UMLS:C0002962 - FACTA Search

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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated different diagnostic strategies for the early diagnosis of acute myocardial infarction, combining sensitivity and specificity of different markers evaluated singly and using combination testing in parallel and serial modes. Myoglobin, cardiac troponin I (TnI), creatine kinase (CK), and CK-MB mass were tested in blood samples from 26 patients with acute myocardial infarction collected at admission (T0; mean = 3.3 hours from the onset of chest pain) and 3 and 6 hours later. The comparison group was made up of 70 patients with renal failure, skeletal muscle diseases, stable angina, unstable angina, and chest pain of nonischemic origin. Single tests showed different sensitivities in relation to the different release kinetics; myoglobin was the most sensitive (69% at T0) although less specific (46%), and TnI showed the highest specificity (90%) and a sensitivity of 54%. Combination testing in a parallel mode using myoglobin and TnI or CK-MB had the same sensitivity and specificity as myoglobin tested singly. The best combination in a serial mode is myoglobin and TnI (at T0 sensitivity, 54%; specificity, 98%), as confirmed by the analysis of the positive predictive value, the negative predictive value, and the accuracy evaluated as a function of different disease prevalences.
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PMID:Strategies for the early diagnosis of acute myocardial infarction using biochemical markers. 1076 62

There is little information about the relation between mild cardiac troponin I (cTn-I) increase after coronary interventions and late outcome. We therefore focused on the long-term outcome and the clinical, morphologic, and procedural correlates of elevation of cTn-I compared with cardiac troponin T, creatine kinase (CK), CK-MB activity and mass, and myoglobin in 105 patients with successful elective percutaneous transluminal coronary angioplasty (PTCA) for stable or unstable angina. Patients with myocardial infarction and those with unstable angina who had a detectable increase in serum markers before PTCA were excluded. Markers were measured before and after the procedure and for 2 days. Patients were followed up to record recurrent angina, myocardial infarction, cardiac death, repeat PTCA, or elective coronary artery bypass graft surgery. Procedure success was achieved in all cases. Elevation in cTn-I (> or =0.1 microg/L) was observed in 23 of 105 patients (22%) (median peak: 0.25 microg/L); 18% had cardiac troponin T (cTn-T) release (> or = 0.1 microg/L, median peak 0.21); 11.4% CK-MB mass (> or =5 microg/L), and 7.6% myoglobin (> or =90 microg/L) release. Five and 2 patients had elevated CK and CK-MB activity, respectively. Fourteen of 18 patients with cTn-T elevation had a corresponding elevation in cTn-I (kappa 0.68; p = 0.001). Patients positive for cTn-I had more unstable angina (p = 0.042) and heparin before PTCA (p = 0.046), and had longest total time (p = 0.004) and single inflation (p = 0.01). By multivariate logistic regression, predictors of postprocedure cTnI elevation were maximum time of each inflation (odds ratio 9.2; p = 0.0012), type B lesions (odds ratio 6.6; p = 0.013), unstable angina (p = 0.041), and age > or =60 years (p = 0.032). Clinical follow-up was available in 103 patients (98%) (mean 19+/-10 months). Kaplan-Meier survival analysis showed that cTn-I elevation was not an important correlate of cardiac events (p = 0.34, by log-rank analysis). The incidence of recurrent angina, myocardial infarction, cardiac death, and repeat revascularization after 12 months was not different in patients positive or negative for cTn-I. We conclude that cTn-I elevation after successful PTCA is not associated with significantly worse late clinical outcome. Levels of cTn-I allow a much higher diagnostic accuracy in detecting minor myocardial injury after PTCA compared with other markers, but there is no association with periprocedural myocardial cell injury and late outcome when cTn-I and other markers are considered.
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PMID:Relation of minor cardiac troponin I elevation to late cardiac events after uncomplicated elective successful percutaneous transluminal coronary angioplasty for angina pectoris. 1040 51

Serum cardiac troponin I-values were compared to conventionally obtained diagnosis in 319 consecutive patients suspected of having myocardial infarction, of which 46 patients were given this diagnosis. All patients with troponin I > 20 micrograms/l (n = 40) also had abnormal creatine kinase and abnormal creatine kinase isoenzyme MB activity. All patients with troponin I values in the range 1.0-19.9 micrograms/l (n = 50) had a diagnosis of heart disease (myocardial angina pectoris, myocardial infarction, arrythmia, heart insufficiency). In this patient group, the creatine kinase measurements showed pathological values in only 12 cases. Troponin I seems to be a sensitive indicator of cardiac cell injury, and measurements of troponin I seems to be useful in ruling out cardiac injury.
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PMID:[Measurement of troponin I levels in suspected myocardial infarction]. 1059 46

The detection of cardiac troponin I(cTnI), including serum or plasma, was evaluated in 114 patients with ischemic heart diseases or other heart diseases. The results were that the sensitivity of cTnI detection(qualitative analysis, cutoff is 0.2 ng.ml-1) was higher than that of creatine kinase(CK), creatine kinase-MB(CK-MB), alpha-hydroxybutyrate dehydrogenase(alpha-HBD), lactic dehydrogenase(LDH), and aspartic transaminase(AST) for diagnosing acute myocardial infarction (AMI) (93.2% vs 68.2%, 68.2%, 65.9%, 65.9%, and 75.0%; P < 0.05; respectively). The specificity of cTnI detection was higher than that of alpha-HBD, LDH, and AST(95.2% vs 81.0%, 73.8%, and 54.0%; P < 0.05; respectively) and similar to CK and CK-MB(95.2% vs 83.3% and 83.3%; P > 0.05; respectively). On the other hand, the sensitivity of cTnI in patients with unstable angina pectoris was 45.5%. It was higher than stable angina pectoris and lower than AMI. The results suggest that the cardiac troponin I is a better cardiac injury marker than other cardiac markers for diagnosing AMI.
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PMID:[Clinical evaluation of cardiac troponin I in ischemic heart diseases]. 1080 70

Programmed myocyte cell death and activation of the immune system have been shown to occur in patients with congestive heart failure. Besides, unstable angina episodes are likely to be associated with immune activation. Our aim was to evaluate the role of changes in circulating levels of soluble Fas (sFas), suggestive of an enhanced inhibitory response to ongoing apoptosis, and soluble IL2 receptor (sIL2-R), indicative of T-lymphocyte activation, in chronic heart failure and unstable angina pectoris. Thirty patients affected by chronic heart failure (20 idiopathic and 10 ischemic cardiomyopathy) and 13 patients with unstable angina were evaluated. Twenty healthy individuals matched for age and gender were used as controls. A complete biochemical determination of indexes of myocardial damage including cardiac troponin I (cTnI) and creatine kinase (MB/CK) was performed. The results demonstrated that mean levels of sFas and sIL2-R were significantly increased in patients affected by chronic heart failure and unstable angina and were not associated with changes in renal function or with serum levels of cTnI. Highest values of sFas were found in NYHA class IV patients (IV NYHA class = 7.39 +/- 0.52 vs. controls = 1.34 +/- 0.12 ng/ml; P < 0.01) and more elevated in idiopathic than in ischemic cardiomyopathy (3.64 +/- 0.40 vs. 1.82 +/- 0.37 ng/ml; P < 0.01). Moreover, in chronic heart failure patients sFas and ejection fraction were negatively correlated (P = 0.01), whereas sFas and sIL2-R were positively correlated (P < 0.01). In unstable angina patients too, sFas and sIL2-R appeared to be correlated (P = 0.03); whereas sFas (angina group = 3.18 +/- 0.39 vs. controls = 1.34 +/- 0.12 ng/ml; P < 0.01) and sIL2-R (angina group = 0.46 +/- 0.11 vs. controls = 0.00 UI/ml; P < 0.01) were higher in angina group than in controls. In most of the cases, the increase of sFas was associated with comparable changes in sIL2-R serum levels, indicating that the activation of Fas system is strictly associated with autoimmune-inflammatory reactions. This phenomenon, both in chronic heart failure and in unstable angina, occurs in the absence of biochemical evidences of myocardial damage and seems to parallel the activation of T cell. Soluble Fas could have a role in sustaining inflammatory response and in prolonging the detrimental effects correlated with it in chronic heart failure and angina pectoris.
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PMID:Soluble antiapoptotic molecules and immune activation in chronic heart failure and unstable angina pectoris. 1082 61

The detection of cardiac troponins in peripheral blood as protein markers of myocardial infarction is a new diagnostic tool in the diagnosis of cardiac disease. In order to increase the sensitivity and specificity of this diagnostic approach, a reverse transcription polymerase chain reaction assay has been developed to detect the mRNA encoding cardiac troponin I from myocardial cells hypothetically released from damaged cardiac tissue. The detection is specific for cardiac troponin I mRNA, with no amplification of homologous sequences of other troponin I isoforms, i.e., troponin I from skeletal muscle cells. However, a strong amplification signal for cardiac troponin I mRNA was detected in samples of peripheral blood from healthy human volunteers. In patients with acute myocardial infarction or angina pectoris, the cardiac troponin I mRNA levels were not increased over background levels. In conclusion, a reverse transcription polymerase chain reaction approach based on the amplification of cardiac troponin I mRNA is not feasible in the diagnosis of cardiac diseases.
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PMID:High background levels compromise the use of cardiac troponin I RNA detection in peripheral blood as a diagnostic tool in cardiology. 1098 26

A number of cardiac interventional procedures are available for the treatment of angina, including percutaneous transluminal coronary angioplasty (PTCA), stent insertion and rotational atherectomy (RA). Variable degrees of myocardial cell injury during PTCA and stent insertion have been observed, based on rises in creatine kinase MB isoenzyme (CK-MB) and cardiac troponin T (cTnT) 6-24 h post-procedure. As there are many variations in technique within each procedure it would be helpful to be able to determine objectively the degree of myocardial damage in order to optimize technique. We measured CK-MB, cTnT and cardiac troponin I (cTnI) to ascertain which is the most sensitive marker for minor myocardial damage in this setting. Blood samples were taken both before and 6, 14 and 24h after the procedure in 109 patients (77 men) with angina, 42 of whom had unstable angina. Of the 109 patients, 86 had a stent inserted (21 as a primary stent), nine had PTCA, eight had RA and six intracoronary brachytherapy. Using the manufacturers' recommended cut-offs--CK-MB 4 microg/L, cTnI and cTnT 0.1 microg/L--five patients were excluded from further analysis as all three markers were raised pre-procedure. Post procedure all three markers were in agreement for 68 patients (44 all normal, 24 all raised). Overall, CK-MB was raised in 28 patients, cTnT in 38 and cTnI in 58. In 19 patients CK-MB and cTnT were normal, but cTnI was raised (15 between 0.11 and 0.30 microg/L). cTnI was the most sensitive indicator of minor myocardial damage, but at the recommended cut-off of 0.1 microg/L may be overly sensitive. We await the results of our follow-up study to determine the clinical implications of these small rises in cTnI.
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PMID:Comparison of cardiac troponin T and I and CK-MB for the detection of minor myocardial damage during interventional cardiac procedures. 1108 20

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after apparently successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatine kinase (CK) and its isoform, creatine kinase-MB (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 50 consecutive patients with stable angina undergoing visually successful PTCA with stenting (n = 35) or without stenting (n = 15). Cardiac TnI, cTnT, CK and CKMB levels were measured before and 6, 24, and 48 hours after the procedures was performed. None of the patients had abnormal cTnI or cTnT levels, CK activity, or CKMB levels before the procedures. Moreover, no patient showed electrocardiographic evidence of myocardial infarction. 13 patients (26%) had abnormal peak values of one or more markers at 24 hours after coronary intervention. Troponin I was elevated in 10/35 patients after coronary stenting (29%) and in 2/15 patients after PTCA (13%) (P = 0.327). Troponin T was elevated in 6 patients (17%) and CKMB activity was elevated in 3 patients (9%) of the coronary stenting group. CTnI was more significant than CKMB (P = 0.023) in detecting minor myocardial injury. When compared with cTnI and CKMB, cTnT did not reach significance (P = 0.129 and 0.489, respectively). 5 out of the 13 patients with abnormal markers (38%) developed side branch occlusion after stenting. In conclusion, cTnI was a very sensitive marker in detecting minor myocardial injury after coronary angioplasty with or without stenting. The frequency of increased serum levels of cardiac troponins was higher in patients undergoing stent implantation than in those treated with angioplasty alone but did not reach significance. Side branch occlusion may have accounted for some, but not all, periprocedural minor myocardial injury in the stent group.
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PMID:Detection of minor myocardial injury after successful percutaneous transluminal coronary angioplasty with or without stenting. 1120 96

An analytical and clinical evaluation of cardiac troponin I (cTnI) on the IMMULITE system is presented. The assay results were compared with those of the Stratus II and the Dimension RxL-HM. A between-run imprecision CV < 20% was found at a cTnI concentration of 0.23 microg/L (functional limit of detection). On the basis of a reference study including 215 patients without ischemic heart disease (97.5th percentile: 0.294 microg/L) and 36 patients clinically classified as having stable angina pectoris (<0.22 microg/L) a preliminary cutoff level of 0.3 microg/L was defined. Assay linearity, sample stability, influence of sample material and method comparison studies were performed. In patients with Duchenne's disease, chronic hemodialysis treatment, pulmonary embolism, coronary artery bypass surgery and minimally cardiac surgery the cTnI results of the IMMULITE agreed better with the Dimension RxL-HM than with the Stratus II data. Of 142 samples from patients with unstable angina 67 samples were classified as cTnI positive with the IMMULITE, 76 with the Dimension RxL-HM, and 62 with the Stratus II. In conclusion, the new assay is sensitive for the determination of cTnI and easy to perform within 45 min.
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PMID:Comparison of diagnostic performance of cardiac troponin I on the IMMULITE system with other automated troponin I assays in minor myocardial damage. 1138 9

Cardiac troponins are sensitive and specific markers for the detection of minor myocardial injury. However, they have been rarely used to monitor myocardial injury after coronary stenting. The purpose of the study was to measure cardiac troponin I (cTnI) and cardiac troponin T (cTnT) levels after elective uncomplicated successful percutaneous transluminal coronary angioplasty (PTCA) with or without coronary stenting and to compare their results with serum creatinine kinase MB isoenzyme (CKMB). CTnI and cTnT levels were compared with those of CK or CKMB in 98 consecutive patients with stable angina undergoing elective uncomplicated successful PTCA with stenting (n = 71) or without stenting (n = 27). Markers were measured before and 6, 12, 24, and 48 hr after the procedure. Peak postprocedural levels for each marker were compared and related to angiographic and procedural characteristics as well as to the occurrence of side-branch occlusion. None of the patients had abnormal markers before the procedure. Abnormal postprocedural values of one or more markers were observed in 28 patients (29%), 23 after stenting and 5 after PTCA alone. The frequencies of abnormal cTnI and cTnT levels were significantly higher than that of CKMB after coronary intervention (26% and 18% vs. 7%; P = 0.00016 and 0.015, respectively), with cTnI being the most significant. When compared with troponin-negative patients, abnormal cardiac troponin values were significantly related to total time of inflation (223 +/- 128 vs. 170 +/- 105 sec; P = 0.008) and inflation maximal pressure (12.9 +/- 2.3 vs. 12.0 +/- 2.7 atm; P = 0.04). Small side-branch occlusion was noticed in 36% of the troponin-positive patients and in 6% of the troponin-negative group (P = 0.00047). In conclusion, minor myocardial injury is not uncommon after elective uncomplicated successful PTCA with or without stenting. Cardiac troponins, especially cTnI, are more sensitive than CKMB for the detection of this minor myocardial injury. Total time of inflation and inflation maximal pressure are predictors of postprocedural elevation of cardiac troponins. Side-branch occlusion may account for some, but not all, periprocedural minor myocardial injury.
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PMID:Minor myocardial injury after elective uncomplicated successful PTCA with or without stenting: detection by cardiac troponins. 1138 2

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