Clinical significance of cardiac contractile proteins for the diagnosis of myocardial injury.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Mair.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVE: To determine whether transient ST-T alterations in patients with unstable angina are associated with an increase in plasma glycogen phosphorylase BB concentrations on admission to hospital. DESIGN: Prospective screening of patients with unstable angina for markers of myocardial cell damage. SETTING: Accident and emergency department of university hospital. PATIENTS: 48 consecutive patients admitted for angina pectoris (18 with transient ST-T alterations). None of the patients had acute myocardial infarction according to standard criteria. MAIN OUTCOME MEASURES: Creatine kinase and creatine kinase MB activities, creatine kinase MB mass concentration, and myoglobin, cardiac troponin T, and glycogen phosphorylase BB concentrations on admission. RESULTS: All variables except for creatine kinase and creatine kinase MB activities were significantly higher on admission in patients with unstable angina and transient ST-T alterations than in patients without. However, glycogen phosphorylase BB concentration was the only marker that was significantly (p = 0.0001) increased above its discriminator value in most patients (16). In the 18 patients with transient ST-T alterations creatine kinase MB mass concentration and troponin T and myoglobin concentrations were significantly (p = 0.0001) less commonly increased on admission (in five, three, and two patients, respectively). CONCLUSIONS: The early release of glycogen phosphorylase BB may help to identify high risk patients with unstable angina even on admission to an emergency department. Glycogen phosphorylase BB concentrations could help to guide decisions about patient management.
Glycogen phosphorylase isoenzyme BB mass release was studied in 20 patients undergoing coronary artery bypass grafting. In 16 patients with uneventful coronary artery bypass grafting, glycogen phosphorylase isoenzyme BB mass concentrations showed a significant, transient increase in the post cross-clamping period and decreased to baseline values within 20 hours (peak concentrations ranged from 12.7 micrograms/l to 47.5 micrograms/l, median 40 micrograms/l). One patient did not fulfil criteria for perioperative myocardial infarction, but clinical data indicated myocardial injury after aortic unclamping. In this patient only glycogen phosphorylase isoenzyme BB mass concentration and not creatine kinase isoenzyme MB catalytic concentration was increased, compared with uneventful patients. In 2 patients with emergency coronary artery bypass grafting for evolving myocardial infarction, glycogen phosphorylase isoenzyme BB mass concentrations, but not creatine kinase isoenzyme MB catalytic concentrations, correlated with clinical evidence of myocardial ischaemia. Our data indicate that glycogen phosphorylase isoenzyme BB mass concentration is a very sensitive laboratory marker of perioperative myocardial injury in patients undergoing coronary artery bypass grafting.
BACKGROUND: As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage. METHODS: This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment. RESULTS: Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion. CONCLUSION: Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.
Cardiac troponin I (cTnI) is a regulatory protein unique to myocardium. We used a cardiospecific 30-min ELISA to measure cTnI in EDTA-plasma samples serially drawn from 28 patients before and after coronary artery bypass grafting (CABG)--26 elective and 2 salvage cases. The cTnI increase in 22 of the elective CABG patients, who did not have perioperative myocardial infarction (not-PMI), reflected the inevitable myocardial damage caused by cannulation and cardioplegic arrest, with peak values of 1.7 +/- 1.0 microgram/L (mean + 2 SD = 3.7 micrograms/L), the peaks occurring on average 8 h (range 4-24) after aortic unclamping. Two of the 22 not-PMI, elective CABG patients showed cTnI peaks > 3.0 micrograms/L (3.9 and 3.4 micrograms/L), indicating more extensive perioperative myocardial damage than the other 20, as confirmed by clinical and electrocardiographic or echocardiographic signs, although creatine kinase isoenzyme MB (CKMB) activity was below our PMI decision limit of 20 U/L (25 degrees C). As classified by electrocardiography, echocardiography, and increased CKMB activity, four of the 26 elective CABG patients did have a PMI. One patient with Q-wave PMI had peak cTnI approximately 30 micrograms/L, and three with non-Q-wave PMI had lower peak values (approximately 5 micrograms/L). The two salvage CABG cases had increased cTnI before surgery. One developed a Q-wave acute myocardial infarction with a 3-h cTnI peak of approximately 35 micrograms/L. We conclude that, after elective CABG, cTnI peaks > 3.7 micrograms/L and concentrations > 3.1 micrograms/L at 12 h or 2.5 micrograms/L at 24 h indicate PMI with high probability.
Explore the source record for details and available documents.
We measured concentrations of guanosine 3',5'-monophosphate (cGMP) in plasma and urine of healthy subjects and patients with congestive heart failure, renal impairment, neoplastic disease, and hepatic cirrhosis. There was no correlation between cGMP concentrations in urine and in plasma. In all patients except those with renal impairment, urinary cGMP concentrations were significantly higher than in healthy persons. Only patients with heart failure or renal impairment showed significantly increased plasma cGMP concentrations. In contrast, cGMP in urine does not relate to the clinically assessed severity of heart failure (New York Heart Association functional classes). Determination of cGMP in plasma results in higher sensitivity and specificity for diagnosing heart failure than measurement of cGMP in urine.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The purpose of this study was to evaluate cardiac troponin T (TnT) in the diagnosis of minor perioperative myocardial tissue damage and small myocardial infarctions during aortocoronary bypass surgery. In 15 patients without enzymatic or electrocardiographic signs of perioperative myocardial ischemia (group 1, uncomplicated bypass surgery), TnT did not exceed 3.55 micrograms/L. In 3 patients with perioperative non-Q-wave infarctions (group 2), TnT was significantly higher than in group 1 patients. In all 3 patients, TnT peak concentrations exceeded 3.5 micrograms/L. Thirteen patients (group 3, borderline cases) showed either signs of perioperative myocardial ischemia by creatine kinase isoenzyme MB (CKMB) activity levels (CKMB > 20 U/L on the first postoperative day, 3 patients) or by electrocardiography (new ST-T segment alterations, 10 patients). TnT concentrations were comparable to group 1 patients and indicated uncomplicated bypass surgery in all 3 patients with solely elevated CKMB activities. On the other hand, TnT concentrations in 3 patients with electrocardiographic signs of perioperative myocardial ischemia were significantly higher than in uncomplicated patients (group 1) with peak values exceeding 3.5 micrograms/L. Thus, TnT indicated perioperative non-Q-wave infarctions not detected by CKMB activity in these 3 patients. These results are in accordance with findings in nonsurgical patients. They suggest a higher sensitivity and specificity of cardiac TnT compared to CKMB activity in the diagnosis of small perioperative myocardial infarctions after bypass surgery.
BACKGROUND: This study compared clinical-chemical estimates of infarct size with scintigraphic estimates of myocardial scar in patients with first-time acute myocardial infarction (AMI). METHODS: Levels of the cardiac isoform of the contractile protein troponin T (TnT), of creatine kinase (CK), and of the isoenzyme MB of CK (CK MB) were tested in serially drawn blood samples from 21 patients (two females and 19 males; median age, 55 years). Of these 21 patients, five had anterior- and 16 had inferior-wall AMI; all patients received intravenous thrombolytic therapy. Single-photon emission computed tomography (SPECT) with technetium-99m-isonitrile (Tc-sestamibi) was performed at rest after the onset of AMI (median time, 5 weeks). Scintigraphic defects were calculated using "bull's-eye" polar coordinate maps. All patients had an uncomplicated course between discharge and myocardial scintigraphy. RESULTS: Scintigraphic defect sizes ranged from 3.2% to 47.8% of the left ventricle (median, 27.3%). Cardiac TnT and CK MB release correlated closely with each other and with scintigraphic estimates of myocardial scar. Significant correlates were found between cardiac TnT and CK MB peak values (r = 0.87, P = 0.0001), CK MB peaks and Tc-sestamibi defect sizes (r = 0.73, P = 0.0014), and TnT peaks and scintigraphic defect sizes (r = 0.73, P = 0.0011). CONCLUSIONS: Because animal studies have already shown a very close correlation between histologic infarct size and SPECT Tc-sestamibi defect size, our results indicate that cardiac TnT is a useful marker to assess infarct size noninvasively in man.
STUDY OBJECTIVES: To evaluate measurements of myoglobin in the diagnosis of perioperative myocardial tissue damage in aortocoronary bypass surgery. A new immunoturbidimetric myoglobin assay, which yields quantitative concentrations of myoglobin within approximately 1 min, was used. DESIGN: Prospective clinical study. PATIENTS: Thirty-two patients scheduled for elective aortocoronary bypass surgery. MEASUREMENTS AND RESULTS: Myoglobin concentrations in patients without perioperative myocardial infarction (n = 27) increased with aortic unclamping, peaked after 1 h, and decreased to almost baseline values within 4 h. By contrast, myoglobin concentrations in patients with perioperative myocardial infarction (n = 5) further increased after 1 h of aortic unclamping and were significantly higher (p < 0.05) than in patients without myocardial infarction as soon as 3 h after aortic unclamping. In all patients with myocardial infarction, myoglobin concentrations exceeded 400 micrograms/L over a minimum period of 4 h. Ten of 27 patients without perioperative myocardial infarction had episodes of minor perioperative myocardial ischemia (defined as ST-T segment changes in the ECG without a concomitant increase in the activity of creatine kinase isoenzyme MB). Myoglobin concentrations (but not creatine kinase isoenzyme MB activity) were significantly higher in these 10 patients when compared to the 17 completely uneventful cases. CONCLUSIONS: Plasma concentrations of myoglobin are a sensitive marker of perioperative myocardial tissue damage in aortocoronary bypass surgery. Myoglobin measurements with the immunoturbidimetric assay have an important contribution to make to the early and rapid diagnosis of perioperative myocardial infarction.
Explore the source record for details and available documents.