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

Unstable angina in patients undergoing CABG surgery is associated with a higher morbidity and mortality compared to patients with stable angina. Mortality ranges between 2 and 10% (20, 21). The importance of the preoperative status is only clear and well documented for patients with unstable angina who are unresponsive to medical treatment, patients who undergo emergency revascularization, and for patients with failed angioplasty. The adverse outcome in elective patients with unstable angina was statistically not significantly different from those with stable angina. Therefore, we may assume that in stabilized patients with unstable angina and minor myocardial cell damage intraoperative determinants like the duration of the aortic clamping period or the degree of revascularization are more relevant than the preoperative ones. These determinants may also be reflected by a marked and significant increase of troponin T in both groups during and after surgery. As for other cardiac enzymes, this increase of troponin T beginning immediately after reperfusion of the cardioplegic heart may limit its diagnostic value after cardiac surgery (6,22). On the other hand, troponin T may serve as a marker in assessing the effectiveness of different cardioprotective measures. Nevertheless, preoperatively elevated troponin T levels may indicate a jeopardized myocardium with an ongoing process of myocardial cell damage and may be of prognostic value. Antianginal and antiischemic therapy, therefore, has to be continued and completed until the day of surgery in these high-risk patients.
 ...
PMID:Troponin T as a marker of perioperative myocardial cell damage. 787 43

A monoclonal enzyme immunoassay for measuring human ventricular myosin light chain isotype 1 (HVMLC1) in serum has been developed. To evaluate the method in patients with suspected myocardial injury, we studied 51 patients (16 acute myocardial infarction (AMI), 19 unstable angina pectoris (UAP), 9 stable angina pectoris, 3 nonischemic heart disease, 4 hip surgery patients), and 190 controls (blood donors). Serial blood-samples were drawn from patients; a single blood-sample from controls. The diagnostic value of the HVMLC1 assay was compared with total creatine kinase (CK), CKMB activity, CKMB mass concentration, lactate dehydrogenase isoenzyme 1 (LD1), troponin T (TnT) and mitochondrial-aspartate aminotransferase (m-ASAT). The detection limit of HVMLC1 was 0.4 microgram/l (linear range 0-20 micrograms/l). Sera from 190 reference persons did not contain detectable levels of HVMLC1 (< 0.4 microgram/l; 99% percentile). The coefficients of variation were 13% (1.0 microgram/l) and 3.1% (17.7 micrograms/l). Cross-reactivity with myosin from skeletal muscle was seen. Times to peak value were: CK 19.3 +/- 2.0, LD1 43.4 +/- 3.2, HVMLC1 72.9 +/- 7.0, and m-ASAT 67.3 +/- 5.6 h. Time-curves of HVMLC1 and m-ASAT were similar, whereas time-curves for HVMLC1 and TnT were quite different in most cases. Peak value of HVMLC1 was five times higher than CK peak value and eight times that of LD1. HVMLC1 appeared in the blood within hours after the onset of chest pain and in the majority remained for more than a week after AMI. Among patients with UAP 16% (3/19) had elevated HVMLC1 in serum, whereas elevated TnT was seen in 26% (5/19) and elevated CKMB mass in 26% (5/19). We conclude that the new HVMLC1 assay offers a sensitive diagnosis of myocardial injury. It is characterized by a wide diagnostic time window. The similarity of the HVMLC1 and m-ASAT curves indicates that it may be used to estimate the extent of myocardial necrosis.
 ...
PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43

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.
 ...
PMID:Troponin T for the differential diagnosis of ischaemic myocardial damage. 843 60

The diagnosis of acute myocardial infarction is straightforward when anginal pain is accompanied by typical ECG changes and in these patients measurements of cardiac markers are unnecessary in deciding whether thrombolytic therapy is appropriate. Cardiac markers in patients with acute ischaemic coronary syndromes, however, may serve to identify a high risk subgroup of patients with small acute infarctions or minor myocardial damage. In many patients with chest pain a valid diagnosis of myocardial cell injury depends on the result of biochemical assays. In 30% of patients with unstable angina, troponin T is elevated although myocardial infarction was ruled out by cardiac enzymes and ECG recordings. The outcome of these patients at 4 weeks and 6 months follow-up is not different from that of patients with definite myocardial infarction. To guide therapeutic decisions on these patients a troponin T test result needs to be available rapidly. The rapid troponin T test strip assay, which allows the determination of troponin T levels in whole blood at the patient's bedside, can be performed conveniently in the emergency room or in laboratories with less sophisticated equipment and has the potential to aid in the triage of chest pain patients and the selection of therapeutic strategies.
 ...
PMID:Troponin T: a diagnostic marker for myocardial infarction and minor cardiac cell damage. 896 Apr 42

We investigated the clinical utility of cardiac troponin T (TnT) and echocardiography in the emergency department to predict subsequent in-hospital diagnosis and adverse cardiac events. TnT is a cardiac-specific protein released during cell injury such as that following acute myocardial inFarction (MI). Unlike creatine kinase-MB isoenzymes, TnT is increased in a subset of patients with unstable angina, and these may be at higher risk for subsequent cardiac events. Echocardiography is a useful noninvasive imaging technique for the assessment of ischemic heart disease in acute care settings because of its mobility and rapid results. Serial TnT determinations and echocardiographic images were prospectively evaluated in 100 patients with chest discomfort and admitted to the hospital. Serum was obtained for CKMB and TnT on presentation to the emergency department and 4, 8, 16 and 24 hours later. TnT was considered increased when at values greater than 0.1 microg/L. Echocardiograms were recorded on videotape in the emergency department and images reviewed in a blinded fashion for wall-motion abnormalities. When available, current echocardiographic results were compared with previous results to determine whether a new wall-motion abnormality was present. Of the 100 patients (57 men, 43 women), TnT was increased in 21 of 21 with acute MI and 15 of 41 with unstable angina. One of the 38 patients with stable angina had an increased TnT value and died 5 months later of a noncardiac cause. Ninety percent of patients who sustained acute MI had a TnT increase detected within 4 hours of presentation. Fifteen of 18 patients with acute MI and 9 of 37 patients with unstable angina had a new wall-motion abnormality on echocardiography. The combination of TnT levels with echocardiography yielded a positive predictive value of 84% and a negative predictive value of 90% for adverse cardiac events in the follow-up population, which was more accurate than either test analyzed separately. TnT and echocardiography are useful tests in emergency department triage of unstable coronary syndromes. Both tests are predictive of discharge diagnosis and follow-up events. However, the combined utility of TnT levels and echocardiographic imaging is a more powerful predictor of adverse cardiac events than isolated results.
 ...
PMID:Clinical utility of troponin T levels and echocardiography in the emergency department. 948 73

The acute coronary syndromes represent a continuum of myocardial ischemia ranging from angina, reversible tissue injury --> unstable angina, frequently associated with minor myocardial damage --> myocardial infarction and extensive tissue necrosis. Historically, coronary artery disease assessment has been mainly binary, using WHO criteria of symptoms, electrocardiography, and biochemical markers. The creatine kinase-MB isoenzyme (CK-MB) has been a benchmark for markers, but it is not specific for myocardium. Cardiac-specific isoforms of troponin T and I have emerged as sensitive myocardial infarction (MI) indicators and, importantly, for risk stratification of acute coronary syndrome patients. In addition to markers of myocardial cell necrosis, markers of plaque disruption (C-reactive protein and serum amyloid A), "angry" platelets (P-selectin), ischemia (glycogen phosphorylase-BB isoenzyme), and the procoagulant state and thrombosis (soluble fibrin) have potential use. Also, CK-MB and myoglobin have been combined with clinical indicators for monitoring reperfusion after thrombolytic therapy. Biochemical markers will continue to be an important clinical adjunct for MI diagnosis, risk assessment, and reperfusion monitoring in the future.
 ...
PMID:Biochemical markers of the acute coronary syndromes. 970 95

Unstable angina is a high-risk phase of coronary heart disease defined by clinical symptoms. Electrocardiographic findings are heterogeneous and creatine kinase is only rarely elevated. However, troponin T and troponin I are found in about 30-40% of patients with angina at rest disclosing minor myocardial cell injury. Several studies in recent years have documented that troponins are the best markers to identify high-risk patients when other life-threatening, non-cardiac diseases are excluded. In addition, first evidence is provided that only these patients benefit from prolonged treatment with low molecular weight heparin or glycoprotein IIb/IIIa receptor blockers. Therefore, this new diagnostic potential should be made available to emergency rooms for risk stratification and in the future to guide therapeutic decision making.
 ...
PMID:Progress in the diagnosis of unstable angina and perspectives for treatment. 985 40

Unstable angina and non--Q-wave myocardial infarction (MI) are at the center of the spectrum of myocardial ischemia, which ranges from stable angina to acute Q-wave MI. In addition to clinical evaluation, cardiac specific markers such as troponin T or I can assist in early diagnosis, triage, and risk stratification. Antithrombotic therapy with aspirin and heparin have been shown to improve the outcome of patients with acute ischemic syndromes. Thrombolytic therapy does not appear to be beneficial in these syndromes. Antiischemic therapy remains an important component of the overall therapy. A strategy of early coronary angiography and revascularization leads to a similar long-term outcome as compared with a more conservative strategy of revascularization for recurrent ischemia, but the early invasive strategy is more expeditious as a large number of conservatively treated patients have recurrent ischemia. At present, many new antithrombotic agents are under active investigation, with the hope that they will lead to further improvement in the clinical outcome of patients with acute ischemic syndromes.
 ...
PMID:Optimizing the Treatment of Unstable Angina. 1060 25

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.
 ...
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.
 ...
PMID:Risk stratification and therapeutic decision making in patients with acute coronary syndrome--the role of cardiac troponin T. 1072 19


1 2 3 4 5 Next >>