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)

The blocking of the creatinphosphokinase by 1-fluoro-2,4-dinitrobenzene (FDNB) allows to investigate the relationship between ATP-supply, contractility and relaxability of the frog's myocardium. In isotonically working isolated ventricles of frogs the time of work, systolic and diastolic volume, velocity of contraction and relaxation as well as the levels of CP, ATP, ADP and AMP were measured at different intervals until termination of each experiment. CP shows a small variation, ATP decreases to 60% and ADP + AMP increase for the same amount under FDNB during the development of a slight inhibition of contractility and a continuously growing inhibition and retardation of relaxation until systolic arrest. ATP content and volume of relaxation correlated strictly. The contracture and the diminished contractility are caused by the decrease of ATP, producing a lack of substrate for Ca transport and actin-myosin-ATPase. This models the course of events during an insufficiency like in angina pectoris and in myocardial infarction.
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PMID:[Mechanical characteristics of isotonic work and high-energy phosphates in frog ventricle after 1-fluoro-2,4-dinitrobenzene]. 31 Jun 11

Ventricular myosin heavy chains serum levels are a new marker of myocardial necrosis. We have studied plasma levels of myosin in 30 patients with unstable angina, 30 patients with acute myocardial infarction and 25 healthy subjects. The myosin peak level was 317 +/- 101 microU/L in angina patients, 2510 +/- 433 microU/L in infarcted patients and 62.3 +/- 17 microU/L in the controls. In both groups, the increase in serum myosin was more marked in those with larger infarction and in those with more severe angina. These data suggest that the measurement of serum myosin can identify the presence of micronecrosis in patients with unstable angina, according to what has been found using other markers of myocellular necrosis.
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PMID:[The determination of myocardial necrosis in unstable angina by the immunoradiometric measurement of circulating myosin]. 129 65

A 64-year-old female patient with a prosthetic mitral valve suffered from recurrent typical angina and dyspnea. Left heart catheterization excluded a dysfunction of the prosthesis and coronary artery disease (CAD). A stress thallium scan demonstrated an ischemic reaction. An antimyosin scintigram was positive, indicating myocytal membrane disruption. Serological tests were suspicious for systemic lupus erythematosus (SLE). Therefore, an endomyocardial biopsy (EMB) was performed and a severe alteration of an intramyocardial artery, comparable with chronic SLE, was diagnosed. EMB is a useful diagnostic tool in patients with typical chest pain, positive thallium and anti-myosin scintigrams, however exclusion of CAD.
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PMID:[Diagnosis by endomyocardial biopsy: angina pectoris as a manifestation of lupus erythematosus]. 175 Feb 31

The aim of the investigation is to study the influence of human myocardium myosin on the quantitative values of T-lymphocytes examined as active rosettes [correction of rosellae] in patients with ischemic heart disease. The study included 99 patients with ischemic heart disease, 49 of them with myocardial infarction and 50--with stenocardia. The controls were 61 clinically healthy donors. It was established that the active rosettes [correction of rosellae] in the patients with myocardial infarction were significantly less than in the controls (p less than 0.05). A significant inhibiting action of the human myocardium myosin on the active rosettes [correction of rosellae] was manifested (p less than 0.002). This action in the patients with stenocardia was less expressed (p less than 0.05). Myosin from a striated muscle did not exert an inhibiting action (p greater than 0.1). The results prove the participation of human myocardium myosin in the pathogenetic mechanism of T-lymphocytes suppression in patients with ischemic heart disease.
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PMID:[The effect of myosin from the human myocardium on quantitative T-lymphocyte values--active rosettes in patients with myocardial infarct and stenocardia]. 208 Jun 8

The manifestations of cardiac involvement in hypertension include: (1) the development of hypertensive heart disease characterized by left ventricular hypertrophy (LVH), and (2) the consequences of coronary atherosclerosis, as angina pectoris, myocardial infarction, and sudden cardiac death. Whereas the former is directly related to increased blood pressure, the latter are sequelae of atherosclerosis per se, and hypertension acts only as a risk factor in this regard. This can partially explain why antihypertensive treatment is effective in diminishing the incidence of congestive heart failure, which is the final consequence of LVH, but is not very effective in preventing coronary complications. It is generally accepted about LVH that increased arterial pressure is the major stimulus to cardiac hypertrophy in hypertension; however, there are a lot of both quantitative and qualitative events suggesting that other factors beside blood pressure levels can modulate the development of LVH, in particular neurohumoral influences. From a morphological point of view, hypertrophy of the cardiac muscle is defined as an increase in the size of existing myocardial fibers. In most experimental models, myocardial hypertrophy is associated with myosin isoenzymatic changes, consisting in a shift from the faster migrating isoenzyme V1 to V3, a form that migrates more slowly. However these changes do not occur in all animal species and particularly in humans. In the hypertrophied human ventricle, a decreased ATPase activity of myofibrils was observed, probably related to changes in myosin light chains. Presently the changes in ATPase activity and in ventricular contractility do not still have a clear molecular basis in humans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heart and hypertension. 252 4

A new scintigraphic method to detect myocardial necrosis has been developed using antimyosin monoclonal antibody F ab labeled with indium-111 (111In-antimyosin). We investigated 111In-antimyosin scintigraphy in 35 patients with myocardial infarction, 5 patients with myocarditis and 3 patients with angina pectoris. 111In-antimyosin F ab was administered iv and antimyosin images were recorded by planar and single photon emission computed tomography (SPECT) 48-72 hrs after injection. Planar images showed discrete localization of 111In-antimyosin in 26 of 27 patients within 16 days after the onset of acute myocardial infarction in 14 of whom creatine kinase, glutamic oxaloacetic transaminase and lactic dehydrogenase had already normalized. In addition, positive scans were also obtained in 4 of 8 patients 1 to 9 months after the onset of the disease. Three patients with acute myocarditis (two of whom were biopsy-proven) had positive scans 2 and 4 weeks after the onset of the disease. Although mechanism of persistent positive anti-myosin images in the chronic stage remains to be clarified, 111In-antimyosin scintigraphy holds potential promise as a noninvasive method for the detection of myocardial injury.
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PMID:[Clinical trial of 111In-antimyosin antibody imaging: (2). Imaging of myocardial infarction and myocarditis]. 279 99

To detect myocardial cell damage, serum samples of 42 consecutive patients with angina at rest were screened for cardiac myosin light chains, which were detected in 22 patients (52%). In 17 of these patients there was a persistent release of myosin light chains lasting until the 4th hospital day, whereas in 7 patients myosin light chains were only detectable during the initial 24 h after admission. The presence of myosin light chains correlated with signs of ischemia in the electrocardiogram (ECG) (p less than 0.05) and with the extent of coronary artery narrowing (p less than 0.05). Cardiac myosin light chains were elevated in serum only if there was a greater than or equal to 75% diameter narrowing in at least one major vessel. In all five patients who developed transmural myocardial infarction during the course of their hospital stay, myosin light chains were detectable greater than or equal to 28 h before the diagnosis of myocardial infarction could be established by ECG criteria and conventional serum enzymes. Thus the detection of circulating cardiac myosin light chains enables one to identify a subgroup of patients with angina at rest having more severe coronary artery disease with a worse outcome.
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PMID:Circulating cardiac myosin light chains in patients with angina at rest: identification of a high risk subgroup. 334 52

In 27 patients presenting with angina pectoris at rest and normal serum creatine kinase (CK) activity, cardiac myosin light chains (CM-LC), myoglobin (MG), and CK-B isoenzyme were determined in 7 serial blood samples by radioimmunoassays. Measurable amounts of CM-LC were found in at least one serum sample in 13 patients. MG was found to be elevated in 9, and CK-B in 8 of these patients. In the 189 serum samples determined, CM-LC were found more frequently elevated (21.7%) than MG (13.2%, P less than 0.05) or CK-B (12.2%, P less than 0.05). Coronary angiograms were obtained in 21 of the 27 patients. Elevated marker protein concentrations were found only in patients with coronary artery stenosis greater than or equal to 70% of at least one coronary artery. The incidence of elevated serum concentrations of any of the 3 marker proteins determined was higher in patients with 3 vessel disease than in those with 1 or 2 vessel disease (33.9% vs 15.6%, P less than 0.05), and it was higher in patients with a history of previous myocardial infarction than in those without (34.5% vs 11.4%, P less than 0.001). The findings suggest that in a subgroup of patients with angina pectoris at rest but without evidence of acute myocardial infarction, ischaemic damage of small myocardial areas can be detected by serological assays of high sensitivity. Among the marker proteins studied, CM-LC were found the most sensitive.
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PMID:Myoglobin, creatine kinase-B isoenzyme, and myosin light chain release in patients with unstable angina pectoris. 366 58

A radioimmunoassay for human cardiac myosin light chains (CM-LC) was developed and evaluated as a selective diagnostic test for acute myocardial infarction (AMI). The assay had a sensitivity of 1.0 ng/ml (+/- 2 standard deviations) in serum. Eighty-three patients with confirmed AMI all showed an elevated plasma concentration of CM-LC at some time during the course of their illness. Of 9 patients from whom early blood samples were obtained, 7 had diagnostic concentrations within 6 hours from the onset of chest pain. Only 2 had an elevated total creatine kinase level at this time. CM-LC concentrations peaked on days 2 to 4, but remained elevated in patients with large AMIs for more than 1 week. In preinfarction syndrome, 8 of 15 patients had elevated CM-LC levels at least once. Of 15 patients with stable angina pectoris, only 1 patient, who had congestive heart failure, showed elevated light chain levels. CM-LC levels were not detectable by this method in the sera of healthy persons (n = 72), patients with recent intramuscular injection (n = 3), or those with a variety of systemic illnesses (n = 14). In initial studies using an antiserum having 25% cross-reactivity between cardiac and skeletal muscle myosin light chains, 3 patients who had extensive skeletal muscle damage appeared to have elevated concentrations. Patients with this finding have not yet been examined with a more specific antiserum (8% cross-reactivity).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diagnosis of acute myocardial infarction by detection of circulating cardiac myosin light chains. 649 59

Isovolumic relaxation abnormalities have been noted in the ischemic left ventricle, but altered end-diastolic distensibility, as well as the role of right ventricular distention, is debated. Accordingly, left ventricular end-diastolic pressure and myocardial segment length were studied in the open-chest dogs with critical (90% diameter reduction) stenoses on both left anterior descending and circumflex coronary arteries. Regional segment length was measured with ultrasonic crystals placed subendocardially, and ischemia was induced by pacing tachycardia for 3 minutes. Transient vena caval occlusion was done to unload the right ventricle and to produce a series of left ventricular end-diastolic pressure and left ventricular end-diastolic segment length points before and after pacing tachycardia. After pacing tachycardia, left ventricular end-diastolic pressure (9.3 +/- 0.9 to 16.9 +/- 1.5 mm Hg, P less than 0.001) and time constant T of left ventricular isovolumic pressure decline (46 +/- 3 to 60 +/- 5 msec, P less than 0.01) increased, with an increase in left ventricular end-systolic segment length (9.8 +/- 0.3 to 10.5 +/- 0.3 mm, P less than 0.001), and a decrease in fractional shortening (17.6 +/- 1.7 to 14.5 +/- 1.3%, P less than 0.01) in the ischemic region, although right ventricular end-diastolic pressure was unchanged. With vena caval occlusion, right ventricular diastolic pressure fell promptly to near zero, followed by decrease in left ventricular pressure and segment length. In each dog, the left ventricular end-diastolic pressure-end-diastolic segment length relation shifted upward after pacing tachycardia. Pacing tachycardia was performed again in six dogs without stenoses. In this group, fractional shortening was preserved after pacing tachycardia (15.7 +/- 2.3 to 15.3 +/- 2.3%, NS), and left ventricular end-diastolic pressure (9.4 +/- 1.8 to 9.8 +/- 1.8 mm Hg, NS) was unchanged. The left ventricular end-diastolic pressure-segment length relation did not shift upward after pacing tachycardia. These data indicate that extrinsic compression of left ventricle by right ventricle is unlikely to be responsible for the upward shift in this model, and the upward shift in end-diastolic left ventricular pressure-segment length relations, as well as dynamic left ventricular diastolic pressure-segment length, supports the concept that persistent myosin-actin interaction throughout diastole plays an important role in the diastolic abnormalities in this angina physiology model.
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PMID:Left ventricular diastolic pressure-segment length relations and end-diastolic distensibility in dogs with coronary stenoses. An angina physiology model. 674 30


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