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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of a degenerative approach lesion in an 83-year-old male with diabetes mellitus, hypertension, and ischemic heart disease. His ECGs changed from first-degree atrioventricular (AV) block 14 years ago, to third-degree AV (A-H) block. A pacemaker was implanted for bradycardia. He died 4 years later from heart and renal failure. Serial sections through the conduction system revealed total depletion and fatty replacement of the atrial muscle at the approaches to the AV node.
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PMID:A degenerative lesion of the approach to the atrioventricular node producing second-degree and third-degree atrioventricular block. 128 48

The experience of the authors performing carotid endarterectomy in Puerto Rico is reported. The study was stimulated by the recently published results of the Carotid Endarterectomy Cooperative Trial groups in North America and Europe. This series consists of 61 carotid endarterectomies performed on 53 patients. The majority of the patients suffered from hypertension, diabetes mellitus, smoking, and ischemic heart disease. Most of the patients presented with Transient Ischemic Attacks (64%) or Reversible Ischemic Neurologic Deficits (19%). One patient died of a presumptive myocardial infarction and one patient had a post-operative worsening of his neurologic condition. The permanent morbidity and mortality rate was 3.2%.
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PMID:Carotid endarterectomy in Puerto Rico. 129

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

To study factor VII (F VII) hyperactivity in chronic dialysis patients, we measured the plasma levels of F VII activity (F VII c) and antigen (F VII Ag), prothrombin activation fragments 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and thrombomodulin in 28 patients on hemodialysis. Marked elevation of F VII c was found in long-term dialysis patients (185 +/- 30%). This hyperactivity was accompanied by both elevation of the F VII Ag level (153 +/- 28%) and enhanced activation of F VII zymogen, expressed as the F VII c/F VII Ag ratio (1.23 +/- 0.23), but pseudocholinesterase activity was decreased. The 6 patients with ischemic heart disease had slightly higher F VII c (200 +/- 25%) than those without ischemic heart disease (181 +/- 30%), although the difference was not significant. Increased F VII c was accompanied by factor Xa hyperactivity (a high plasma F1 + 2 level) in the long-term dialysis patients, but there was no significant elevation of plasma TAT levels when compared with controls matched for age, sex, and the presence or absence of diabetes mellitus. Plasma TAT levels were significantly correlated with plasma thrombomodulin levels, suggesting that thrombin generation in blood as a result of hemodialysis could induce systemic endothelial cell injury.
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PMID:Factor VII hyperactivity in chronic dialysis patients. 133 12

Radionuclide ventriculographic studies were performed at rest and during exercise in 15 middle-aged asymptomatic patients with non-insulin-dependent diabetes mellitus (NIDDM) whose mean age was 58.7 +/- 10.5 years (mean +/- SD), and in 10 age- and sex-matched normal control subjects. The patients had neither clinical evidence of cardiovascular diseases nor obvious perfusion defects during maximal exercise testing with thallium-201 myocardial scintigraphy. The average left ventricular ejection fraction (LVEF) at rest was 69.1 +/- 5.3% in the diabetic patients and 65.6 +/- 4.2% in the control subjects, and during exercise, the average LVEFs were 68.3 +/- 6.9% and 72.1 +/- 5.0%, respectively. The changes in LVEF during exercise were -0.7 +/- 7.6% in the diabetic group and +6.5 +/- 2.6% in the control group (p < 0.01). However, the filling fraction during the first third of diastole at rest was significantly less in the diabetic group than in the control group (p < 0.05), the time to peak filling rate (TPF) was longer, and the TPF/R-R, normalized by the R-R interval and expressed as a percentage, was greater in the NIDDM patients than in the control subjects. There was close correlation between the abnormal response of LVEF to exercise and the reduced early diastolic filling in the diabetic patients. We concluded that 1) not only the response of LVEF to exercise but also the early left ventricular diastolic filling at rest are impaired in middle-aged asymptomatic NIDDM patients, and 2) some common factors could cause dysfunction of both the systolic and diastolic left ventricles in NIDDM patients, possibly latent global myocardial ischemia or metabolic myocardial disturbances.
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PMID:Systolic and diastolic left ventricular dysfunction in middle-aged asymptomatic non-insulin-dependent diabetics. 133 1

The purpose of this investigation was to determine if endurance exercise training would alter the degenerative effects of streptozotocin diabetes on cardiac function and alter the responses of streptozotocin diabetic rats to induced myocardial ischemia. Diabetic rats experienced a significant (p < 0.05) reduction in cardiac function as evidenced by left ventricular peak systolic pressure (LVPSP), maximal time rate of change of pressure (+dP/dTmax), rate pressure product (RPP), and heart rate (HR). Exercise training apparently reduced the effect of diabetes since the function of non-ischemic hearts from trained diabetic rats was not different from that of non-diabetic rats. It also was not different from the sedentary diabetic rat hearts. Training did not alter the response of the hearts of either group of diabetic rats to induced myocardial ischemia.
Diabetes Res 1992
PMID:Streptozotocin-induced diabetes and the effects of endurance exercise training. 134 14

To elucidate the clinical characteristics of pulmonary edema in unstable angina, 120 patients with unstable angina who admitted to the hospital within 6 hours after the onset of chest pain were studied. The criteria for the diagnosis of pulmonary edema included interstitial pulmonary edema and diffuse alveolar edema. Pulmonary edema was present in 24 patients. In these patients, the duration of chest pain was relatively longer, and the incidences of diabetes mellitus, emergency coronary revascularization and multiple-vessel coronary artery disease were higher than in those without pulmonary edema. In addition, in-hospital mortality rate in patients with pulmonary edema was higher than in those without it (21 vs 1%, p < 0.001), which is probably due to a large area of myocardial ischemia. For these patients, therefore, early diagnosis and appropriate therapy to save viable segments of the myocardium are mandatory.
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PMID:[Clinical characteristics of pulmonary edema in patients with unstable angina]. 134 24

In a case-controlled study into the risk factors for admission to hospital with stroke, 400 subjects and 400 age and sex-matched controls were recruited. All bar two subjects were followed until death or 6 months. Previous stroke and regular snoring (p = 0.0013 and p less than 0.0001 respectively) were the only two risk factors adversely to effect mortality. Transient ischaemic attack, ischaemic heart disease, hypertension, atrial fibrillation, diabetes mellitus did not significantly effect prognosis. An apparent beneficial effect of drinking alcohol and smoking became insignificant when the confounding influence of age was taken into account.
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PMID:Effect of the risk factors for stroke on survival. 135 99

The information explosion characteristic of recent years has presented a series of findings enabling a more effective prevention of ischemic heart disease by controlling low density lipoprotein (LDL) levels of cholesterol. The detection of LDL receptors has provided new information on the mechanisms regulating the level of plasma LDL. Data on competitive inhibitors of endogenous cholesterol synthesis have afforded new possibilities of pharmacological control of LDL levels. Studies of primary prevention of ischemic heart disease have yielded evidence showing that a 1% decrease of cholesterol level reduces coronary risk by 2%. A prospective study of the relationship between cholesterol levels and coronary mortality, absolutely unique as to its extent (368,000 middle-aged men followed up over a period of 6 years) has demonstrated that there is no borderline cholesterol level below which coronary risk would be absolutely excluded. Between total cholesterol level and coronary mortality there is a close, continual and graded relationship. In light of these findings, total cholesterol levels have been reclassified: desirable levels -5.2 x 10(-3) mol.l-1, borderline risk levels under 5.2-6.2 x 10(-3) mol.l-1, and high risk levels--above 6.2 x 10(-3) mol.l-1. In subjects with several risk factors (smoking, hypertension, familial occurrence of heart, heart disease, obesity, diabetes mellitus, HDL cholesterol below 0.9 x 10(-3) mol.l-1) the level of total cholesterol should be brought down below 4 x 10(-3) mol.l-1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Plasma cholesterol levels and ischemic heart disease: new findings and new approaches]. 139 27

The authors investigated selected indicators of the lipid metabolism in 31 children with insulin-dependent diabetes for a period of 3 to 14 years. They divided the patients into two groups those with a glycosylated haemoglobin below or above 9 mumol/1 g haemoglobin. They compared the assembled results of the two groups and also with the results obtained in a control group. The total cholesterol was in both diabetic groups higher than in healthy subjects and was higher than the value which is considered from the aspect of the genesis and development of atherosclerosis as a risk value. Children with poorly compensated diabetes, i. e. with a glycosylated Hb level above 9 mumol had a higher cholesterol level as compared with well compensated diabetic children. The pre-beta fraction of lipoprotein increased in both groups of patients, however, more in those where the disease was not well compensated. There was a parallel decrease of the alpha fraction and the lipoprotein profile had a markedly atherogenic character. The apolipoprotein B concentration was in patients with well compensated diabetes lower, as compared with controls but in patients with poorly compensated diabetes after 4-5 years treatment is was significantly higher. Poor compensation of diabetes led after 4-5 years duration to a significant rise of the serum triglyceride level. As the blood lipid levels are influenced in a significantly way by diet, compensation of the disease and a low-fat diet are essential with regard to the results assembled in this investigation for prevention of ischaemic heart disease in diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Variations in lipid metabolism in long-term monitoring of children treated for diabetes mellitus]. 139 53


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