). Furthermore, multivariate regression analysis showed LTL significantly shorter in hypertensive cases than in normotensive cases (p = 0.04, β = −0.07). One hundred seventy-one cases (86%) ended the average follow up of 9±5 years, 92 (54%) presented a major cardiovascular event. At multivariate regression analysis the LTL detected at enrollment did not represent a predictive factor of major cardiovascular events nor it significantly impacted with cumulative events. Based on present cohort of young Italian patients, the LTL did not represent a marker of acute myocardial infarction nor had a predictive role at medium term follow up.

Myocardial infarction marker levels are influenced by prothrombin and tumor necrosis factor-α gene polymorphisms in young patients

Polymorphisms of genes encoding key factors for the control and activation of inflammatory response and coagulation cascade regulation may play a role in genetic susceptibility to acute myocardial infarction (AMI). This study sought to analyze the effect of TNF −308G/A and pro-thrombin (FII) 20210G/A polymorphisms on the laboratory parameters of young patients affected by AMI. Results indicated that TNF −308A positive genotype frequencies were increased in these patients and that a genetically determined higher production of TNF-α is associated in young subjects to a more severe cardiac damage as depicted by higher levels of troponin, Creatine kinase-MB Isoenzyme (mCK-MB) and a significant increased plasma fibrinogen levels. Similar and probably additive effects on might have a genetically determined increased production of pro-thrombin even if no significant differences in genotype frequencies of pro-thrombin (FII) 20210G/A polymorphisms were observed in this study. All together these results, indicating the relationship among genetically determined TNFα and FII production and increased levels of tissue damage markers of AMI, suggest that a complex genetic background, might be involved in susceptibility to AMI in young men influencing the extension and severity of the disease.

Soluble Amyloid Precursor Protein 770 Is Released from Inflamed Endothelial Cells and Activated Platelets

Separate monitoring of the cleavage products of different amyloid β precursor protein (APP) variants may provide useful information. We found that soluble APP770 (sAPP770) is released from inflamed endothelial cells and activated platelets as judged by ELISA. sAPP770 is an indicator for endothelial and platelet dysfunctions. How sAPP770 is released in vivo has been shown. Most Alzheimer disease (AD) patients show deposition of amyloid β (Aβ) peptide in blood vessels as well as the brain parenchyma. We previously found that vascular endothelial cells express amyloid β precursor protein (APP) 770, a different APP isoform from neuronal APP695, and produce Aβ. Since the soluble APP cleavage product, sAPP, is considered to be a possible marker for AD diagnosis, sAPP has been widely measured as a mixture of these variants. We hypothesized that measurement of the endothelial APP770 cleavage product in patients separately from that of neuronal APP695 would enable discrimination between endothelial and neurological dysfunctions. Using our newly developed ELISA system for sAPP770, we observed that inflammatory cytokines significantly enhanced sAPP770 secretion by endothelial cells. Furthermore, we unexpectedly found that sAPP770 was rapidly released from activated platelets. We also found that cerebrospinal fluid mainly contained sAPP695, while serum mostly contained sAPP770. Finally, to test our hypothesis that sAPP770 could be an indicator for endothelial dysfunction, we applied our APP770 ELISA to patients with acute coronary syndrome (ACS), in which endothelial injury and platelet activation lead to fibrous plaque disruption and thrombus formation. Development of a biomarker is essential to facilitate ACS diagnosis in clinical practice. The results revealed that ACS patients had significantly higher plasma sAPP770 levels. Furthermore, in myocardial infarction model rats, an increase in plasma sAPP preceded the release of cardiac enzymes, currently used markers for acute myocardial infarction. These findings raise the possibility that sAPP770 can be a useful biomarker for ACS.

98 Assessing QT Prolongation as an Early Electrocardiographic Marker in Acute Myocardial Infarction

Background: Treatment guidelines and triaging in patients with acute myocardial infarction currently depends on whether there is ST elevation (STE) MI, an ECG diagnosis or non-STEMI, diagnosed by absence of STE in the presence of elevation of cardiac enzymes. Numerous studies have shown that cardiac wall motion abnormality precedes STE, hence there is an intense research into finding earlier EKG changes that will predict myocardial ischemia before the onset of wall motion abnormalities. Associations between the QT interval on an electrocardiogram (ECG) and acute myocardial infarction have been reported for over 20 years.

Tartrate-resistant acid phosphatase 5a in sarcoidosis: Further evidence for a novel macrophage biomarker in chronic inflammation

Tartrate-resistant acid phosphatase (TRACP) 5a is expressed strongly in inflammatory macrophages (MΦ). Serum TRACP5a is elevated in rheumatoid arthritis patients with extra-articular manifestations of rheumatoid nodules, in a percentage of patients with end-stage chronic kidney disease, and may be a risk marker for acute myocardial infarction. This proof-of-concept study was undertaken in patients with sarcoidosis to further substantiate our hypothesis that TRACP5a protein is a biomarker for macrophages in other chronic inflammatory diseases. Immunohistochemical staining for TRACP5a and CD68 was performed in tissues of 19 patients with sarcoidosis. We also measured circulating TRACP5a protein and other inflammation biomarkers including interkeukin-6, angiotensin-converting enzyme, and C-reactive protein in 13 patients. Twenty healthy age-matched nonsmoking individuals were used as the reference group. All sarcoidosis tissues showed strong staining for TRACP5a and CD68 in the non-caseating granulomatous lesions and localized specifically to MΦ, multinucleate giant cells, and epithelioid MΦ. Serum TRACP5a protein was elevated significantly in active sarcoidosis patients compared with the control group, and levels fluctuated with disease activity in one patient studied longitudinally. TRACP5a protein is expressed abundantly in the granulomatous tissues and may be elevated in a significant proportion of sarcoidosis patients. These findings further support our hypothesis that serum TRACP5a is derived from systemic inflammatory MΦ and thereby may be a biomarker of inflammation for sarcoidosis and also reflect its disease activity.

Prognostic Value of Cardiac-Specific Troponins in Intracranial Hemorrhage

Cardiac-specific troponin (Tn) serum concentrations have proved to be important diagnostic and prognostic markers for acute myocardial infarction. Elevated levels in the setting of noncardiac diseases such as intracerebral hemorrhage also may provide useful prognostic information regarding outcome. A systematic review of the English-language medical literature was performed using PubMed. Articles reporting original data were included. Ten reports qualified for review. A spectrum of cardiac abnormalities was observed in studied patients, sometimes more frequently in those with Tn elevations, whereas some had no such abnormalities, even if Tn was detected. Although some studies suggested a worse outcome in patients with elevated Tn levels, the findings were inconsistent. At this time, although the literature suggests an association between cardiac-specific Tn elevations and clinical events in patients with intracranial hemorrhage, data are insufficient to conclude that there is a consistent predictive value or to recommend routine Tn monitoring for prognosis.