Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early sensitivities of creatine kinase (CK), CKMB (activity and mass), CKMM and CKMB isoform ratios, myoglobin, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) were compared to find the most sensitive serum marker for acute myocardial infarction (AMI) during the first hours after onset of chest pain. In a prospective study we investigated 37 consecutive patients with AMI who were admitted to the coronary care unit within 4 h after onset of chest pain. Blood samples were drawn every hour for the first 10 h after admission. CKMB mass concentrations, CKMM and CKMB isoform ratios, myoglobin, cTnI, and cTnT increased significantly (P < or = 0.0067) earlier than CK and CKMB activity and were also significantly (P < or = 0.046) and markedly more sensitive on admission. Differences in early sensitivities of myoglobin, CKMB mass, CK isoform ratios, cTnI, and cTnT were small and not significant. Therefore, turnaround time and practicality for emergency determination of methods, specificities of markers, the required specificity in the individual patient, and costs mainly determine the choice among myoglobin, CKMB mass, CK isoforms, cTnI, and cTnT.
 ...
PMID:Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction. 765 36

It is important to establish as soon as possible whether patients who present with chest pain are having an acute myocardial infarction (AMI). Ideally, sensitive and specific serum myocardial markers could provide the basis for early detection as well as determine the status of reperfusion following thrombolytic therapy. The present study examined the utility of cardiac troponin I (cTnI), CK-MB, and myoglobin for the sensitive and specific detection of AMI in 98 consecutive patients presenting to the emergency department (ED) with chest pain. In addition, cardiac troponin T (cTnT), CK-MB, and myoglobin samples were measured over a 90 min time period following thrombolytic therapy in nine separate AMI patients to assess reperfusion. In the ED study, CK-MB, myoglobin, and cTnI were equally sensitive (100%) for the detection of AMI in patients who presented 7.4-14 h after onset of chest pain. However, cTnI was the most specific serum marker (specificity 91.9% compared to CK-MB 85.6%, myoglobin 61.4%). Five of the six non-related AMI patients who had an elevated cTnI had clinically documented myocardial involvement. In the reperfusion study, cTnT, CK-MB and myoglobin, relative increases were greater in reperfused compared to non-reperfused patients. Within the reperfused group, the relative increase of cTnT was greater than CK-MB and myoglobin at 90 min following thrombolytic therapy. These findings show the clinical utility of cardiac-specific troponins as markers for the early detection of AMI and monitoring of reperfusion following thrombolytic therapy.
 ...
PMID:Cardiac troponin, CK-MB and myoglobin for the early detection of acute myocardial infarction and monitoring of reperfusion following thrombolytic therapy. 766 79

The screening by immunoenzymometric assay (IEMA) of 784 monoclonal antibody (MAb) combinations resulted in the selection of an optimal pair of MAbs for measuring human cardiac troponin I (TnI). Using a one-step IEMA described here, we were able to detect TnI within the range of 0.2-20 micrograms/L in 30 min at room temperature. No cross-reactivity was observed with the skeletal isoforms of troponin up to a concentration of 500 micrograms/L. This assay was used to measure cardiac TnI in the plasma of 43 patients with acute myocardial infarction (AMI). TnI was detected relatively early after the onset of chest pain (4.3 +/- 2.1 h, mean +/- SD); the peak occurred after 12.2 +/- 4.6 h in a population that had undergone fibrinolysis. TnI disappearance was generally observed between 5 and 9 days after the onset of chest pain. No cardiac TnI could be detected in 145 healthy donors or in a control group of 6 patients (with skeletal damage or rhabdomyolysis). This assay allows a specific diagnosis of AMI in its early acute phase, with a high diagnostic specificity and sensitivity.
 ...
PMID:Cardiac-specific immunoenzymometric assay of troponin I in the early phase of acute myocardial infarction. 850 66

We used a cardiospecific enzymoimmunometric assay to measure cardiac troponin I (cTnI) in samples serially drawn from 78 patients with acute myocardial infarction (AMI), 7 patients with unstable angina (Braunwald class III), 22 multi-traumatized patients, and in 30 athletes after eccentric exercise, as well as in 101 non-traumatic chest pain patients on admission to the emergency department. cTnI assay crossreactivity with crude human skeletal muscle homogenates was < 0.1%. cTnI could not be detected in athletes or multi-traumatized patients except for 2 trauma patients with myocardial damage. Increased cTnI concentrations were found in 6 of 7 patients with unstable angina at rest and in all AMI patients. After AMI, cTnI increased about 3.5 h (median) after the onset of chest pain, reached peak values parallel to CKMB, and stayed increased for at least 4 days. Cardiac troponin T (cTnT) increased and mostly peaked parallel to cTnI. cTnT sensitivity on the 7th day after AMI was significantly higher than that of cTnI. In contrast to cTnI, cTnT mostly showed a second, usually smaller, peak about day 4 after AMI. During the first 4 h after the onset of chest pain and before thrombolytic therapy the sensitivities of myoglobin (0.43) and CKMB mass (0.56) were significantly higher than those of both troponins (cTnI, 0.29; cTnT, 0.25). Areas under receiver operator characteristic curves indicated only moderate diagnostic accuracies of bio-chemical markers for early AMI diagnosis in non-traumatic chest pain patients that cTnI is a highly sensitive and specific marker for myocardial damage which is suitable for early and late diagnosis.
 ...
PMID:Cardiac troponin I in the diagnosis of myocardial injury and infarction. 864 13

Serial plasma concentrations of myoglobin, creatine kinase MB (CK-MB) isoenzyme, and cardiac troponin I (cTnI) were measured in 25 patients with a confirmed diagnosis of acute myocardial infarction (AMI), and 74 patients who were suspected of AMI but were subsequently ruled out for this diagnosis. The cutoff concentration for the cTnI assay was optimally determined to be 2.5 ng/mL. Of the three markers, myoglobin had the highest clinical sensitivity (50 percent) when blood was collected between 0 to 6 h after the onset of chest pain. Assays for all serum markers used had high clinical sensitivity (> 93 percent) 6 to 24 h after onset. The CK-MB remained highly sensitive for 48 h, while cTnI was sensitive for up to 72 h. Between 72 and 150 h, cTnI had a clinical sensitivity of 70 percent as compared to 21 percent and 18 percent for myoglobin and CK-MB, respectively. The clinical specificity of cTnI for non-AMI patients was equivalent to CK-MB and significantly higher than for myoglobin. The clinical efficiency of cTnI for all samples was better than either CK-MB or myoglobin, owing mainly to the wider diagnostic window. The specificity of cTnI for 59 patients with chronic renal failure, skeletal muscle trauma and disease was better than all of these markers including cardiac troponin T (cTnT). Results of this study show that cTnI is an effective marker for the retrospective diagnosis of AMI, and consideration should be given to its use in place of CK-MB.
 ...
PMID:Comparison of myoglobin, creatine kinase-MB, and cardiac troponin I for diagnosis of acute myocardial infarction. 880 Apr 29

This study compared the diagnostic accuracy of the measurement of serum cardiac troponin I (cTnI) with creatine kinase (CK) MB mass in patients with minor myocardial injury whose measured total CK activity did not exceed twice the upper reference limit (300 U/L for men; 200 U/L for women). Forty-eight consecutive patients presenting with chest pain and with in-hospital documentation of myocardial injury were enrolled. Electrocardiogram, echocardiogram, and serial serum CK-MB mass, cTnI, and total CK were measured over 36 h after admission. Peak total CK activity was within normal limits in 28 patients (58%). The mean (+/- SD) peak CK-MB mass and cTnI concentrations were: 16.4 (11.8) micrograms/L and 132 (13.0) micrograms/L; respectively. The peak biochemical marker index (defined as CK-MB or cTnI divided by its respective upper reference limit) was significantly (P < 0.05) higher for cTnI than for CK-MB from 7 to 36 h. The clinical sensitivity for detection of myocardial injury for cTnI was 100% [95% confidence interval (CI): 87.2% to 100%], compared with 81.8% (CI: 67.3% to 91.8%) for CK-MB. Thus, cTnI was more sensitive than CK-MB mass for detection of myocardial injury in patients with small increases of total CK.
 ...
PMID:Improved detection of minor ischemic myocardial injury with measurement of serum cardiac troponin I. 936 87

We evaluated whether recent cocaine use alters the specificity of CK-MB, myoglobin, and cardiac troponin I for acute myocardial infarction (AMI) in patients who are seen in the emergency department for chest pain. Patients <60 years old with potential myocardial ischemia underwent a standardized history and physical examination and routine CK-MB assays every 8 to 12 hours and had study serum obtained at presentation for CK-MB, myoglobin, and cardiac troponin I immunoassays, as well as benzoylecgonine, cocaine's main metabolite. We enrolled 97 patients, 19 (20%) of whom had recent used cocaine. Patients with and without cocaine use were similar with regards to sex, race, renal and muscular disease, diabetes, family history, and hypertension and rate of AMI (12% vs 11%, p = 1.0). In patients without MI, the mean myoglobin level was higher in cocaine users than noncocaine users (179 vs 74 ng/ml; Mann-Whitney p = 0.003), but the mean values were similar for CK-MB (2.2 vs 2.1 ng/ml; Mann-Whitney p = 0.58) and for cardiac troponin-I (0.02 vs 0.02 ng/ml; Mann-Whitney p = 0.87). The specificities of the markers in patients with and without cocaine use were as follows: cardiac troponin I, 94% vs 94%, (p = 1.0); CK-MB, 75% vs 88% (p = 0.24); and myoglobin, 50% vs 82%, (p = 0.02), respectively. Our data demonstrate that the specificity of myoglobin was altered by recent cocaine use. The specificity of CK-MB was affected less and the specificity of cardiac troponin I was not affected by recent cocaine use.
 ...
PMID:Effect of recent cocaine use on the specificity of cardiac markers for diagnosis of acute myocardial infarction. 948 72

The prognosis and extent of injury to the myocardium have previously been assessed by increased serum creatine kinase (CK) MB levels. We report findings from 39 consecutive, acute myocardial infarction (AMI) patients presenting 4.5 h (range, 0.7-12.1 h) after the onset of chest pain. We compared CK MB mass (upper reference limit, 5.0 ng/ml) and cardiac troponin I (cTnI; upper reference limit, 0.8 ng/ml) (Stratus II, Dade International) in serial serum specimens obtained over 36 h after chest pain from AMI patients; within 6 h after onset of chest pain. While the appearance of the kinetics of CK MB and cTnI were similar during the initial 24 h following the onset of chest pain, cTnI was increased significantly (p < 0.05) over CK MB after 9 to 12 h. Half-life determinations (mean+/-S.D.) in 22 of the 39 AMI patients demonstrated a significantly (p < 0.01) shorter half-life in non-Q-wave infarcts [t1/2 6.8 h (+/-5.6)] vs. Q-wave infarcts [t1/2 20.4 h (+/-10.7)]. Further serial time versus marker (mean+/-S.D.) results were significantly correlated (p < 0.001, r = 0.66). Sixteen of twenty patients assessed by echocardiography had an abnormal left ventricular ejection fraction (LVEF); mean 37.6 (S.D. 15.2)%, ranging from 15.4 to 67.6%. LVEF was significantly and inversely correlated to peak CK MB (r = .50, p = 0.03), as well as to peak cTnI (r = 0.46, p = 0.04). Based on these findings, cTnI shows excellent promise as a useful marker of infarct size, for the assessment of left ventricular function, and may potentially replace CK MB as the cardiac-specific marker for AMI detection.
 ...
PMID:Assessment of left ventricular function using serum cardiac troponin I measurements following myocardial infarction. 958 57

Detection of cardiac troponin I (cTnI) in patients suspected of having an acute coronary syndrome is highly predictive for an adverse outcome. We evaluated a bedside test for cTnI that uses a polyclonal capture antibody and two monoclonal indicator antibodies. Clinical studies were performed in patients with acute coronary syndrome and patients with chest pain but no evidence of acute myocardial injury. The whole-blood, 15-minute assay had a concordance of 98.9% with an ELISA for cTnI and a detection limit of 0.14 microg/L, and the device tolerated temperatures between 4 degrees C and 37 degrees C. Diagnostic sensitivity for myocardial infarction at arrival (3.5 +/- 2.7 h after onset of symptoms) was 60% [creatine kinase isoenzyme MB (CK-MB) mass, 48%; CK activity, 36%; P < 0.01], and 4 h later, diagnostic sensitivity was 98% (CK-MB mass, 91%; CK activity, 61%; P < 0.01). In 38% of the patients with unstable angina, at least one positive cTnI test was found (CK-MB mass, 4%; CK activity, 2%). No false-positive test results were found in renal failure or injury of skeletal muscle. We conclude that the diagnostic efficacy of the cTnI rapid test was comparable with the cTnI ELISA and superior to CK-MB determination. Therefore, this device could facilitate decision-making in patients with chest pain at the point of care.
 ...
PMID:Analytical performance and clinical application of a new rapid bedside assay for the detection of serum cardiac troponin I. 973 78

Acute chest pain patients without ECG-signs of acute myocardial infarction (AMI) on admission need to be earlier and better diagnosed to reduce use of expensive intensive care beds and to treat more patients with acute recirculation therapy. We investigated whether total CK-activity, CK-MB mass, CK-MB2, myoglobin, cardiac troponin I (cTnI) and T (cTnT) measured in venous blood on admission and after 1 and 2 h could be used to identify or exclude acute myocardial damage (AMD) in 22 acute chest pain patients without ECG-signs of AMI admitted to hospital within 6 h after onset of pain. Increases in CK-MB mass, CK-MB2, myoglobin and cTnI identified AMD in three patients classified retrospectively as AMI. Likewise, CK-MB mass, CK-MB2, cTnI and cTnT increased with time in three of seven patients classified as having unstable angina pectoris. CK-MB2 and cTnI increased with time in two patients with tachycardia belonging to the other heart disease group. The remaining seven patients of the non-heart disease group showed no change in any of the cardiac markers. Thus, early serial measurements of selected cardiac markers appear useful in identifying or excluding AMD 3 h after admission in these acute chest pain patients.
 ...
PMID:Serial measurements of cardiac markers to rule in or out acute myocardial damage less than 3 h after admission in acute chest pain patients without ECG-signs of acute myocardial infarction. 974 21


1 2 3 4 5 6 7 8 Next >>