Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Troponin T is a structurally bound protein found in striated muscle cells. We tested concentrations of its cardiac-specific isotype in peripheral venous blood samples serially drawn from 72 patients with confirmed myocardial infarction. Fifty-nine patients received thrombolytic treatment with intravenous streptokinase, urokinase, or recombinant tissue-type plasminogen activator; because of contraindications, the remaining 13 patients did not. Concentrations of troponin T in plasma, measured by an enzyme-linked immunosorbent assay, started increasing within a few hours after the onset of symptoms (median, 4 h; range, 1-10 h). The sensitivity of troponin T for detecting myocardial infarction was 100% from 10 to 120 h after the onset of symptoms; sensitivity on the seventh day after admission was 84%. Concentrations were increased for up to three weeks in some patients with late or high peak values. Successful reperfusion in Q-wave infarction obviously influences the release of troponin T into plasma, with all such cases showing peak values less than or equal to 26 h (median, 14 h) after the onset of symptoms. Troponin T concentrations in these patients returned to within the reference interval more rapidly than in nonreperfused subjects. In the 13 patients without fibrinolytic therapy, troponin T tended to peak approximately 48 h (median) after the onset of chest pain. Troponin T concentrations in patients for whom thrombolysis was unsuccessful resembled those in patients without fibrinolytic therapy. The specificity of the assay was 96% as tested in samples of 96 emergency-room patients. The reference interval (less than 0.5 micrograms/L) was established from samples of 100 healthy blood donors. Troponin T measurements are a specific and sensitive method for the early and late diagnosis of acute myocardial infarction and could, therefore, provide a new criterion in laboratory diagnosis of its occurrence.
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PMID:Cardiac troponin T in diagnosis of acute myocardial infarction. 159 99

Troponin T has been used successfully to risk stratify patients with acute coronary syndromes, but the utility of this approach using a rapid bedside assay in patients undergoing thrombolysis for ST-segment elevation acute myocardial infarction has not been assessed in a large population. We assessed whether a point-of-care, qualitative troponin T test at enrollment could independently risk-stratify patients randomized to receive alteplase or reteplase in the GUSTO-III trial. Complete troponin T data were available for 12,666 patients (84%) enrolled at 550 hospitals. The primary end point was mortality at 30 days, and the predictive ability of an elevated baseline troponin T level was analyzed (after adjustment for baseline characteristics) with multiple logistic regression. Patients with an elevated troponin T result at enrollment (8.9%) had significantly higher mortality at 30 days (unadjusted 15.7% vs 6.2% for negative patients; p = 0.001), which persisted even after adjustment for age, heart rate, location of infarction, Killip class, and systolic blood pressure. In a multivariable regression model, a positive troponin T result added independently to the prediction of 30-day mortality (chi-square 46, p = 0.001). A positive result with qualitative troponin T testing on admission is an independent marker of higher 30-day mortality. Troponin T testing could be a valuable addition to the evaluation strategy for patients with acute myocardial infarction.
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PMID:Risk stratification with a point-of-care cardiac troponin T test in acute myocardial infarction. GUSTOIII Investigators. Global Use of Strategies To Open Occluded Coronary Arteries. 1061 91

Patients with acute coronary syndromes (ACS) frequently present with signs of disturbed fibrinolysis. The present study investigates the correlation of alterations in the fibrinolytic system and the amount of myocardial damage characterized by troponin release. In 85 patients with ACS markers of plasmin activation, plasminogen activator system and troponin T (TnT) were measured initially and after 48 h. Patients with TnT release (> or = 0.01 microg/l) at admission had higher TPA levels than those without release (10.2+/-0.7 ng/ml vs. 7.6+/-0.5 ng/ml; p <0.01). Additionally, patients with positive TnT had higher D-dimer levels initially (457+/-39 ng/ml vs. 316+/-22 ng/ml; p <0.01) and 48 h later (451+/-42 ng/ml vs. 275+/-37 ng/ml; p <0.01). The association of myocardial damage with a prothrombotic state and an enhanced fibrinolysis may explain the high prognostic value of troponin measurements in respect to future coronary events.
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PMID:Myocardial troponin T release is associated with enhanced fibrinolysis in patients with acute coronary syndromes. 1181 3

The efficacy and safety of fibrinolysis and subsequent transluminal (FAST) therapy were evaluated in 195 patients with acute myocardial infarction (AMI) for the early achievement of thrombolysis-in-myocardial-infarction grade 3 (TIMI-3) flow in the infarct-related artery. Intravenous thrombolysis using the optimal dose of a thrombolytic agent was initiated immediately after arrival in the emergency room, followed by coronary angiography and adjuvant percutaneous coronary intervention. A comparison of the thrombolysis alone (n=83) and thrombolysis plus intervention (n=112) groups showed significant differences in the time interval from hospital arrival to achievement of TIMI-3 flow (66.2+/-23.7 vs 111.6+/-29.6 min, p<0.0001), creatine kinase-MB release (295+/-201 vs 468+/-322 U/L, p=0.0003) and peak troponin T (23.6+/-16.9 vs 38.9+/-25.9 ng/ml, p<0.0001). No significant differences were observed in either 30-day mortality or complications. The TIMI-3 flow at the initial angiography was significantly higher with a single bolus of mutant tissue-type plasminogen activator (t-PA) monteplase than with an accelerated infusion of t-PA (60% vs 32%, p=0.005). In conclusion, the early restoration of TIMI-3 flow by FAST therapy reduced the degree of myocardial damage with a low risk of complications. TIMI-3 flow was achieved at an earlier stage with monteplase and this agent may be beneficial in the FAST therapy.
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PMID:An early and complete reperfusion strategy for acute myocardial infarction using fibrinolysis and subsequent transluminal therapy--The FAST trial. 1207 77

Diagnostic approaches in acute pulmonary embolism include evaluation of clinical likelihood, D-dimers, echocardiography and spiral CT angiography and pulmonary scintigraphy. Determination of D-dimers is only meaningful in patients with low or intermediate clinical likelihood. It is safe not to initiate anticoagulation treatment (or to discontinue such treatment) in patients with low clinical likelihood of acute pulmonary embolism and negative D-dimer test (only if methods with 99-100% sensitivity are used). Duplex sonography and pulmonary scintigraphy are only necessary at the centres with a first generation spiral CT and not those with multidetector devices. Investigations in normotensive patients should include echocardiography that should also include assessment of the right ventricular function using echocardiography and determination of biomarkers of pulmonary embolism. Right ventricular dysfunction together with elevated troponins identifies a normotensive group at an increases risk. Highly sensitive troponin T (hsTnT) appears to be particularly valuable. Echocardiography reading might the decisive factor for treatment initiation in patients with massive acute pulmonary embolism. Negative or unclear echocardiography finding warrants spiral CT angiography (CTA). Ventilation/perfusion scan or pulmonary arteriography are recommendable in patients with unclear CTA finding and patients with high clinical likelihood of pulmonary embolism and negative CTA finding. A combination of CTA and CTV also appears useful as it increases the overall sensitivity of the investigation and enables imaging of pelvic veins. Thrombolytic treatment is indicated in haemodynamically unstable patients, patients with a high risk of a massive pulmonary embolism associated with cardiogenic shock or hypotension (systolic pressure below 90 mmHg or a decrease in systolic pressure by > 40 mmHg) or symptoms of acute right-sided heart failure. Thrombolytic treatment is also indicated in pulmonary embolism not receding following heparin treatment, in recurring or expanding pulmonary embolism, in the presence of thrombi in the right heart and in patients with right-to-left shunting through patent foramen ovale. This treatment should also be considered in patients with submassive pulmonary embolism associated with a dysfunction of the right ventricle and increased troponins, and particularly in patients lacking even a relative contraindication of thrombolytic treatment. A thrombolytic of choice is alteplase. Embolectomy or catheterization should be used if thrombolytic treatment is contraindicated or ineffective. Long-term monitoring of massive and submassive acute pulmonary embolism is highly recommended. Low molecular weight heparins or unfractioned heparin or fondaparinux are used in haemodynamically stable patients.
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PMID:[Diagnosis and treatment of acute pulmonary embolism in 2010]. 2135 57