Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to evaluate the efficacy of the newly developed Troponin T (TNT) enzyme immunoassay for predicting the prognosis of patients with angina pectoris. TNT, creatine kinase (CK) and MB isoenzyme of creatine kinase (CK-MB) were monitored in 134 patients with angina pectoris. There was no abnormality with any of these tests in 40 patients with stable angina pectoris and 30 patients with unstable angina pectoris of Class 1 and 2 according to Braunwald's criteria. None of them developed acute myocardial infarction or other cardiac events. Elevation of TNT concentration with normal level of CK and CK-MB was found in 34 of the 64 cases of unstable angina pectoris of Class 3. Among the 34 patients, 11 had acute myocardial infarction within 10 days during hospitalization. In contrast, only one of the patients with unstable angina pectoris of Class 3 with normal value of TNT developed acute myocardial infarction. As the incidence of angina pectoris is quite high clinically but only a small number of patients developed myocardial infarction, it is necessary to have a new assay of high sensitivity and high negative predictive value. TNT determination could meet these requirements as it had high sensitivity (92%) and high negative predictive value (98%) for the prognosis of unstable angina pectoris. If there is no rise of circulating TNT level, a favorable outcome can be expected with a high degree of probability. Determination of serum TNT level would be adopted as a routine procedure for evaluating the prognosis of angina pectoris and it is superior to other enzyme tests such as CK and CK-MB.
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PMID:Prognostic efficacy of troponin T measurement in angina pectoris. 758 97

The diagnostic performance of a new enzyme linked immunosorbent assay for the cardiac structural protein troponin T in the differential diagnosis of ischaemic cardiac damage was assessed. A well documented set of patients admitted to the coronary care unit of a district general hospital were studied. At a cutoff value of 0.2 micrograms/L, troponin T measurements 12-24 h after admission or 12-16 to 24-48 h from onset of chest pain showed an overall efficiency of 97.6% for diagnosis of proven myocardial infarction. Troponin T was not detectable in patients when ischaemic heart disease could be excluded but was present in four patients with angina. Detectable troponin T in these angina patients was associated with subsequent cardiac events.
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PMID:Troponin T for the differential diagnosis of ischaemic myocardial damage. 843 60

Troponin T (TpT) is a protein implicated in skeletal muscle contractions, including myocardium. It was shown that the presence of troponin TpT in unstable angina patients' blood is associated with poor prognosis. In the present study amongst 25 patients with unstable angina 12 were found to have TpT present in their blood. TpT concentration was higher in patients with III and IVo CCS symptoms in comparison with class I and IIo CCS symptoms: 0.207 +/- 0.275 and 0.144 +/- 0.186 ng/mL respectively (p = 0.053; nonparametric Kolmogorow-Smirnov test). Patients were subjected to percutaneous transluminal coronary angioplasty (PTCA). After 3 months of follow up 17 patients (the rest of them dropped out) were assigned to two groups: A (n = 8)--without and B (n = 9)--with clinical and electrocardiographic signs of restenosis. Retrospective analysis revealed the presence of TpT before PTCA in 6 group B patients and 2 group A patients. Relative risk of stenocardia recurrence was calculated as 2.25. TpT was present in the blood of 20 patients in the first 24 hours after PTCA, and group B patients had higher mean TpT concentration; that could result from reperfusion of more ischaemic myocardium. It seems that the presence of TpT in unstable angina patients' blood may be an important factor characterizing patients with more serious prognosis.
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PMID:[Troponin T--is it a marker of restenosis after transluminal percutaneous angioplasty in unstable angina patients?]. 1059 26

It is still uncertain to what extent PTCA contributes to a rise of the myocardial ischemic marker troponin T. The purpose of this study was to determine the release of troponin T in patients with unstable and stable angina pectoris pre- and post-PTCA. Serial troponin T measurements were performed in 66 patients with unstable angina (group A) and 55 patients with stable angina pectoris (group B) pre-PTCA and 4, 8 and 24 hours post-PTCA. In group A, 39 (59%) patients with unstable angina pectoris showed pathologic troponin T concentrations (troponin T > or = 0.1 ng/ml); in 27 (41%) patients already pre-PTCA the troponin T was elevated beyond the normal values. Medians of troponin T rose from initially 0.045 ng/ml pre-PTCA to a maximum of 0.21 ng/ml 8 hours post PTCA. In group B medians of troponin T were at all times within normal limits; there was no rise in the observation interval. Using the Chi-square test there were statistically significant differences between group A and B regarding the troponin T values pre- and post-PTCA. In group A medians of total creatine kinase ranging between 24 U/L and 30 U/L were to all times within normal limits. Also in group B medians of total creatine kinase were always within normal limits. Statistically significant differences between the two groups could not be shown. Our study could show a difference in the periinterventional course of the ischemic marker troponin T in patients with unstable and stable angina pectoris. The data indicate a PTCA induced reversible ischemia of the cardiac muscle cell with additional release of the cytoplasmatic bound part of troponin T in patients with unstable angina pectoris. Troponin T also appears to be a more sensitive marker of very short myocardial ischemia than creatine kinase.
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PMID:[Release of troponin T following PTCA in patients with unstable and stable angina pectoris]. 1064 59

Patients with chest pain represent an inhomogeneous group with greatly varying severity of coronary artery disease and cardiac risk. The proper selection of different treatment strategies in these patients requires reliable risk assessment. Patients with definitive myocardial infarction: in patients with ST-segment elevation on ECG, a positive troponin T (cTnT) on admission identifies a group of patients having a threefold higher mortality rate than patients with a negative cTnT test. The differences in risk based on cTnT are found for patients treated with thrombolytic as well as mechanical recanalization therapy. These differences in mortality based on admission cTnT may be explained by more severe coronary artery disease, worse left ventricular function, and less efficient microvascular reperfusion in the cTnT-positive patients. Patients with rest angina: in patients with angina at rest, a positive cTnT value on admission identifies a subgroup having a threefold higher cardiac event rate than cTnT-negative patients. The cTnT-positive patients seem to benefit from treatment with low molecular weight heparin and fibrinogen receptor antagonists, while cTnT-negative patients do not. The differences in risk and response to therapy may be due to more severe coronary artery disease, more critical coronary artery stenoses, and a higher rate of intracoronary thrombus formation in the cTnT-positive versus negative patients. Low risk chest pain patients: in low risk chest pain patients, (i.e. no rest angina, no ECG-changes) cTnT-positive patients on admission have a twofold higher cardiac event rate than cTnT-negative patients. The proper treatment strategy for the low risk cTnT-positive patients remains to be determined. Troponin T versus troponin 1: many of the findings on cTnT also relate to troponin I. However, there is a high interassay variability of troponin I assays, which has to be taken into consideration.
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PMID:Risk stratification and therapeutic decision making in patients with acute coronary syndrome--the role of cardiac troponin T. 1072 19

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

Release of cardiac enzymes has been reported in patients with stable angina who undergo elective percutaneous coronary intervention (PCI) and has been associated with adverse clinical outcomes. The aim of the present study was to investigate whether impaired microvascular integrity can be detected using myocardial contrast echocardiography in patients undergoing elective PCI, and whether it is related to the extent of postprocedural troponin T elevation. We investigated consecutive patients with stable angina (n = 19) who were scheduled for elective angioplasty with stent placement. Myocardial contrast echocardiography was performed before and 2 to 4 hours and 24 hours after coronary intervention. Contrast images were analyzed visually and quantitatively measuring the peak signal intensity (A) and the slope of the signal intensity rise (beta) in 16 myocardial segments. The product of A x beta was calculated in each segment to estimate the regional myocardial blood flow. Troponin T was collected serially before and 2 to 4 hours and 24 hours after PCI. Five patients (26%) had elevated troponin T 24 hours after PCI (range 0.03 to 0.46 microg/L). Eight patients (42%), including all 5 patients with elevated troponin T levels, demonstrated impaired microvascular integrity 2 to 4 hours after PCI in >or=2 myocardial segments (range 2 to 4) within the perfusion territory of the target vessel. Of the 11 patients without evidence of impaired myocardial perfusion by myocardial contrast echocardiography, none had elevated troponin T levels at follow-up. Quantitative analysis of myocardial blood flow showed that impaired perfusion after PCI was partially reversible. Thus, A x beta had decreased significantly at 2 to 4 hours after PCI (3.4 +/- 1.6 vs 8.8 +/- 3.4 dB/s baseline, p <0.01), reincreased after 24 hours (6.4 +/- 2.3 dB/s at 24 hours vs 3.4 +/- 1.6 dB/s at 2 to 4 hours, p <0.01), but did not return to baseline (8.8 +/- 3.4 dB/s at baseline vs 6.4 +/- 2.3 dB/s at 24 hours, p <0.01). The perfusion defect size 2 to 4 hours after PCI was closely related to the troponin T levels after 24 hours (r(2) = 0.80, p <0.0001). In conclusion, impaired microvascular integrity is partially present in patients with stable angina who undergo elective PCI, is partially reversible, and is closely related to the release of troponin T. Because judgment of interventional success has shifted downstream to tissue level perfusion, myocardial contrast echocardiography may be useful to monitor such alterations in myocardial tissue perfusion.
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PMID:Usefulness of real-time myocardial perfusion imaging to evaluate alterations of myocardial blood flow in patients with stable angina pectoris undergoing elective percutaneous coronary interventions. 1618 10

The purpose of this study was to investigate whether thyroid hormone levels have any predictive value for mortality in patients presenting to the emergency department with acute myocardial infarction (AMI). Three groups of patients admitted to the emergency department within the 11-month study period were considered eligible: 95 patients with chest pain and proven AMI, 26 patients with chest pain and no AMI, and 114 patients who served as controls with no evidence of any major disease. Cardiac enzymes and the following thyroid hormones were analyzed and compared between groups, regarding effects of historical and demographic factors: thyrotrophin, free triiodothyronine (FT3), total triiodothyronine (TT3), free thyroxine (FT4), and total thyroxine (TT4). Sixteen patients with AMI (16.8%) died within the study period. Troponin T and creatine kinase-B with an M-type subunit levels were significantly higher in the nonsurvivors when compared with survivors. Survivors in the AMI group had higher TT3, TT4, and lower FT4 levels, while the nonsurvivors in the AMI group had higher thyrotrophin and lower TT3, FT3 and FT4 levels than controls. In the AMI group, the nonsurvivors had lower TT3 and FT3 levels than the survivors. A history of diabetes mellitus and/or angina, TT3, or FT3 was an independent predictor of mortality. TT3 and FT3 appear to be independent prognostic factors in patients with AMI.
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PMID:Prognostic value of thyroid hormone levels in acute myocardial infarction: just an epiphenomenon? 1633 Sep 14

We describe a case of a 41-year-old female patient who was admitted with typical signs of thrombotic-thrombocytopenic purpura. Markers of myocardial ischemia (Troponin T, CK, CK-MB) were even present at admission without symptoms of angina pectoris. Only a few hours after admission the patient developed all signs of cardiogenic shock with subsequently cardiac arrest. Postmortal coronary angiographies showed occlusions in all coronary arteries with significant myocardial necrosis. We are unaware of any report that describes macrovascular occlusions in thrombotic-thrombocytopenic purpura.
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PMID:Extensive coronary thrombosis in thrombotic-thrombocytopenic purpura. 1702 82

A 65-year-old man had been medically treated under a diagnosis of ulcerative colitis for 12 years as an outpatient at another facility. Two weeks before admission, he complained for the first time of mild chest pain limited to exertion. He was seen again by his previous physician in the morning and admitted to that facility later that day. Laboratory findings showed elevated serum creatine kinase (CK) at that time, so non-ST-elevated acute coronary syndrome was suspected and the patient was referred to our hospital. On admission, CK-MB was elevated but troponin T was negative. No findings of myocardial damage were observed during the admission period. Elective coronary angiography was performed and the diagnosis was effort angina pectoris. Elevated CK activity persisted but was not cardiogenic and instead due to the presence of elevated macro CK-1 associated with ulcerative colitis. Troponin T and isoenzyme electrophoresis were highly specific for the differential diagnosis of non-cardiogenic elevated CK.
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PMID:[Differentiation of acute coronary syndrome and ulcerative colitis as causes of elevated macro creatine kinase in a patient with effort angina pectoris: a case report]. 1713 24


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