Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 sought to identify differences in coronary anatomic pathology in patients with unstable angina and elevated versus nonelevated serum troponin T values. Previous studies have shown a worse prognosis in unstable angina patients with elevated serum troponin T values. Consecutive patients (n = 117) with Braunwald class IIIB angina were included in the study. Serum samples for troponin T were obtained at admission and every 6 to 8 hours for 18 to 24 hours. Acute myocardial infarction was excluded by routine creatine kinase measurements. All patients underwent coronary angiography before discharge. Cardiac events including cardiac death and myocardial infarction were recorded. Two thirds of the patients with unstable angina had no increase in serum troponin T (<0.1 microg/L) (n = 80). They had a lower incidence of 3-vessel disease (26% vs 46%, p <0.001), left main disease (5% vs 16%, p = 0.04), visible thrombus (4% vs 22%, p = 0.006), and less severe stenosis of the culprit artery (65% vs 84%, p <0.004) than patients with elevated serum troponin T values (> or =0.1 microg/L) (n = 37). The 1-year cardiac event rate was 0% versus 19% in patients with troponin T values <0.1 microg/L compared with patients with serum troponin T values > or =0.1 microg/L (p <0.0001). It was concluded that patients with unstable angina and no release of troponin T have less severe coronary artery disease, and have an excellent prognosis. It is suggested that these patients may be managed more conservatively and without invasive evaluation before discharge.
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PMID:Coronary angiographic findings and troponin T in patients with unstable angina pectoris. 1075 18

Unstable angina is a critical phase of coronary heart disease with widely variable symptoms and prognosis. A decade ago, a classification of unstable angina based on clinical symptoms was introduced. This system was then validated by prospective clinical studies to correlate with the prognosis and was linked to angiographic and histological findings. It has been used to categorize patients in many large clinical trials. In recent years, the pathophysiological roles of platelet activation and inflammation in unstable angina have been elucidated. Subsequently, improved markers of myocardial injury, acute-phase proteins, and hemostatic markers that may be associated with clinical outcomes have been identified. Particularly, cardiac-specific troponin T and troponin I have been shown to represent the best predictors of early risk in patients with angina at rest. Accordingly, it is suggested that the original classification be extended by subclassifying one large group of unstable angina patients, ie, those with angina at rest within the past 48 hours (class IIIB), into troponin-positive (T(pos)) and troponin-negative (T(neg)) patients. The 30-days risk for death and myocardial infarction is considered to be up to 20% in class IIIB-T(pos) but <2% in class IIIB-T(neg) patients. Initial results suggest that troponins may function as surrogate markers for thrombus formation and can effectively guide therapy with glycoprotein IIb/IIIa antagonists or low-molecular-weight heparins. These observations provide additional impetus for adding the measurement of these markers to the clinical classification and represent a novel concept of treating these high-risk patients.
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PMID:A classification of unstable angina revisited. 1088 Apr 24

This article summarizes the design and findings -- both at 3 months and at 1 year follow-up -- of the Fragmin during Instability in Coronary Artery Disease (FRISC) II trial. This multicentre randomized trial compared both an early invasive with an early non-invasive stategy, and prolonged treatment with dalteparin as opposed to placebo, in patients with unstable coronary artery disease. The results show that an early invasive strategy with coronary angiography and, if appropriate, revascularization procedures within 7 days after admission reduces the subsequent rate of mortality and myocardial infarction. The benefits of the invasive treatment were noticeably more marked in patients with any high-risk indicator -- for example, male gender, age above 65 years, previous severe angina, or signs of ischaemia (ST depression on ECG) or of myocardial damage (elevated levels of troponin T). Treatment with dalteparin reduced the risk of death and myocardial infarction in high-risk (i.e. troponin-positive) patients, particularly during the first month of treatment. However, continuation with dalteparin therapy after revascularization procedures conferred no benefit. It is concluded that extended treatment with dalteparin is useful as a bridge to revascularization in this high-risk subgroup of patients with unstable coronary artery disease.
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PMID:Low-molecular-weight heparin as a bridge to timely revascularization in unstable coronary artery disease -- an update of the Fragmin during Instability in Coronary Artery Disease II Trial. 1125 53

We evaluated the chemiluminescence immunoassays for the detection of the cardiac markers troponin I, myoglobin and CK-MB on the IMMULITE System (Diagnostic Products Corporation) in comparison to the same analytes of other companies. The IMMULITE assays are two-site solid phase immunometric assays using a murine monoclonal capture antibody on the solid phase and a polyclonal antibody conjugated with alkaline phosphatase (except CK-MB monoclonal, murine) for detection. Precision was investigated using serum pools with a low, a cutoff and a high concentration of the respective analyte. The results were satisfactory with an intra-assay precision coefficient of variation, CV of 1.7% - 3.2% for troponin I, 2.6% - 5.1% for myoglobin, 2.7% - 5.3% for CK-MB and an interassay precision of 5.1% - 6.9% for troponin I, 5.7% - 7.3% for myoglobin and 3.8% - 8.4% for CK-MB. In linearity studies with various dilution steps, a mean value of 105% was found for troponin I, 103% for myoglobin and 117% for CK-MB. The average recovery was 85% for troponin I, 100% for myoglobin and 95% for CK-MB. The clinical validity of the assays in the diagnosis and therapy of myocardial infarction was investigated in 120 patients who were sent to the hospital with suspected myocardial infarction. Four hours after admission all patients with clinically verified myocardial infarction showed troponin I and troponin T values above the cutoff value. A maximum rate of 32% of the patients (IMMULITE Troponin I) with an instable angina pectoris showed troponin values above the cutoff for myocardial infarction (1.0 microg/L), 4 hours after admission. A cutoff-reduction to 0.2 pg/L for troponin I increased the number of patients to 45%. The negative predictive value was constantly 67%. The results obtained by IMMULITE assays were compared to the Elecsys cardiac assays (Roche Diagnostics) and the AxSYM-cardiac assays (Abbott Diagnostics). The highest correlation (r = 0.99) was found for IMMULITE Troponin I (DPC) and Troponin I (Abbott). The Abbott-Troponin I showed the highest diagnostic sensitivity within 4 hours after admission. All compared methods showed a similar diagnostic sensitivity (close to 100%) > 4 hours after admission. For all investigated methods the percentage of discrepant results decreased to a minimum 4 hours after admission.
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PMID:Evaluation of the chemiluminescence immunoassays for the measurement of troponin I, myoglobin and CK-MB using the IMMULITE system in comparison to other measuring systems. 1193 24

Elevated C-reactive protein (CRP) can identify patients with coronary artery disease who are prone to future acute events. We investigated whether elevated CRP is related to the activation of the terminal complement cascade in 66 patients with unstable angina pectoris (UAP), in 45 patients with stable angina pectoris, and in 42 controls. CRP, additional acute phase reactants, the terminal complement complex (sC5b-9), leukocytes, and troponin T were measured. In 47 patients with UAP the CRP values were regarded as elevated (>0.3 mg/dl). In patients with UAP and elevated CRP, the plasma levels of sC5b-9 were markedly higher than in patients with UAP and lower CRP (245 +/- 14 vs 188 +/- 19 ng/ml, p <0.02) and in patients with stable angina pectoris with slightly (0.4 +/- 0.1 mg/dl) increased CRP (sC5b-9 173 +/- 21 vs 130 +/- 7 ng/ml [controls; p <0.05]). A further acute phase reaction was present only in patients with UAP and elevated CRP already on admission (p <0.01). sC5b-9 was not related to troponin release. Thus, elevated CRP levels are associated with activation of the plaque destabilizating terminal complement system in patients with UAP during the acute phase reaction. This may explain the prognostic value of CRP in acute coronary syndromes (ACS).
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PMID:Comparison of C-reactive protein and terminal complement complex in patients with unstable angina pectoris versus stable angina pectoris. 1195 Apr 26

From the clinical standpoint a cardiomyopathy can be classified as primitive when other causes, i.e. ischemic, infiltrative, systemic diseases, can be ruled out. Initial symptoms usually include a progressive dyspnea and fatigue with tachycardia in a patient previously healthy. Congestive heart failure may be the initial manifestation. Angina is often present, not only because of coronary heart disease. Auscultatory findings usually include a gallop rhythm with a third heart sound, not rarely a four-sound gallop. Blood test to evaluate renal and liver function should be performed. The dosage of troponin I and/or troponin T, plasma renin activity, brain natriuretic peptide or endothelins has recently gained some reputation to indicate prognosis, but there is no reason to believe that these measures are superior to cardiopulmonary stress test.
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PMID:[Dilated cardiomyopathy: role of clinical and laboratory evaluation]. 1202 82

Nicorandil has been reported to have a preconditioning effect which suppresses the ST-segment shift or lactate production during coronary angioplasty in patients with stable angina pectoris. The present study investigated whether the preconditioning effect of nicorandil affects troponin T (TnT) levels after coronary angioplasty. Twenty-four patients with stable angina pectoris were randomized to receive a 1-minute intravenous infusion of nicorandil (100 microg/kg) or normal saline. Five minutes later they underwent three 2-minute balloon inflations 5 minutes apart. The sum of ST-segment elevation in all leads (Sum-ST) was determined at the end of each balloon inflation. Serum levels of TnT were measured 6 and 18 hours after the procedure, and the higher value of the two measurements was compared between the groups. SumST decreased progressively during the three sequential balloon inflations in both groups and was less in the nicorandil group than in the control group. The TnT level after the procedure was significantly lower in the nicorandil group than in the control group (0.05+/-0.05 vs 0.11+/-0.10 ng/mL). In conclusion, pretreatment with intravenous nicorandil suppresses TnT release after coronary angioplasty as well as ST-segment elevation during coronary angioplasty, suggesting pharmacological preconditioning by nicorandil.
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PMID:Nicorandil-induced preconditioning as evidenced by troponin T measurements after coronary angioplasty in patients with stable angina pectoris. 1245 2

Unstable coronary artery disease is in most cases associated with plaque rupture, activation of the coagulation system and subsequent intracoronary thrombus formation which may cause myocardial cell damage. The aim of the present analysis was to assess the relation between troponin T, markers of coagulation activity, i.e. prothrombin fragment 1+2, thrombin-antithrombin complex, soluble fibrin and D-dimer, and ischemic events, i.e. death, myocardial (re-)infarction or refractory angina. 320 patients with unstable coronary artery disease were randomized to 72 hours infusion with inogatran, a low molecular weight direct thrombin inhibitor, or unfractionated heparin. Patients with elevated troponin levels had higher levels of prothrombin fragment 1+2, soluble fibrin and D-dimer before, during, and at 24 hours after cessation of anticoagulant treatment. These troponin-positive patients tended to have worse short-term clinical outcome, without relation to markers of coagulation activity. Troponin-negative patients with unchanged or early increased thrombin generation during treatment had a cluster of ischemic events within 24 hours after cessation of the study drug. The 30-day ischemic event rate was 19 % in troponin-negative patients with unchanged or early increased prothrombin fragment 1+2, and 5.7 % in patients with decreased prothrombin fragment 1+2, p=0.006, and similarly 15 % in troponin-negative patients with unchanged or early increased thrombin-antithrombin complex and 4.5 % in patients with decreased thrombin-antithrombin complex, p=0.02. In conclusion, in unstable coronary artery disease a troponin elevation indicates higher risk and higher coagulation activity. However, among the troponin negative patients, with a lower risk and lower coagulation activity, a part of the patients seem to be non-responders to treatment with a thrombin inhibitor expressed as unchanged or raised coagulation activity and a raised risk of ischemic events early after cessation of treatment.
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PMID:Myocardial damage, coagulation activity and the response to thrombin inhibition in unstable coronary artery disease. 1496 Nov 68

Nicorandil, ATP sensitive potassium channel opener, is shown to reduce coronary events for patients with stable angina. The present study was designed to examine the protective potential of nicorandil for patients undergoing off-pump coronary artery bypass grafting. Twenty-four patients undergoing off-pump coronary artery bypass grafting were randomly assigned to two groups, one receiving continuous infusion of nicorandil (1.0 microg.kg(-1).min(-1)) (n = 12) through anesthesia to next day and the other receiving no nicorandil for control (n = 12). For assessing myocardial injury, heart type fatty acid binding protein, troponin T, and creatine kinase MB isoform were determined during the first 15 hours after reperfusion. The concentration of heart type fatty acid binding protein in the nicorandil group was significantly lower than that in the control group. On the other hand, the concentrations of troponin T and creatine kinase MB isoform in the nicorandil group were lower than those in the control group, but the differences did not reach statistical significance. Furthermore, nicorandil did not affect the patients' hemodynamic variables. Our data suggest that the infusion of nicorandil provides small myocardial protection without affecting hemodynamic parameters during perioperative treatment of patients undergoing off-pump coronary artery bypass grafting.
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PMID:Prophylactic effect of intravenous nicorandil on perioperative myocardial damage in patients undergoing off-pump coronary artery bypass surgery. 1545 60

We performed a pilot study to assess the significance of modest, asymptomatic, elevated serum cardiac markers--troponin T (TnT) and creatinine kinase-MB (CK-MB)--18-24 h following successful elective percutaneous coronary intervention (PCI) and to explore their relationship with changes in aerobic exercise capacity, as measured by peak oxygen consumption (VO2), 6 weeks following the procedure. Twenty-three patients with single-vessel disease and chronic angina performed an incremental cardiopulmonary exercise test before and 6 weeks after successful uncomplicated PCI. A venous blood sample was taken at rest before PCI and 18-24 h after the procedure. Successful PCI resulted in a trend towards an increased peak VO2 [21.62 +/- 0.64 (pre) vs. 23.03 +/- 0.75 ml/ kg/min (post), p = 0.07; mean +/- SEM]. There was a significant increase [median (IQR)] in TnT, from 0.00 (0.00) microg/l at baseline increasing to 0.02 (0.03) microg/l at 18-24 h, p = 0.002. CK-MB levels showed no significant difference. In the group of 15/23 (65%) patients with an elevation in serum TnT (>/=0.01 microg/l), 18-24 h after successful PCI, there was no significant increase in peak VO2 [23.31 +/- 0.96 (pre) vs. 23.89 +/- 1.09 ml/kg/min (post), p = 0.57]. In 8 (35%) patients with no rise in TnT at 18-24 h, a significant increase in peak VO2 was observed following successful PCI [23.10 +/- 0.91 (pre) vs. 25.09 +/- 0.75 ml/kg/min (post), p = 0.02]. Although 7 of these 8 patients increased their peak VO2, the absence of a TnT rise at 18-24 h was not significantly associated with an increase in peak VO2 following successful PCI (p = 0.18). To confirm these interesting initial results and investigate the relationship of serum cardiac markers following successful PCI and subsequent exercise capacity, further studies are required.
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PMID:Relationship of serum cardiac markers following successful percutaneous coronary intervention and subsequent exercise capacity in patients with chronic stable angina: a pilot study. 1553 83


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