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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A radioimmunoassay for human myoglobin has been used to study the serum myoglobin level in 13 normal individuals and 68 patients admitted to a Coronary Care Unit because of chest pain. Values in normal individuals ranged from 3 to 75 and averaged 25 +/- 23 (SD) ng/ml. Thirty-two patients with myocardial infarction initially examined within 12 hours of the onset of chest pain all showed clear-cut elevations in serum myoglobin, peak values ranging from 200 to 5500 and averaging 1368 +/- 1357 ng/ml. Seventeen patients with clinically atypical chest pain and no subsequent evidence of myocardial necrosis had myoglobin levels in the normal range, as did 11 of 19 patients with chest pain thought clinically to represent myocardial ischemia but no subsequent evidence of myocardial necrosis by conventional criteria. The final eight patients in the latter group showed mild elevations of serum Mb, peak values ranging from 102 to 280 and averaging 162 +/- 52 ng/ml; the basis for these elevations remains to be clarified.
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PMID:Radioimmunoassay for human myoglobin. Initial experience in patients with coronary heart disease. 56 27

Phytic acid stimulated the myoglobin-t-butylhydroperoxide (TBHP)-catalysed oxidation of uric acid, but inhibited the peroxidation of erythrocyte membrane lipids induced by the same system. Butylated hydroxytoluene, a free radical chain reaction-terminating antioxidant, also suppressed the myoglobin-TBHP-induced lipid peroxidation. Moreover, phytic acid inhibited the hydroxyl radical-induced degradation of deoxyribose, but the extent of inhibition in this system was reduced by increasing the ferric ion concentration, suggesting that these effects of phytic acid on the myoglobin-TBHP-mediated oxidation are more likely attributable to its metal chelating properties rather than to a free radical scavenging action. The effectiveness of phytic acid, a naturally occurring antioxidant, in the inhibition of both iron- (as previously shown) and myoglobin-dependent lipid peroxidation suggests its possible therapeutic application as a non-toxic antioxidant for ameliorating the extent of oxy-radical-mediated myocardial ischemia/reperfusion damage.
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PMID:Effects of phytic acid on the myoglobin-t-butylhydroperoxide-catalysed oxidation of uric acid and peroxidation of erythrocyte membrane lipids. 201 Nov 17

This study was undertaken to assess the effect of a calcium antagonist, nicardipine (N), added in a cardioplegic solution on the ischemic myocardium. Isolated rat hearts were perfused with oxygenated Krebs Ringer Bicarbonate (KRB) solution by Langendorff's perfusion method and were subjected to 2 hours of ischemic arrest at 30 degrees C with multidose cardioplegia (every 30 min, for 5 min) and a subsequent 60 min of reperfusion. HR, LVP, coronary flow and oxygen tension of coronary effluent were monitored. Oxygen saturation of intracellular myoglobin and redox state of mitochondrial cytochrome aa3 in the myocardial cell were continuously measured throughout studies by a spectrophotometer. Oxygenated crystalloid cardioplegic solution (KRB) containing 25 mM of potassium was used. 40 rats were divided into 4 groups (10 rats each) according to the concentration of N (none, 0.5, 1 and 2 mg/L) in fully oxygenated potassium cardioplegic solution (PO2: 601 +/- 31 mmHg). The percent recovery of pressure-rate product after reperfusion was compared in each group and the optimal concentration of N was found to be 1 mg per liter of cardioplegic solution. No significant difference was found between Group Ia (N = 0 mg/L) and Group Ib (N = 1 mg/L) in metabolic or hemodynamic recovery after reperfusion. In other experiments, 40 rats in Group IIa (N = 0 mg/L, n = 20) and Group IIb (N = 1 mg/L, n = 20) received 10 ml of poorly oxygenated cardioplegic solution (PO2: 215 +/- 10 mmHg) on each reinfusion followed by a 25 min interval of ischemic arrest. The index of oxygen utilization, MVO2/pressure-rate product after reperfusion was significantly lower in Group IIb than in Group IIa (p less than 0.05). The results show that the addition of N (1 mg/L) to the cardioplegic solution preserved a more aerobic state (higher intracellular oxygen level) in the myocardium by further suppressing myocardial oxygen demand during the ischemic period which resulted in better myocardial protection. Therefore, it is concluded that the addition of N to the cardioplegic solution enhances myocardial preservation during myocardial ischemia.
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PMID:[Functional and metabolic effects of nicardipine on ischemic rat hearts with multidose potassium cardioplegia]. 237 97

The present study investigated whether the lack of enzyme increase is reason enough to exclude necrosis in patients with ischemic heart disease who develop electrocardiographic sustained ST-T changes in the absence of Q waves. In 15 consecutive patients with angina who developed sustained ST-T changes during hospitalization, the presence of myocardial necrosis was investigated by a prospective multiparametric approach. Serum enzymes and myoglobin, pyrophosphate uptake, 2-dimensional echocardiography, perfusion scintigraphy, left ventriculography and coronary angiography were evaluated. According to creatine kinase and creatine kinase-MB peak at twice the upper normal value, the diagnosis of acute myocardial infarction applied only to 40% of patients. However, myoglobin was positive in 80% and a perfusion defect could be documented by an electrocardiographic gated microsphere technique in 100% of patients. The positivity of myoglobin increased to 100% and of creatine kinase and creatine kinase-MB to 87 and 60%, respectively, when a peak value twice the individual lowest value was considered for positivity. The 100% presence of perfusion defects associated with the high prevalence of both positive pyrophosphate uptake (87%) and regional dyssynergies (87 and 73%, respectively, by left ventriculography and echocardiography) strongly suggest that sustained (greater than or equal to 7 days) ST-T changes in this population were indicative of myocardial necrosis. Thus, by conventional enzymatic approach, diagnosis of non-Q-wave infarction can be missed in a sizable number of patients and present important clinical implications.
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PMID:Multiparametric approach to diagnosis of non-Q-wave acute myocardial infarction. 253 2

Altogether 106 patients with different types of acute CHD (large and small local MI, unstable angina) and stable angina were investigated. Combined assessment of perfusion disorder permits differentiation of necrotic and ischemic myocardial lesions. A degree and type of RP accumulation corresponds to a size of necrotic myocardial lesion determined by means of biochemical markers of necrosis. Parallelism of myoglobin concentration, isoenzyme activity in the blood serum and the results of scintigraphy was revealed. In focal RP accumulation, myoglobin concentration reached maximum values; a moderate increase and decrease up to normal values in the absence of accumulation were observed in diffuse accumulation. Diffuse RP accumulation in patients with stable and unstable types of angina was indicative of transient perfusion disorders resulting from myocardial ischemia.
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PMID:[Scintigraphy of the myocardium in ischemic heart disease]. 254 77

Endomyocardial biopsies were taken from the apex of the left ventricle in 15 patients operated on for aortic valve disease or ischaemic heart disease and from papillary muscles in six patients operated on for mitral valve disease. Activities of cardiac phosphofructokinase (PFK), total lactate dehydrogenase (LD), its isoenzyme LD1, aspartate aminotransferase (ASAT), total creatine kinase (CK), its isoenzyme MB, citrate synthase (CS) and myoglobin content (MYO) were related to the angiographically determined left ventricular function. Activities of total LD, PFK and PFK/CS ratio were lower in patients with decreased, than in those with normal, left ventricular function. Myoglobin content and activities of CS and ASAT were not related to left ventricular function. It is suggested that depressed left ventricular contractility is associated with a decreased glycolytic capacity while the oxidative capacity is mainly unaltered.
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PMID:Key enzymes of myocardial energy metabolism in patients with valvular heart disease: relation to left ventricular function. 297 29

Detailed review of the literature for chest discomfort evaluation in the Emergency Department leaves the clinician without a precise guideline as to whom to admit or send home. It is clear that the seasoned physician's instinct (the sum total of the history, physician examination, and ancillary laboratory tests) is as good an indicator as existing statistical decision models. Current decision rules appear most helpful as teaching aids for physicians-in-training and for providing reassurance to seasoned physicians. Although ancillary tests such as echocardiography and rapid myoglobin analysis may play more important roles in the future, emergency physicians must now rely primarily upon their clinical impression to guide admission decisions. Vigorous attempts to minimize the admission of patients without ischemia to the CCU will increase the incidence of infarction patients released from the Emergency Department. The liberal use of intermediate care unit beds may represent one future disposition alternative. Nonetheless, each physician must establish his or her own threshold for admission. Several studies have found a 5 per cent unintentional release of infarction patients from the Emergency Department. Decreasing the admission threshold may lower this rate substantially. Patients with chest discomfort who are released from the Emergency Department require close followup. At urban teaching hospitals, where private physician referral is often limited, the institution may need to establish a clinic specifically for this purpose. Unrecognized myocardial ischemia is one rationale for close followup; however, the pursuit of alternative diagnoses including gastrointestinal and psychiatric (e.g., panic disorders) etiologies may minimize subsequent morbidity in the released population.
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PMID:Detection of myocardial ischemia/infarction in the emergency department patient with chest discomfort. 328 Mar 3

As early as in the graphical RKG-RCG period a close inverse correlation could be established between the LV-EF and the serum myoglobin level during the acute course of myocardial infarction, in 10 patients in repeated follow up examinations. Corr. coeff. -0.91, p less than 0.01. In the mid seventies it could be shown by RKG-RCG, in 15 IHD patients with angina pectoris that the decrease of the basal LV-EF during ergometric load reflected the severity of IHD, compared with the increasing LV-EF tendency of 15 normal subjects. This fact could be verified on 19 middle age males (mean age, 41 years) by 99mTc RBC gamma camera ventriculography, i.e. that under modest load (100 W ergometry) a more than 10% decrease was a non-specific sign of main branch or three-vessel coronary heart disease. So in this extreme case our nuclear stethoscope-like RKG-RCG method alone may be satisfactory for staging and screening of coronary ischaemic heart disease (IHD) patients. All the 11 normal subjects belonged to the load-reaction group with more than 5% LV-EF increase, while the extensive anterior and inferior scar patients reacted without exception with more than 10% deficit (their basal LV-EF value was already under 45%). Supported by data in the literature in the comparison of load ECG and coronarography and two-step load, we could gain more refined data, but in accordance with the one-step load on the same patients. As regards the reproducibility of our global LV-EF investigations with gamma camera computer program Supersegams, it was within 5%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiological significance of the global and regional left-ventricular ejection fraction (LV-EF) on ischaemic heart disease patients at rest and during ergometric exercise load (from radiocardio-cyclography (RKG-RCG) to parametric amplitude and phase scan). 361 51

Recently, prostacyclin (PGI2) has been reported to have a role of potential importance in myocardial ischemia. The direct effects of PGI2 on ischemic myocardial injury (60 minutes ischemia at 30 degrees C) were examined, using a hemoglobin free isolated rat heart perfused by the Langendorff's technique. Dual-wavelength reflectance spectrophotometry was used to measure myoglobin oxygenation in cardiac tissue, from which the intracellular oxygen concentration was calculated. The effect of PGI2 on cardial function under normoxic perfusion condition was studied. PGI2 was infused for 10 minutes with the doses of 5ng/g X body weight per minute. PGI2 infusion increased heart rate, LV dp/dt and myocardial oxygen consumption. The average 9.7% increase in myoglobin oxygenation was noted during PGI2 infusion which indicated the improvement in tissue oxygen metabolism. The global ischemia was produced for 60 minutes at 30 degrees C, following to the pretreatment of 10 minutes infusion of PGI2, by the discontinuation of Langendorff's perfusion. Recovery of cardiac function such as double product and LV dp/dt at 15 minutes after reperfusion was significantly higher in the PGI2 treated group than in hearts receiving only the vehicle. Infusion of PGI2 inhibited the decrease in ATP level of the ischemic myocardium at 15 minutes after reperfusion (P less than 0.025, P less than 0.05). PGI2 prevented the increase in lactate release from the ischemic myocardium, observed in vehicle group at 1 minutes after reperfusion. In summary, prostacyclin seems to have a direct cytoprotective effect on ischemic myocardium.
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PMID:[Effects of prostacyclin on the cardiac functions and energy metabolism in the perfused rat heart]. 389 89

Human myocardium with focal myocytolysis (vacuolar degeneration, colliquative myocytolysis) was examined by routine light microscopy and by immunoperoxidase staining techniques for creatine kinase (CK) M and B, myoglobin, lactate dehydrogenase (H4)(LDH-1), and aspartate aminotransferase (AST, GOT). Sections of myocardium were selected from autopsy and surgical specimens from patients with and without clinical morphologic evidence of ischemic heart disease. Areas of coagulation necrosis showed loss of enzyme staining, while both normal and myocytolytic cells stained darkly. These results indicate that fibers with myocytolysis retain enzymes and other proteins, indicating sarcolemmal integrity, which is not present in fibers with coagulation necrosis. The implication of these findings is that fibers with myocytolysis are viable; thus, myocytolysis may be a reversible form of myocardial alteration that does not necessarily lead to cell death and eventual myocardial fibrosis.
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PMID:Myocytolysis (vacuolar degeneration) of myocardium: immunohistochemical evidence of viability. 620 21


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