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

Changes in serum myosin light chain I (MLCI) due to elective percutaneous transluminal coronary angioplasty (PTCA) were studied after PTCA (0, 8 and 48 hours) in 57 patients with old myocardial infarction (MI group) and 20 patients with angina pectoris (AP group). The AP group showed no increase after PTCA. In contrast, in the MI group there were 16 patients in whom MLCI at 48 hours was increased by 1.0 ng/ml or more (MI1 group) and another group of 41 patients who showed no increase in MLCI (MI2 group). The MI1 group had a significantly higher incidence of (1) non-Q wave myocardial infarction (62.5% vs. 17.1%, p < 0.01), (2) 99% stenosis of a coronary artery (50.0% vs. 12.2%, p < 0.01), and (3) redistribution in a hypoperfusion area found in the delayed image of resting thallium-201 (201Tl) myocardial scintigraphy (85.7% vs. 15.8%, p < 0.01). The left ventricular ejection fraction (LVEF) was significantly improved in the MI1 group, 3 to 4 months later (from 0.49 +/- 0.12 to 0.58 +/- 0.11, p < 0.01), in contrast to the patient of MI2 group who did not show any improvement. The AP group was not considered to have a bulk of myocardium impaired enough to show a release of MLCI due to PTCA-associated transient coronary occlusion. In the MI1 group, however, MLCI was probably released from the chronically under-perfused, but still salvageable, portion of the myocardium. This is consistent with the improvement in LVEF observed 3 to 4 months after the relief of severe coronary stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase in serum cardiac myosin light chain I associated with elective percutaneous transluminal coronary angioplasty in patients with ischemic heart disease. 148 36

A highly specific enzyme-linked "sandwich" immunoassay was developed for determining cardiac myosin light chain II (MLC II) in serum by using an anticardiac MLC II monoclonal antibody and a solid phase consisting of glass rods coated with another monoclonal antibody. We can detect as little as 0.2 ng of cardiac MLC II per assay. The measurable range of cardiac MLC II concentration in serum is 1 to 30 micrograms/L. The assay demonstrated no cross-reactivity with a skeletal muscle MLC within the measurable range. The mean coefficients of variation were 6.1% within assay and 5.1% between assay. The concentration of cardiac MLC II in sera from healthy subjects ranged from 0 to 4.0 micrograms/L (mean 0.75 micrograms/L and median 0 micrograms/L). The concentrations of cardiac MLC II in serum of patients with skeletal muscle disease due to various causes (n = 15) and patients with effort angina (n = 25), in general, were not significantly elevated above normal. In all patients with myocardial infarction, the concentrations of cardiac MLC II were over 4.0 micrograms/L at 12 h after onset. The mean (+/- 1 SD) peak concentration of cardiac MLC II was 16.2 (+/- 4.4) micrograms/L at 90 h (mean) after onset. On the 5th day, the cardiac MLC II concentrations in all patients with myocardial infarction were significantly elevated above normal; none showed abnormal MB-creatine kinase (CK-MB) activity at this time. Thus, the measurement of cardiac MLC II concentration in serum may be useful to provide a specific and sensitive diagnosis of myocardial necrosis at any time period following myocardial infarction.
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PMID:Clinical assessment of specific enzyme immunoassay for the human cardiac myosin light chain II (MLC II) with use of monoclonal antibodies. 228 10

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

The accurate estimation of myocardial damage is desirable for the assessment of myocardial protection and surgical treatments. The purpose of the study was to estimate myocardial damage by measuring cardiac myosin light chain I (CMLCI). Forty-nine patients undergoing cardiac surgery (for angina or valvular disease) were arbitrarily divided into four groups according to the maximum CMLCI level. Group 1: max CMLCI < 10 micrograms/L (37%); Group 2: max CMLCI 10-20 micrograms/L (39%); Group 3: max CMLCI 20-30 micrograms/L (16%); Group 4: max CMLCI > 30 micrograms/L (8%). Electrocardiogram (ECG) and serum creatine kinase MB isoenzyme (CK-MB) were conventionally used as standards of myocardial damage, and compared with CMLCI. Perioperative myocardial infarction, injury and minimum damage were determined by combinations of ECG pattern changes and CK-MB levels. The max CMLCI level was usually seen on the third postoperative day. None of the patients in group 1 had any ECG changes. The number of patients with ECG changes was much higher as the max CMLCI level increased, and evidently increased when the max CMLCI was over 20 micrograms/L. The number of patients with high CK-MB > 100 micrograms/L followed the same pattern. Furthermore, perioperative infarction was only seen when the max CMLCI was > 30 micrograms/L. The peak CMLCI level was significantly higher in the infarction group than injury and minimum damage groups. This study showed that CMLCI was able to estimate the actual extent and severity of the myocardial damage and enhanced the diagnosis of perioperative infarction.
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PMID:Detection of perioperative myocardial structural damage by the estimation of cardiac myosin light chain I. 830 Jul 19

To establish serum myosin light chain I (MLCI) as a severity and prognostic marker for patients with acute myocardial infarction (AMI), we measured the serum levels of MLCI in 71 patients with first AMI daily for 1 week after the onset and classified them into four groups by the peak LCI: group 1, > or =2.5 ng/ml but <10 ng/ml; group 2, > or =10 ng/ml but <25 ng/ml; group 3, > or =25 ng/ml but <50 ng/ml; and group 4, > or =50 ng/ml (MLCI grade). The patients in group 1 were likely to show non-Q-wave infarction. The patients in groups 1 and 2 were likely to show redistribution on exercise thallium-201 scintigraphy, suggesting frequent residual ischemia in these groups. The patients in group 4 were likely to show higher Forrester's subset and lower cardiac index at admission and lower left ventricular ejection fraction at discharge. Recurrent angina was equally found in all groups. Severe complications or death were found in patients in groups 3 and 4. Thus the MLCI grade can be used as a simple marker for evaluating the severity of patients with AMI.
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PMID:Myosin light chain I grade: a simple marker for the severity and prognosis of patients with acute myocardial infarction. 948 84

Plasma myosin heavy chain assay, which can be easily performed during the acute phase of myocardial infarction, is a recent method allowing quantitative assessment of the extent of infarction. However, to our knowledge, its prognostic value has not been studied in contrast with serum myosin light chain assay. We monitored the state of health of 40 patients (including 37 men with a mean age of 56 years) for two years after a first myocardial infarction, thrombolized during the acute phase. Their survival (mortality) and the development of "cardiac events" (MI, angina, sudden death, etc.) were evaluated at 2 years. The results observed at 2 years were correlated with the initial plasma myosin assay results and other direct and indirect methods of assessment of the extent of infarction, performed during the acute phase of myocardial infarction (cardiac enzymes, contrast angiography). The main result of this study is the demonstration that an unusual plasma myosin release kinetic (complex appearance) is predictive for the medium-term development of heart failure (p = 0.04) and/or destabilization of coronary insufficiency (p = 0.02). These results need to be emphasized, as with only 5 serum myosin assays performed over a 10-day period, it seems possible to identify a group of patients at high risk of medium-term complications, who possess a complex release kinetic during the acute phase of myocardial infarction and a value for area under the curve greater than 10.470 microliters U/L (cut-off value, p = 0.043).
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PMID:[Mid-term prognostic value of plasma heavy-chain myosin in thrombolysed myocardial infarction]. 1255 65

Coronary vasospasm is currently considered to be an exaggerated contractile nonspecific response of the vascular smooth muscle in the large coronary artery to various agonists or stimulation, that is established after the process of inflammation and fibrocellular proliferation. Endothelial dysfunction with reduced nitric oxide bioavailability has been reported in angiographically normal coronary arteries in Japanese patients with coronary spastic angina. Recently, several interesting findings concerning the exact mechanism of calcium hypersensitivity of spastic vascular smooth muscle have been reported. In animal models with coronary spasm Rho-kinase is upregulated at the spastic site and plays a key role in inducing vascular smooth muscle hypercontraction by inhibiting myosin light chain phosphatase, resulting in enhancement of its phosphorylation. Also, oxidative stress has been given attention as an important mediator of the spastic conversion of vascular smooth muscle cell "phenotype." The incidence of coronary spastic angina in the Japanese population is reported to be remarkably high compared with that in Caucasians. Clinical and pathophysiological differences between Japanese and Caucasian patients with respect to coronary vasospasm are characterized by a lower prevalence of fixed coronary artery stenoses and diffuse coronary hyperreactivity in the Japanese patients. Recently, several distinct characteristics have been recognized to be associated with coronary vasospasm in studies analyzing data obtained from Japanese patients. In the present review, we will discuss our point of view on the mechanisms and predisposing factors in coronary vasospasm. Predisposing factors include smoking, lipid metabolic disorders, and gene expression, all of which may be interrelated issues.
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PMID:Recent insights into the mechanisms, predisposing factors, and racial differences of coronary vasospasm. 1570 Jan 95