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

The ferritin level in serum was investigated in 9 patients with myocardial infarction, all with a history of chest pain of less than 4 hours before admission. A significant rise in serum ferritin level was found in 8 patients. The rise was generally smaller than that seen in acute infection and not significantly correlated to the size of infarction, as estimated from changes in serum levels of myoglobin, ASAT and LDH. The rise started after a mean of 30 hours, the peak being reached within a week (M 4.3 days). Serum ferritin then fell to 120--300% (M 190) of the initial level, where it remained. An initial rise in serum iron levels was unexpectedly seen within 12 hours in 7 patients.
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PMID:Serum ferritin during inflammation. A study on myocardial infarction. 52 35

Using a solid-phase radioimmunoassay for detection of serum myoglobin, the pattern of myoglobinemia was investigated in patients with acute myocardial infarction. All patients with acute infarcts had a marked rise in serum myoglobin concentration. Peak serum myoglobin concentration was found on an average 9 h after the initial onset of chest pain. Late onset of myoglobin peaks without signs of reinfarction as well as sustained abnormal myoglobinemia, in the majority of patients, could be explained by impaired renal function. The peak serum level of myoglobin correlated (r = 0.92) to the peak level of ASAT supporting the idea that the detection of myoglobin in serum may be a useful diagnostic aid in the qualitative diagnosis of myocardial infarction.
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PMID:Myoglobinemia after myocardial infarction; influence of renal function. 72 98

Fifty-six patients with a preliminary diagnosis of possible acute myocardial infarction (AMI) were studied on the second or third day after onset of symptoms by 99mtechnetium stannous pyrophosphate myocardial imaging. The scintigraphy was positive in 25 (44.6%). The final clinical diagnoses upon discharge were: definite AMI in 11 with positive scintigraphy in 9 (82%), intermediate coronary syndrome (ICS) in 37 with positive scintigraphy in 15 (40.5%), postinfarction failure in 4 with positive scintigraphy in 1, no diagnosis of coronary heart disease in 4 patients with negative scintigraphy in all. Of the 37 patients with a final diagnosis of ICS, 25 were admitted to the Coronary Care Unit with chest pain as the only symptom. In this group the mean percentage increase in ASAT was significantly higher in 9 patients with positive scintigrams than in 16 with negative. It is therefore assumed that among patients with ICS, a positive scintigraphy may reflect a more serious myocardial injury than a negative scintigram. Of six patients with an acute tachyarrhythmia and ICS, scintigraphy was positive in the three with the most long-lasting or severe arrhythmmias. False negative scintigrams may be seen in some patients with definite AMI.
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PMID:Myocardial scintigraphy with 99mtechnetium stannous pyrophosphate in patients with possible acute myocardial infarction. 89 72

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.
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PMID:Human ventricular myosin light chain isotype 1 as a marker of myocardial injury. 817 43