Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Defibrotide (D) is a natural polydeoxyribonucleotide from mammalian lungs with profibrinolytic and antithrombotic activities. D also has PGI2-stimulating and tissue plasminogen activator (TPA)-releasing activities, but has no anticoagulant properties. The protective effects of D were demonstrated very recently in a model for non-lethal ischemia in the cat. In the experiments reported here Defibrotide was tested in a model for acute myocardial ischemia leading to ventricular fibrillation (VF) and death of the cat. Occlusion of the coronary artery (LAD) at its origin induced VF and death in 17 of 20 control cats. When cats were treated with D (32 mg Kg-1, bolus i.v., + 32 mg Kg-1 h-1, i.v., after LAD occlusion) 19 of 20 animals survived until the end of experiments. D also prevented changes in plasma and myocardial CPK, hemodynamics and ECG. D was compared with a variety of pharmacological agents which are used clinically for specific cardiovascular diseases. The ability of D to promote considerable generation of PGI2 from vascular walls plus its ability to prevent the decreases in CPK-activity and ATP in the myocardial tissue may have roles in its beneficial effects against ischemic heart in the cat. However, the mechanism/s of the substantial protective effect of D against cardiac death has still to be clarified.
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PMID:Protective activity of defibrotide against lethal acute myocardial ischemia in the cat. 308 10

Acute myocardial ischemia followed by protracted asynergy and subsequent resolution was defined as reversible ischemic myocardial damage. The purpose of this study was to confirm the existence of this entity and to illustrate the clinical features. The subjects consisted of 26 patients with typical acute myocardial ischemia who satisfied the above definition, and serial changes in left ventricular wall motion were observed by two-dimensional echocardiography. The left ventricle was divided into 11 segments and the movement was scored according to the dynamic behavior of each segment by five points ranging from normal (0) to dyskinesis (4), and evaluated semiquantitatively using the total score sum as the total asynergy score. Compared to the initial value, this score decreased to 57% after one week, 38% in two weeks, 22% in three weeks and 17% in four weeks. The asynergy persisted 23.7 +/- 13.5 days and ranged from two days to three months. The peak CPK ranged from 32 to 561 IU (mean 212 +/- 157 IU). Coronary arteriography revealed undisturbed flow of the responsible artery in both acute and chronic phases including four cases of successful PTCR. Comparison of the electrocardiographic changes and asynergy showed that diminished R wave amplitude, ST segment elevation and inverted T waves are frequently associated with persistence of asynergy, extensive asynergy can even occur in cases without a diminished R wave or abnormal Q wave and when asynergy resolves, ST segments tend to return to the baseline, but T wave inversion commonly persists. A transient Q wave was observed in 38% of the patients examined. The electrocardiogram became normal in an average of 111.3 +/- 75 days. In conclusion, there is a subgroup of reversible asynergy among cases of unstable angina pectoris or subendocardial infarction. The mechanism for this may be myocardial "stunning" following transient transmural ischemia. Recognition of this fact seems very important in the diagnosis and treatment of acute myocardial ischemia.
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PMID:[Reversible ischemic myocardial damage: clinical observation using two-dimensional echocardiography]. 365 11

We investigated the effects of Defibrotide (D), a natural polydeoxyribonucleotide, on acute myocardial ischemia (AMI) in anesthetized cats. A permanent ligature was placed around the left anterior descending coronary artery (LAD) 12-14 mm from its origin. Ventricular fibrillation and death were exceptional and when they occurred the cats were not included in the evaluation. Pretreatment of cats with D, 32 mg Kg-1 h-1, i.v. infusion, maintained throughout the 5 h occlusion period, reduced AMI-ST segment increases and increased the diminished pressure-rate index (PRI). AMI-induced changes in lactate, ATP and CPK in ischemic tissue were prevented by D. PGI2 gave the same results as D. Atenolol prevented the loss of myocardial CPK, but had no favourable effects on lactate and ATP in ischemic tissue. The beneficial effects of D in AMI reported here could be partly attributed to its ability to enhance PGI2 release from vascular walls; D might also relieve ischemia by improvement of local tissue oxygenation, energy supplies and platelet function by its ability to deaggregate platelet clumps.
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PMID:Cardioprotective effects of defibrotide in acute myocardial ischemia in the cat. 389 Feb 60

Haemorrheological disturbances have already been described in ischaemic heart disease. However, it has not been established whether these changes are secondary to the ischaemia and/or myocardial infarction or whether they play a role in initiating or sustaining the haemodynamic abnormalities which cause infarction. We report our results observed in 14 patients aged 48 to 75 years admitted to the coronary care unit with a diagnosis of acute coronary insufficiency defined as typical persistent anginal pain resistant to glyceryl trinitrate associated with specific ECG changes (without pathological Q waves or increased serum CPK concentrations). Blood samples were obtained on admission for determination of: haematocrit, total blood viscosities at different levels of shear with the patients hematocrit and with corrected hematocrits, total blood filtrability, plasma viscosity and plasma albumin fraction. All patients received 800 mg lidocaine, 40 mg chlorezepate, adequate anticoagulant doses of heparin and a specific antianginal drug: amiodarone, nifedipine or diltiazem. Six patients had a favourable outcome and were discharged from the Coronary Care Unit without myocardial infarction (Group I); the remaining 8 patients (Group II) developed documented changes of myocardial infarction between the 12th and 4th day after admission (see the Table in the text). The haemorrheological parameters on admission of the two patients groups were compared. The abnormalities observed were significantly more severe in the group developing myocardial infarction. This suggests that these changes may play a major role in initiating conditions leading to myocardial necrosis. These observations confirm the results of other workers who have also shown a relationship between the severity of infarction and the incidence of haemodynamic complications and changes in blood viscosity and filtrability.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemorheologic disorders in the threatened myocardial infarct syndrome]. 393 83

The purpose of this prospective study in 66 patients with acute ischemic heart disease was to analyze the possible effects of moderately elevated levels of carboxyhemoglobin (COHb) on the early course of this disease. Thirty-one patients presented with a level of COHb less than or equal to 2% and 35 with a level of greater than 2%. In the group with elevated COHb, more patients developed transmural infarction, but the difference was not significant (p = 0.123). Patients with transmural infarction had higher maximum CPK values (p less than 0.01), when COHb levels were greater than 2%. During the first 6 h after admission to hospital, these patients needed an antiarrhythmic treatment significantly more frequently (p = 0.003). Differences in rhythm disorders were still present at a time when nicotine, due to its short biological half-life, was already eliminated. We conclude that a moderately elevated level of COHb is not just a marker for recent smoking but may aggravate the course of acute ischemic heart disease.
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PMID:Influence of moderately elevated levels of carboxyhemoglobin on the course of acute ischemic heart disease. 407 Aug 1

Acute ligation of the left coronary artery of rats produced abnormal Q-wave in the electrocardiogram, tachycardia and frequent ventricular fibrillation. Serum CPK level was elevated, reaching a maximum at 3 to 5 hours after ligation and returning to near the pre-ligation level 24 hours later, when CPK activity in the left ventricle markedly decreased. Pretreatment with bucumolol at 2.5 mg/Kg s.c. and 5 mg/Kg s.c. lessened these changes and increased the survival rate in a dose related manner. d-Bucumolol at 5 mg/Kg, on the other hand, increased survival rate primarily by suppressing ventricular fibrillation without any significant effect on other parameters. These results suggest that the membrane stabilizing action does not contribute to protective actions of bucumolol against myocardial ischemia.
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PMID:Effects of bucumolol, a beta-adrenergic blocking agent, and its d-isomer on myocardial infarction produced by coronary artery ligation in rats. 611 77

Many isotopic methods have been proposed recently for the investigation of normal and diseased myocardium in ischaemic heart disease. The results of myocardial scintigraphy with Technetium 99 m marked methylene diphosphonate in the supine, left lateral and 30 degrees or 45 degrees right anterior oblique incidences are reported. A preliminary study of the tracer's fixation on diseased myocardium was performed in 18 patients. Scintigraphy every 30 minutes over a five hour period showed the optimal time for investigation to be situated between the third and fourth hour after the injection of the tracer. Seventy eight patients were then investigated; 82 scintigraphies were performed, 58 in patients with acute myocardial infarctions confirmed by the usual biological and electrocardiographic changes. A 74% sensitivity and 67% specificity were obtained with the methylene diphosphonate method. These figures varied according to the type of necrosis, subendocardial or transmural and with its extent, chronicity and degree of CPK elevation. Methylene diphosphonate scintigraphy would appear to be less sensitive and more specific for diseased myocardium than other isotopic methods. It may be carried out at the bedside and could improve the diagnosis of acute myocardial infarction when the clinical history and electrocardiographic changes are difficult to interpret.
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PMID:[Myocardial scintigraphy using technetium-99m labelled methylene diphosphonate in coronary care units. 82 cases]. 645 75

Three cases (one, newborn infant and two infants--one of them recently published--) who present electrocardiographic and enzymatic alterations comparative with diagnosis of ischemia and myocardial infarction are reported. Rarity of this entity in infants is stressed as most of published cases are secondary to ananomolous coronary artery. Etiology of the cases presented shows a myocardiac fibrosis with Schwachman's syndrome in one case, a coronary thrombosis secondary to a disseminated intravascular coagulation in a second case, and finally a generalized hypoplasia of coronary arteries. Hypoxia appears in these cases a factor acting in favour of myocardial ischemia. Diagnostic criteria of acute myocardial infarction are based on typical electrocardiogram and rise of isoenzymes of LDH and CPK-MB. Although rare, it is a diagnosis to be considered in cases of unknow cardiac insufficiency in newborns and infants.
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PMID:[Myocardial infarction and myocardial ischemia in newborn children and infants, not secondary to an abnormal coronary]. 666 Jun 44

The activity of glycogen phosphorylase (GP) and creatine phosphokinase isoenzyme MB (CPK MB) was measured in patients with myocardial infarction over 72 hours after the anginal attack. In most clinical observations, CPK MB and GP patterns were similar, however, the GP activity reached its peak 4-6 hours earlier, and sooner returned to normal, as compared to that of CPK MB. The measurement of GP and CPK MB activity at early dates of myocardial infarction provides more evidence of new lesion foci or expanding necrotic area. In one-third of the infarction patients, the said enzymes showed different patterns of activity. It is suggested that the assessment of GP and CPK MB activity in cases of myocardial infarction may contribute to better insight into both necrotic and ischemic myocardial processes associated with myocardial infarction, with similar trends in enzyme patterns indicating necrotic myocardial changes, and high GP activity coupled with unchanged CPK MB signalling myocardial ischemia.
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PMID:[Glycogen phosphorylase activity in acute myocardial infarction]. 685 63

On a model of reversible coronary blood flow disturbances in dogs short-term myocardial ischemia (2 to 15 min) in 16 chronic experiments caused an increase in the activity of total blood CPK by 57.3 +/- +/- 11.7 mE/ml (p less than 0.001) and of MB fraction by 6.9 +/- 1.23 mE/ml (p less than 0.001). Experiments in which the disturbances in coronary blood flow were repeated at intervals of 2-3 days showed that the changes in the activity of the enzymes occurred in definite stages. The results obtained on this model present new possibilities for elaborating diagnostic criteria of microfocal myocardial lesions.
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PMID:[Activity of total serum creatine phosphokinase and its MB fraction in reversible coronary blood flow disorders in dogs in a chronic experiment]. 735 98


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