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PubMed2001

A double-blind, multicentered study comparing the accuracy of diagnostic markers to predict short- and long-term clinical events and their utility in patients presenting with chest pain.

BACKGROUND: Millions of patients present annually with chest pain, but only 10% have myocardial infarction (MI). We recently reported comparative sensitivity and specificity of available markers in the diagnosis of MI; however, optimum interpretation of marker results requires prognostic follow-up data. HYPOTHESIS: The study was undertaken to study the accuracy of CK-MB subforms, troponin I and T, myoglobin, and CK-MB in predicting clinical events at 30 days and 6 months. METHODS: In all, 955 consecutive patients with chest pain were enrolled in a prospective, multicenter, double-blind study to test the prognostic accuracy of these markers. RESULTS: Myocardial infarction was diagnosed in 119 by CK-MB mass criteria and unstable angina (UA) in 203 patients by clinical criteria. Follow-up at 30 days and 6 months was available in 824 and 724 patients, respectively, with mortalities of 2.8 and 4.14%, respectively. Cumulative 6-month mortality was 5.6% in MI, 4.4% in UA, and 3.0% in others. Revascularization was reported in 9.3% of patients by 6 months. A positive test on each of the markers except myoglobin was predictive of revascularization. The composite endpoint of death or revascularization occurred in 107 patients by 6 months and a positive result on each of the markers was predictive of this composite endpoint (p < 0.05). The relative risk of death or revascularization for patients who did not have MI but tested positive on each of the markers was > 1.0 but did not reach statistical significance. CONCLUSIONS: With the possible exception of myoglobin, each of the diagnostic markers displayed similar prognostic performance in patients with chest pain presenting to emergency departments. The most appropriate markers to triage patients with chest pain, which has both adequate early diagnostic sensitivity and prognostic accuracy, are the CK-MB subforms.

Adult↗
PubMed2002

C-reactive protein as a marker for active coronary artery disease in patients with chest pain in the emergency room.

BACKGROUND: Markers of inflammation, such as C-reactive protein (CRP), were found to be related to risk for cardiovascular disease (CVD) events in patients with angina pectoris. In addition, recent studies have shown that, in the case of atherosclerosis, increased CRP concentration reflects the inflammatory condition of the vascular wall. HYPOTHESIS: The study was undertaken to determine whether CRP levels in individuals with chest pain attending the emergency room (ER) may be used as a marker of active CVD. METHODS: Serum CRP level was measured in 226 of 326 consecutive patients (128 men, 98 women; mean age 61.3 +/- 5.9 years; range 19-87 years) referred to the ER with chest pain. The decision whether to admit orrelease the subjects was determined without taking the CRP level into account. Follow-up was then performed for 1 year. RESULTS: Eighty-four patients were admitted to the hospital. Of these, 9 with acute coronary syndrome (ACS) had very high levels of CRP (25-40 mg/l), 35 had had an acute coronary event within the preceding 3 months, with levels of CRP 14-20 mg/l. Only eight patients with nonsignificant CVD had elevated CRP levels. Twenty-eight subjects who were released from the ER had elevated CRP levels (7-14 mg/l); 8 of these, in addition to 4 subjects with normal CRP levels, had a late coronary event. CONCLUSION: This study indicates that in patients referred to the ER with chest pain and no other indication for hospitalization, a normal level of CRP suggests safe release. Most hospitalized patients with normal CRP will not have acute coronary syndrome. Patients who will develop early coronary events have very high CRP levels. High serum CRP level, after excluding other inflammatory sources, was proven to be a sensitive diagnostic and prognostic marker for significant coronary disease.

Adult↗
PubMed2004

Bail-out stenting for left main coronary artery dissection during catheter-based procedure: acute and long-term results.

BACKGROUND: The optimal treatment of patients with left main coronary artery (LMCA) dissection during catheter-based procedure remains uncertain. HYPOTHESIS: In cases with significant LMCA dissection occurring during catheter-based procedure, prompt stent implantation may be safe and associated with favorable clinical outcome. METHODS: We evaluated the acute and long-term results of bail-out stenting for LMCA dissection occurring during a catheter-based procedure in 10 patients. RESULTS: Initially, there was no significant stenosis of LMCA segments in these patients. Catheter-induced dissection occurred in eight patients (during diagnostic angiography in three patients and during guiding catheter manipulation in five patients). Two patients suffered dissection in the setting of stent deployment in other vessels. Therefore, bail-out stenting for LMCA dissection was performed in a total of 10 patients. In four patients, hypotension developed and an intra-aortic balloon pump was placed during the procedure. Stents were successfully deployed in all patients; there was no in-hospital mortality. Six-month angiographic follow-up was performed in eight patients. No angiographic restenosis (diameter stenosis > or = 50%) was observed in any patient at follow-up study. During a mean follow-up of 31 +/- 25 months after hospital discharge, there was no major adverse cardiac event (death, myocardial infarction, and target lesion revascularization). CONCLUSIONS: Bail-out LMCA stenting is technically feasible and showed good acute and long-term results in a small series of patients.

Aged↗
PubMed2004

Elevation of the soluble thrombomodulin levels is associated with inflammation after percutaneous coronary interventions.

BACKGROUND: Thrombomodulin (TM) is an endothelial cell surface thrombin-binding protein with anticoagulation ability by thrombin-mediated activation of protein C. An increase of plasma soluble TM level is reported to be associated with severity and worse outcome of coronary artery disease. HYPOTHESIS: This prospective study investigated the relation of the elevated levels of plasma soluble TM and inflammatory and myonecrotic markers in patients undergoing percutaneous coronary intervention (PCI). METHODS: Plasma levels of soluble TM, C-reactive protein (CRP), and creatine kinase and its MB isoenzyme were measured before and after PCI in 100 patients undergoing PCIs. RESULTS: Peak TM levels after PCIs were significantly higher than baseline (3.39 +/- 1.63 vs. 2.90 +/- 1.57 ng/ml, p < 0.001). The peak TM levels after PCIs correlated significantly with the peak CRP and MB levels, and the maximal inflation duration (r = 0.423, p < 0.001; r = 0.212, p = 0.034; r = 0.307, p= 0.002, respectively). CONCLUSIONS: Soluble TM levels increase significantly after PCI. The elevation of the soluble TM after PCI shows better correlation with inflammation than myocardial injury, indicating an endothelial origin. Measurement of soluble TM could be useful and calls for further studies on the prognostic effects of this marker in this clinical condition.

Aged↗
PubMed2004

Serum levels of cardiac enzymes before and after renal transplantation.

BACKGROUND: Cardiac troponins are very sensitive and specific indicators of myocardial damage; however, they are sometimes found to be increased in patients with end-stage renal disease (ESRD). HYPOTHESIS: The aim of this study was to determine cardiac troponin I (cTpI) and creatine kinase myocardial isoform (CK-MB) levels and to assess their diagnostic and prognostic importance before and after renal transplantation. METHODS: Thirty-four patients with ESRD (mean age 31.8 +/- 8.6 years, 11 women) were enrolled. Serum levels of cTpI and CK-MB were measured pre- and postoperatively on Days 1, 7, and 30. Patients were followed up for cardiac events, and possible myocardial damage was investigated by exercise thallium-201-labeled myocardial perfusion scintigraphy. Mean cTpI levels were 0.24 +/- 0.11 ng/ml (preoperative), and 0.34 +/- 0.27 ng/ml (Day 1), 0.26 +/- 0.11 ng/ml (Day 7), and 0.28 +/- 0.30 ng/ml (Day 30). RESULTS: Compared with preoperative levels, cTpI was increased in 16 (47%), decreased in 6 (17.6%), and did not change in 12 (35.4%) patients. However, the increase did not exceed the myocardial infarction reference level of 2.3 ng/ml in any patient. Mean CK-MB levels were 12.6 (8.7U/l (preoperative), and 16.8 +/- 9.2U/l (Day 1), 16.3 +/- 8.1U/l (Day 7), and 13.3 +/- 6.6U/l (Day 30). Creatine kinase-MB was increased to above normal levels of 24 U/l in 13 (38.2%) patients on postoperative Days 1 or 7, and decreased to normal at the end of Month 1. No cardiac events occurred, and there was no abnormality in any patient on thallium scintigraphy. CONCLUSION: There was no significant difference in the levels of cTpI in patients with ESRD without cardiac events before and after renal transplantation (p > 0.05). Our findings show that cTpI has very high sensitivity and specificity for detecting cardiac damage in patients with ESRD after renal transplantation.

Adult↗
PubMed2005

The new definition of myocardial infarction--can we use it?

BACKGROUND: A joint committee of the European Society of Cardiology and the American College of Cardiology (ESC/ACC) recently redefined myocardial infarction. HYPOTHESIS: The objective of this study was to examine the outcome of diagnoses from more than 500 patients admitted to a university hospital coronary care unit (CCU), when the ESC/ACC committee cut-off levels were compared with the Swedish diagnostic criteria for acute myocardial infarction (MI), comparable with everyday practice in most countries. METHODS: Creatine kinase-MB, troponin I, and troponin T were measured in 525 patients admitted consecutively to the CCU, Huddinge University Hospital, with possible myocardial ischemia lasting <12 h before arrival. RESULTS: The ESC/ACC definition of MI increased the number of MIs by 3-32% compared with the number achieved when Swedish diagnostic criteria for acute MI were used. A significant number of patients with elevated cardiac enzymes presented with acute heart failure, tachycardia, pulmonary embolism, and sepsis as initial symptom. CONCLUSIONS: In this study of more than 500 patients with possible myocardial ischemia admitted consecutively to the CCU at a university hospital, the ESC/ACC definition of MI increased the number of MIs by 3-32% compared with the number achieved when Swedish diagnostic criteria for acute MI were used. A majority of the patients identified with ESC/ACC cut-off levels presented with myocardial ischemia as the primary symptom, whereas many of the other patients had acute heart failure and tachycardia as initial symptom. It is unclear whether patients in this latter group should be labelled as having MI; there are no clinical studies providing guidance in this situation.

Aged↗
PubMed2005

Interleukin-1 receptor antagonist levels correlate with extent of myocardial loss in patients with acute myocardial infarction.

BACKGROUND: Interleukin-1 receptor antagonist (IL-1Ra) levels are elevated early in patients with acute myocardial infarction (MI) and often precede release of markers of necrosis; however, IL-1Ra levels did not correlate previously with infarct size and prognosis in such patients. HYPOTHESIS: The goal of our study was to evaluate prospectively the correlation between IL-1Ra levels upon emergency department (ED) presentation and the extent of myocardial necrosis and prognosis in patients with ST-segment elevation MI. METHODS: Levels of IL-1Ra were measured upon ED presentation in 44 consecutive patients (40 men, aged 55 +/- 10 years). Peak values of creatine kinase (CK) and CK-MB were determined during hospitalization, and left ventricular ejection fraction (LVEF) was evaluated by echocardiography before discharge. All patients were followed prospectively and underwent clinical and echocardiographic assessment at 42 +/- 3 months after the infarction. RESULTS: Levels of IL-1Ra upon ED presentation correlated directly with CK (p = 0.002) and CK-MB (p = 0.01) peak levels and correlated inversely with LVEF before discharge (p = 0.009). Patients with in-hospital adverse events had significantly higher IL-1Ra levels upon ED admission (n = 10,2620 +/- 4706 pg/ml) than those without events (n = 34,598 +/- 457 pg/ml) (p = 0.015). CONCLUSIONS: In patients with MI, levels of IL-1Ra upon ED presentation correlated significantly with the extent of myocardial necrosis, as measured by cardiac enzymes peak and reduction of LVEF, and are predictive of in-hospital events. Results of this study may influence early therapeutic approach in patients with acute MI.

Adult↗
PubMed2004

Cardiotoxicity of doxorubicin/paclitaxel combination in rats: effect of sequence and timing of administration.

The higher incidence of cardiotoxicity of doxorubicin (DOX)/paclitaxel (PTX) combination compared with DOX alone remains to be a major obstacle against effective chemotherapeutic treatment. We investigated the effect of sequence and time interval between administration of both drugs on the severity of cardiotoxicity of the combination. Male Wistar rats were divided into seven groups. DOX was administered intraperitoneally (i.p.) at a single dose of 5 mg x kg(-1) every other 2 days, 2 doses per week for a total cumulative dose of 20 mg x kg(-1). PTX was administered by an i.p. route at a dose of 20 mg x kg(-1) every other 2 days. Both drugs were injected either alone or sequentially in combination. In one case, DOX preceded PTX by 30 min and 24 h and in the other case, PTX preceded DOX by 30 min and 24 h. Cardiotoxicity was evaluated by both biochemical and histopathological examination, 48 h after the last DOX dose. DOX-induced cardiotoxicity was manifested by abnormal biochemical changes including marked increases in serum creatine phosphokinase isoenzyme (CK-MB), lactate dehydrogenase (LDH), glutathione peroxidase (GSH-Px), and aspartate aminotransferase (AST) activity levels. Myocardial tissue from DOX-treated rats showed significant increases in malondialdehyde (MDA) production and total nitrate/nitrite (NOx) levels, parallel with depletion of "endogenous antioxidant reserve," including GSH contents and GSH-Px activity level. PTX treatment produced significant changes in the biochemical parameters measured by a lower magnitude than those changes produced by DOX alone. Combination of both drugs resulted in aggravation of DOX-induced cardiotoxicity regardless the sequence and time interval between administration of either drug. Administration of PTX 30 min and 24 h after DOX treatment showed exaggeration of combination-induced cardiotoxicity compared with the reverse sequence. This exacerbation was manifested by much more pronounced changes in serum and cardiac tissue parameters measured. Histopathological examination of ventricles of rat's heart revealed that DOX treatment produced myo-cytolysis and myocardial necrosis. Administration of PTX following DOX treatment showed extensive myocardial necrosis compared with those rats treated with either DOX alone or the reverse sequence of administration. Moreover, rats treated with PTX 24 h after DOX treatment showed exaggeration of the combination-induced cardiotoxicity. In conclusion, PTX might synergistically aggravate DOX-induced cardiotoxicity. The effect might be much more pronounced with those rats treated with PTX 24 h after DOX treatment.

Animals↗
PubMed2001

Evaluation of Stratus CS stat fluorimetric analyser for measurement of cardiac markers Troponin I (cTnI), creatine kinase MB (CK-MB), and myoglobin.

Myoglobin, CK-MB, and Troponin I (cTnI) are cardiac muscle necrosis markers that are useful for detecting acute myocardial infarction (AMI). The Stratus CS (Dade Behring, Inc.) is a discrete fluorimetric immunoassay analyser designed for the determination of the three cardiac markers from a single sample of whole blood or plasma. Overall analytical performances of the Stratus CS provided by Dade Behring were evaluated according to the French Society of Clinical Biology guidelines. Within-run imprecision (n = 20) for the three parameters at three levels gave values under 5%, whereas CVs for between-run imprecision (n = 20) were under 6%. The sensitivities were 0.03 microg/L for cTnI and 0.4 microg/L for CK-MB. Linearities extended from 0-50 microg/L for cTnI, 0-140 microg/L for CK-MB, and 1-900 microg/L for myoglobin. The results, particularly those obtained on whole-blood samples, correlated well with those obtained on Stratus II. We did not find any interference with haemolysis, icterus, or lipemia. The system was very easy to use, and fulfills the requirements for the analysis of the three cardiac markers in patients with acute chest pain in emergency situations.

Chemistry, Clinical↗
PubMed2001

Negative interference of bilirubin and hemoglobin in the MEIA troponin I assay but not in the MEIA CK-MB assay.

Troponin I is a sensitive and specific marker for the diagnosis of myocardial infarction. Several commercially available immunoassays measure the concentration of troponin I in serum. The microparticle enzyme immunoassay (MEIA) for troponin I (Abbott Laboratories, Abbott Park, IL) is widely used in clinical laboratories, including our hospital laboratory. We studied the effect of bilirubin and hemolysis on the MEIA for troponin I and compared our assay with a newly available chemiluminescent assay (CLIA) for troponin I (Bayer Diagnostics, Tarrytown, NY). We also measured CK-MB concentration using the MEIA CK-MB assay. One serum pool was prepared by combining several specimens of one patient with elevated troponin I and with a diagnosis of myocardial infarction. Other serum pools were prepared by combining sera with similar troponin I values. All serum pools showed normal bilirubin concentrations and had no hemolysis. Then we supplemented aliquots of serum pools with various concentrations of bilirubin (5.0, 10.0, 15.0, and 20.0 mg/dL). After supplementation, troponin I concentrations were measured again using the MEIA and CLIA. We observed a statistically significant decrease in troponin I concentration in the presence of bilirubin with the MEIA. For example, in serum pool 1, the troponin I concentration was 16.3 (bilirubin: 0.8 mg/dL). In the presence of 5.0, 10.0, 15.0 and 20.0 mg/dL of added bilirubin, the cardiac troponin I concentrations were 13.9, 13.4, 13.3 and 13.0 ng/ml respectively. We observed similar negative interference of bilirubin in troponin I measurement by the MEIA in other pools. The troponin I value decreased slightly (not statistically significant) in one pool and did not change in two other pools in the presence of bilirubin when we measured troponin I concentration using the CLIA. Interestingly, bilirubin did not interfere with the MEIA CK-MB assay. Moderate hemolysis did not have any effect on the troponin I assay using either the MEIA or CLIA. However, gross hemolysis (hemoglobin > 40 mg/dL) interfered with both assays for troponin I.

Bilirubin↗
PubMed2001

Dual influence of disease and increased load on diaphragm muscle in heart failure.

We have recently shown that mitochondrial function and energy metabolism are altered in the myocardium as well as in slow and fast locomotor muscles of rats subjected to prolonged congestive heart failure (CHF) suggesting a generalized metabolic myopathy in heart failure. Here, we investigate whether the diaphragm of CHF animals, which experiences both increased work and the general systemic influence of heart failure, will also be susceptible to altered energy metabolism. Biopsies were obtained from the costal diaphragm of failing rats 8 months after aortic banding. A marked increase in type I and type IIa myosin heavy chains at the expense of types IIx and IIb, suggests an adaptation towards a slower phenotype. Glycolytic enzymes decreased in CHF diaphragm with an increase in the H:M lactate dehydrogenase isoenzyme ratio. These results suggest a reorientation of the diaphragm muscle towards a slow, fatigue-resistant phenotype. However, maximal oxidative capacity assessed in saponin-permeabilized fibers in the presence of ADP was considerably reduced in CHF diaphragm (7.7+/-0.4 v 11.8+/-0.7 micromol O2/min/g dry weight in sham P<0.001), suggesting an alteration in oxidative phosphorylation. Furthermore, ADP sensitivity of CHF mitochondria was significantly increased (apparent Km for ADP 308+/-21 v 945+/-106 microM in sham P<0.001), whereas sensitivity to ADP in the presence of creatine was comparable (Km 79+/-12 v 90+/-11 microM in sham). In heart failure, therefore, the diaphragm muscle seems to adapt towards a more slow and economical contraction as a result of increased workload, but this adaptation is limited by the disease-induced altered mitochondrial function.

Animals↗
PubMed2002

Cardiac necrosis markers associated with low nitric oxide levels in the plasma of rabbits after treatment with vasopressin: protective effects of nitroglycerin administration.

It has been reported that the administration of vasopressin induces myocardial ischaemia in rats, which causes electrocardiographic ST segment alterations according to many authors. But rat electrocardiogram (ECG) lacks ST segment. Consequently it appears important to study the effects of vasopressin in rabbits, which show ST segment present in the ECG. Since cardiac necrosis markers are released in the plasma of humans with myocardial infarction, as well as in a variety of experimental models of myocardial necrosis, it is possible that the same may occur in rabbits with myocardial ischaemia induced by vasopressin. The main aim of this study was to investigate whether the administration of vasopressin causes the appearance of specific myocardial necrosis markers, such as cardiac troponin I, myoglobin or creatine kinase MB (CK MB) in rabbits in the presence or absence of modified ECG profile, and to also verify whether these markers are associated with the alterations in some coagulation parameters, that are known to be induced by vasopressin. As the effects of vasopressin are counteracted by nitric oxide (NO), another aim was to verify whether vasopressin also affects plasma NO levels and whether the administration of a NO donor can reverse these effects. Vasopressin was administered to rabbits and caused ischaemic alterations such as electrocardiographic changes, and significantly increased the levels of plasma cardiac necrosis markers (c-troponin I, myoglobin and CK MB). It also elevated diastolic blood pressure (BP), lowered heart rate (HR), increased procoagulation activity, and lowered plasma NO levels. The appearance of heart necrosis, demonstrated by plasma cardiac necrosis markers in the animals receiving vasopressin, was attributed to a drug-induced increase in vasoconstriction and coagulation activity. The intense vasoconstriction and thrombosis may lead to endothelium necrosis and a consequent drop in NO production. The administration of the NO donor nitroglycerin (NG) in the vasopressin treated animals restored NO values, and was capable of preventing the appearance of the plasma cardiac necrosis markers and altered coagulation values. The protective activity of NG was attributed to NO release, which lowers BP values and counteracts coagulation activity in vasopressin-treated animals. The described procedure may also be proposed for the study of early ischaemic myocardial lesions and the screening of NO donors preventing myocardial damage.

Animals↗
PubMed1992

The significant role of membrane stabilization in hypothermic cardioplegic cardiac preservation in a canine experimental model.

Isolated mongrel hearts were preserved for 6 h at 5 degrees C followed by normothermic reperfusion for 2 h. The dogs were divided into three groups; K+-cardioplegic solution alone, group C, n = 7; K+-cardioplegic solution with lidocaine 200 mg/l, group L, n = 7; and K+-cardioplegic solution with betamethasone 250 mg/l and lidocaine 200 mg/l, group B + L, n = 7. Ventricular fibrillation occurred early during reperfusion in all dogs in group C, in one of seven in group L, and in two of seven dogs in group B + L. The serum MB fraction of creatinine kinase (MB-CK), mitochondrial aspartate aminotransferase (m-AAT) and calcium overload were suppressed to a greater extent in both groups L and B + L during reperfusion compared to group C. Myocardial ATP, total adenine nucleotide, and creatine phosphate did not differ between the three groups at the end of reperfusion. Myocardial ADP and AMP declined significantly during reperfusion in group C, however, they remained unchanged in group B + L and increased in group L which showed significantly higher levels compared to group C. Left ventricular functional recovery during reperfusion was consistently better in both group L and B + L compared to group C. These results suggested that membrane stabilization prevents myocardial damage from hypothermia and cardioplegia and provides better myocardial viability and functional recovery in donor heart preservation.

Animals↗
PubMed2006

Aortic operation after previous coronary artery bypass grafting: management of patent grafts for myocardial protection.

OBJECTIVES: Aortic surgery for progressive aortic valve disease or aortic aneurysm after previous coronary artery bypass grafting (CABG) is a challenging procedure. We report the outcome of aortic reoperation after previous CABG and evaluate our management of patent grafts and our methods for obtaining myocardial protection. METHODS: From February 2001 to July 2003, 6 patients with progressive aortic valve disease and aneurysm of the thoracic aorta were operated on. The group comprised 3 men and 3 women with a mean age of 67.6 years. There were 4 patients with an aneurysm of the aortic arch, 1 with chronic ascending aortic dissection, and 1 with progressive aortic valve stenosis. The interval between previous CABG and aortic surgery was 74.0 +/- 44.2 months. All reoperations were performed via median resternotomy. Myocardial protection was obtained by hypothermic perfusion of patent in-situ arterial grafts following cold-blood cardioplegia administration via the aortic root under aortic cross clamping. RESULTS: The operative procedure was aortic arch replacement in 4 patients, ascending aortic replacement with double CABG in 1, and aortic valve replacement in 1. All patients survived the reoperation. Postoperative maximum creatine kinase-MB was 49.2 +/- 29.8 and no new Q-waves occurred in the electrocardiogram nor were any new wall motion abnormalities recognized on echocardiography. There were no late deaths during a follow-up of 30.7 months. CONCLUSION: Reoperative aortic procedures after CABG can be performed safely with myocardial protection via hypothermic perfusion of a patent in-situ arterial graft.

Aged↗
PubMed2003

Effects of lipoteichoic acid induced delayed preconditioning on ischemia-reperfusion injury in isolated rat hearts.

To explore the potential of lipoteichoic acid (LTA) induced cardioprotection against ischemia-reperfusion (I/R) injury in isolated rat hearts and whether endogenous nitric oxide (NO) participates in the protection, the rats were pretreated with LTA (1 mg/kg, i.p.) 24 h before the experiment, and the isolated hearts were subjected to 30 min no-flow normothermic global ischemia and 60 min reperfusion after a 20-min stabilization period by the langendorff method. Cardiac functions were evaluated at the end of stabilization, and at 30 min, 60 min of reperfusion. The amounts of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase(LDH) and total NO oxidation products in the coronary effluent were measured spectrophotometrically at the end of reperfusion. It was revealed that pretreatment with LTA could significantly improve the recovery of cardiac function, reduce the release of CK-MB and LDH, and increase the concentrations of NO in coronary effluent. The protective effects were abrogated by pretreatment of the rats with L-NAME. It was concluded that LTA could induce the delayed cardioprotection against I/R injury, and endogenous NO may be involved in the mechanisms.

Animals↗
PubMed2004

Role of heart-type fatty acid binding protein in early detection of acute myocardial infarction in comparison with cTnI, CK-MB and myoglobin.

Heart fatty acid-binding protein (H-FABP) is supposed to be the most sensitive biomarker of early acute myocardial infarction (AMI). To evaluate the diagnostic value of H-FABP for AMI in the early stage, the plasma levels of H-FABP were measured by sandwich ELISA in 93 patients with suspected AMI at admission within 6 h after onset of chest pain and 69 normal healthy subjects. The plasma concentrations of cardiac troponin-I (cTnI), creatine kinase-MB (CK-MB) and myoglobin (Mb) were assayed at the same time by using corpuscle chemiluminescence for those patients. The patients were classified as AMI group (n=32) and non-AMI group (n=61) retrospectively. The diagnostic validity was evaluated in terms of sensitivity, specificity and receiver operating characteristic (ROC) curve analysis. The results showed the cutoff value of H-FABP for AMI was 16.8 ng/ml, and its diagnostic sensitivity for AMI was 64.29% within 3 h and 84.38% within 6 h after onset of chest pain, and the diagnostic specificity for non-AMI was 100% within 3 h and 91.8% within 6 h. H-FABP had higher sensitivity than that of cTnI and CK-MB at all time points (P<0.05), whereas there was no significant difference in specificity among the four markers. But the area under the ROC curve of H-FABP was significantly greater than that of cTnI, CK-MB and Mb within 3 h. These results revealed that H-FABP possessed high diagnostic sensitivity and specificity for AMI in early stage, especially within 3 h after onset of persistent angina pectoris. In conclusion, H-FABP can be used as a sensitive marker for AMI in the early stage.

Angina Pectoris↗
PubMed2000

Variation of perioperative blood cTnT levels in patients undergoing cardiopulmonary bypass and its clinical implication.

The clinical value of cardiac Troponin T (cTnT) as a marker in assessing myocardial cell damage in the patients undergoing open heart surgery was studied. Serum cTnT and CK-MB levels were measured in serial blood samples from 20 patients undergoing open heart surgery before operation, at aorta clamping, aorta opening, the end of CPB and the operation, and subsequently one h, one day, 3 days and one week after operation respectively. Ten patients receiving thoracic surgery were also subjected to the measurement of cTnT and CK-MB before and 24 h after operation. The results showed that peak concentrations were reached earlier in cTnT than in CK-MB, and the circulation cTnT remained high when CK-MB had already decreased to normal. In 10 patients receiving thoracic surgery, cTnT level was normal and CK-MB was increased in 4 patients after surgery. It was concluded that the sensitivity and specificity of cTnT was more than those of CK-MB and cTnT could be used as a routine indicator for myocardiac protection.

Adolescent↗