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)

Although L-carnitine is not considered as an essential nutrient, endogenous synthesis may fail to ensure adequate L-carnitine levels in neonates, especially those born prematurely. Free L-carnitine is found in many foods, mainly those from animal sources. Absorption of free L-carnitine is virtually complete. Lysine and methionine are necessary ingredients for the biosynthesis of L-carnitine. All tissues in the body can produce deoxy-carnitine but, in humans, the enzyme that enables hydroxylation of deoxy-carnitine to carnitine is found only in the liver, brain and kidneys. Complex exchanges of carnitine and its precursors occur between tissues. Muscles take up carnitine from the bloodstream and contain most of the body carnitine stores. L-carnitine and L-carnitine esters are eliminated mainly through the kidneys, which may play a central role in the homeostasis of this compound. Thyroid hormones adrenocorticotrophin (ACTH), and diet all influence urinary excretion of L-carnitine. Free L-carnitine can be assayed in plasma and urine and is occasionally measured in muscle biopsy specimens. Plasma L-carnitine levels may not accurately reflect L-carnitine body stores. L-carnitine ensures transfer of fatty acids to the mitochondria where they undergo oxidation. This process is associated with production of short-chain acylcarnitine which exit from the mitochondria or peroxisomes. L-carnitine ensures regeneration of coenzyme A and is thus involved in energy metabolism. L-carnitine also ensures elimination of xenobiotic substances. Carnitine deficiencies are common. Currently, these deficiencies are classified into two groups. In deficiencies with myopathy, only the muscles are deficient in L-carnitine, perhaps as a result of a primary anomaly of the L-carnitine transport system in muscles. In systemic deficiencies, L-carnitine levels are low in the plasma and in all body tissues. Systemic L-carnitine deficiencies are usually the result of a variety of disease states including deficient intake in premature infants or long-term parenteral nutrition; renal failure; organic acidemias; and Reye's syndrome. Modifications in L-carnitine metabolism have also been reported in patients with diabetes mellitus, malignancies, myocardial ischemia, and alcohol abuse. A large number of supplementation trials have been carried out.
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PMID:[L-carnitine: metabolism, functions and value in pathology]. 129 65

The purpose of this study was to determine whether the selective type IV cAMP-phosphodiesterase inhibitor rolipram could reduce the reperfusion injury that occurs during myocardial infarction in the anesthetized dog. This question was tested in pentobarbital-anesthetized dogs subject to 90 min of regional myocardial ischemia and 5 h of reperfusion. Dogs were treated with 1 mg/kg of rolipram (i.v., 15 min before reperfusion) followed by a 1 mg/kg/h infusion over the duration of the 5 h of reperfusion. Rolipram was tested in vitro for efficacy in inhibition of isolated human neutrophil superoxide generation. Rolipram produced significant inhibition of superoxide production over the concentration range of 0.1-100 microM rolipram when neutrophils were stimulated with a 10(-7) M concentration of the chemotactic peptide f-Met-Leu-Phe. Rolipram significantly inhibited superoxide generation from human and canine granulocytes in whole blood stimulated by zymosan. Therapeutic concentrations of rolipram in the blood of dogs were achieved during the course of the experiments with a plasma concentration of 0.761 +/- 0.095 micrograms/ml (2.76 +/- 0.34 microM) at the time of reperfusion, and 0.574 +/- 0.098 micrograms/ml (2.08 +/- 0.36 microM) at the end of the reperfusion period. The relative severity of myocardial ischemia between the two treatment groups was similar as assessed with radiolabeled microsphere measurement of myocardial blood flow. Transmural myocardial blood flows were not significantly different between the two groups after coronary occlusion (control, 0.05 +/- 0.01 ml/min/g, n = 6, vs. rolipram, 0.18 +/- 0.07 ml/min/g, n = 6; p = 0.48).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of granulocyte cAMP-phosphodiesterase by rolipram in vivo is not sufficient to protect the canine myocardium from reperfusion injury. 137 23

A study is presented of the blood plasma level of opioid peptides in patients with progressive stenocardia. Results indicate non-homogeneity of the patients concerning the content of neuropeptides. Two subgroups were singled out: 1. patients with progressive stenocardia of exertion in which beta-endorphin and leucin-enkephalin were above normal; 2. patients with a severe course of ischemic heart disease. Here the content of same peptides was lower than in the compared group. Similar dependence of changes of the content of methionine-enkephalin was not revealed.
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PMID:[Enkephalins and endorphins in unstable stenocardia]. 233 Jul 14

Recent evidence indicates that different forms of stress, including hypoxia, can induce specific proteins called heat-shock or stress proteins in various types of mammalian cells. These studies examined whether myocardial ischemia can result in increased levels of proteins with molecular weight and isoelectric point characteristics similar to those described for heat-shock or stress proteins. The left anterior descending coronary artery of the dog heart was completely occluded; normal and ischemic myocardial samples were obtained 6 hours after occlusion; and total cardiac proteins and RNA were prepared. Ribonucleic acid was translated in vitro in a modified rabbit reticulocyte lysate system, and [35S]-methionine-labelled translational products as well as unlabelled cardiac proteins were separated by two-dimensional gel electrophoresis. Total proteins were visualized by silver staining and in vitro translation products quantified by fluorometry. A translatable mRNA coding for a 71,000 dalton peptide with an isoelectric point of 5.8 was markedly increased in the ischemic myocardium after 6 hours of ischemia. A protein with similar migration characteristics was detected in ischemic myocardium but not in normal myocardium. These results indicate that an mRNA coding for a translational product with similar migration characteristics of heat-shock protein 71 is induced by ischemia in the dog heart.
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PMID:Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71. 242 3

Few studies have presented a thorough analysis of young adults with symptoms of arterial occlusive disease. To learn more about the possible risk factors of vascular disease playing a role in these young patients, we have reviewed all patients of 45 years of age and younger with symptoms of arterial occlusive disease who had been referred to our department between 1978 and 1987. Thirty-seven patients (28 males and 9 females) were included in the study. The mean age at which the first symptoms occurred was 34 years. Most patients presented with chronic arterial obliterations of the lower extremities (31/37, 84%). In addition, 4 patients showed signs of ischaemic heart disease. A strongly positive family history of arteriosclerosis was obtained from 13 patients (35%). Hypertension was present in 7 patients (19%), diabetes in three (8%) and nicotine abuse was found in 27 patients (73%). Fifty-four percent of the patients (20/37) had undergone vascular reconstructive surgery, 19% (7/37) underwent transluminal dilatation, and 3 had had subsequent treatment of newly developed lesions. For this study, all patients were recalled to the outpatient clinic. A complete case history was taken followed by a physical examination and ECG. Laboratory examinations were performed to analyse parameters of: (a) coagulation; (b) fibrinolysis; (c) fat- and (d) methionine metabolism. Clear-cut laboratory abnormalities were found in 33 patients (33/37, 89%). Coagulation parameters were abnormal in 11 patients (30%) (protein S deficiency: 3 pts). Fibrinolysis was impaired in 15 patients (40%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective survey of risk factors in young adults with arterial occlusive disease. 274 53

Accurate use and interpretation of exercise test results depend on an understanding of physiologic principles, meticulous attention to proper methodology, and realization of the appropriate applications and limitations of testing. Understanding the relationship between myocardial and ventilatory oxygen consumption and exercise test variables will aid in the diagnosis and prognostic evaluation. Use of proper methodology in preparing the patient, performing the examination, and interpreting the results is critical to obtaining the maximum information with maximum safety for each individual patient. Improvements in methodology including the use of the Borg scale to estimate individual effort, abandonment of the predicted maximum heart rate, and the increased use of ventilatory oxygen uptake measurements should be applied. Exercise capacity should not be reported in total time but rather as the VO2 or MET equivalent of the workload achieved. This permits the comparison of the results of many different exercise testing protocols. The most useful exercise ECG variable for the diagnosis of coronary artery disease remains the ST segment shift. Unfortunately, it is not as helpful in localizing myocardial ischemia. Diagnostic accuracy can be improved by adjusting ST depressions for exercise-induced heart rate increase. Accuracy can be further increased by combining ECG, clinical, and radionuclide variables in probabilistic formulas that retain the independent diagnostic information from each variable and accurately predict disease probability. To avoid errors in clinical decision making, care must be used to insure that the mathematical formula used was derived from a population of patients that is similar to those being tested. The clinical applications for exercise testing include diagnosis of patients with chest pain syndromes, determination of disease severity, and prognosis in patients with known coronary artery disease, evaluation of arrhythmias, screening of asymptomatic patients, and evaluation of medical, surgical, and angioplastic therapy for coronary disease. In spite of studies involving thousands of patients, controversy exists regarding the diagnostic power of exercise testing. The large differences in reported accuracies are largely due to methodologic problems that have been encountered by various investigators. Clinicians should be made aware of these problems when reading the literature on ECG and radionuclide exercise testing. Such awareness will help them understand the limitations of these noninvasive procedures.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise testing: uses and limitations considering recent studies. 305 66

The uses of the exercise test continue to grow and diversify. Familiarity with the mechanics, logistics, and interpretation of these tests leads to their optimal use. The application of exercise testing for competitive or recreational sports, cardiovascular fitness exercise training, and cardiac rehabilitation is the focus of this review. Many test protocols are available, but treadmill testing is the most widely used. The inclusion of thallium scintigraphy in the exercise protocol requires additional time and expense and is best reserved for those in whom the exercise electrocardiographic response cannot be adequately interpreted. Exercise testing is a relatively safe procedure, providing that adequate screening of individuals for unstable cardiac or medical conditions has been performed. The test must be administered by experienced personnel in a setting where the necessary emergency resuscitative equipment is available. Adequate interpretation of the exercise test requires knowledge of the individual being tested and of the reason the test is being performed. Complete analysis of the exercise test includes electrocardiographic response (ST segment changes and rhythm disturbances), hemodynamic response (heart rate and blood pressure before, during, and after exercise), and functional capacity (exercise duration, symptoms, conversion to MET's). When exercise tests are employed to establish a diagnosis of coronary artery disease, an assessment of the pretest likelihood (prevalence) of disease is essential in deriving a reasonable assessment of the probability of disease after the test has been performed and reviewed. This information is particularly important when screening asymptomatic subjects for underlying coronary disease before they engage in an exercise program. Exercise testing of individuals with known cardiac disease prior to engaging in competitive or recreational sports can yield much useful information. In addition to a knowledge of the underlying cardiac condition, the type and intensity of the sport being performed must be taken into account when exercise testing is performed for athletic screening. Individuals with congenital or acquired valvular heart disease, coronary artery disease, and rhythm disturbances should undergo an exercise test as part of the pretraining evaluation. Patients with ischemic heart disease, especially those who have had a recent myocardial infarction or have undergone coronary artery bypass surgery, require counseling regarding their ability to perform certain activities of daily living and to return to work. Exercise testing can be a useful tool in establishing activity guidelines for these individuals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Exercise testing for sports and the exercise prescription. 355 96

Precocious atherosclerosis occurs in homocystinuria due to cystathionine beta-synthase deficiency and there is evidence that homocysteine may produce endothelial damage. Mild homocysteinemia has been reported in heterozygotes after methionine loads and it has been suggested that they could have an increased risk of atherogenesis. We measured plasma amino acids before and after a methionine load (100 mg per kg) in 17 obligatory heterozygotes, in 20 men under 50 yr with established ischemic heart disease, and in matched controls, to determine whether methionine loading allows identification of heterozygotes, and whether there is an altered rate of methionine metabolism in patients with premature coronary artery disease. The obligate heterozygotes had higher mean plasma concentrations of methionine and total homocysteine at 4, 8 and 12 hours after the load than their controls, and lower concentrations of total cysteine and taurine in fasting and all post load samples; however, there was considerable overlap of measurements in heterozygotes and their controls even when differential weightings were applied. There were no differences in mean plasma concentrations of methionine, total homocysteine or total cysteine between the patients with ischemic heart disease and their controls at any measurement point. However, two patients with premature coronary artery disease, identical twins, had persistent elevation of total plasma homocysteine and an exaggerated homocysteine response to methionine. Oral folate restored homocysteine concentrations before and after methionine to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Homocysteinemia, ischemic heart disease, and the carrier state for homocystinuria. 668 24

To determine the exercise workload, ECG, and thallium-201 image parameters that are most closely associated with a poor prognosis from ischemic heart disease, the test results of 268 patients were reviewed. Only patients with unequivocal thallium-201 redistribution were selected. A multivariate analysis was performed to find the variables that were most strongly associated with the outcomes of coronary revascularization, myocardial infarction, and cardiac death during a follow-up period of 25 +/- 19 months. Patients who underwent early elective revascularization had poorer exercise tolerance and more thallium image abnormalities than those with no events. In the remaining patients myocardial infarction was most closely related to the extent and severity of thallium ischemia (p = 0.0086), whereas cardiac death was associated with abnormal thallium lung uptake (p = 0.0082) and an inability to exercise to 9.6 MET (p = 0.0144). Thus unlike myocardial infarction, cardiac death is best predicted by variables that reflect poor left ventricular function rather than those that indicate ischemia.
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PMID:Variables associated with a poor prognosis in patients with an ischemic thallium-201 exercise test. 842 25

Similarly as in other inborn metabolic diseases the cause of hyperhomocysteinaemia are interactions between genetically conditioned changes most frequently due to reduced cystathionine-beta synthase activities and negative factors of the external environment. Negative environmental factors include above all a high dietary animal protein consumption which is the main methionine donor and a low intake of protein of plant origin. Another negative factor is a low intake of foods of plant origin. Fruits and vegetables are among others important sources of folic acid and pyridoxine. Substitution therapy with vitamin preparations is essential in homozygotes and in high risk heterozygotes of cystathionine beta-synthase. This treatment is also necessary during the periconception period in hyperhomocysteinaemic fertile women to reduce the risk of neurotubal defects in their future children. So far investigations are lacking which would provide evidence of a reduced risk of ischaemic heart disease and other cardiovascular diseases in isolated treatment of mildly elevated levels of plasma homocysteine. To elucidate the part played by hyperhomocysteinaemia in hastening of the atherogenetic process further studies are essential, focused on the interaction of elevated homocysteine plasma levels, dyslipoproteinaemias, hyperfibrinogenaemia and other metabolic indicators in this process.
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PMID:[Hyperhomocysteinemia]. 870 82


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