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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abdominal fat distribution estimated by the waist/hip ratio (WHR) was studied in 85 subjects (55 men, 30 women) with treated noninsulin-dependent diabetes mellitus (NIDDM), and its association with cardiovascular disease and cardiovascular risk factors was analyzed. In men, WHR was highly correlated with the body mass index (BMI; r = 0.697), but this was not true in women (r = 0.091). In men, WHR was significantly and positively correlated with mean diastolic blood pressure (DBP) level. In women, this correlation was also positive, but of lesser degree. Fasting plasma insulin was highly correlated with BMI and WHR in men, but not in women. In both sexes, WHR was positively correlated with fasting serum triglyceride and negatively correlated with serum high-density lipoprotein cholesterol. In addition, mean WHR, but not BMI, was significantly greater in subjects with cardiovascular disease (positive electrocardiographic signs and/or history of angina, myocardial infarction, stroke, intermittent claudication).
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PMID:Male-type fat distribution is associated with cardiovascular risk factors and the prevalence of cardiovascular disease in noninsulin-treated diabetics. 215 Dec 25

The content of cyclic nucleotides (cAMP and cGMP), hormones (T3, T4, insulin, protein-bound iodine and thyroid-stimulating hormone) and phosphodiesterase activity were examined in the acute period and over time in blood plasma of patients with ischemic stroke. The parameters under study were found to be interrelated. Also, it has been established that the T4/T3 and cAMP/cGMP ratios and the content of insulin may serve as important biochemical criteria for the gravity of ischemic stroke.
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PMID:[Plasma levels of cyclic nucleotides, phosphodiesterase, thyroid hormones and insulin in patients with ischemic stroke]. 217 82

Cardiovascular diseases are the major cause of morbidity and mortality in the diabetic patient. The acceleration of atherogenesis occurs in all types of diabetes and culminates in such fatal complications as myocardial infarction, stroke and gangrene. Subjects with non-insulin-dependent diabetes mellitus exhibit a 3-4 times higher rate of cardiovascular mortality than non-diabetic persons. Since it was not possible to explain the excess risk by the traditional cardiovascular risk factors, various hypothesis have been put forward. These include certain aspects of blood pressure elevation, lipid changes, hyperinsulinemia, abnormal hemostasis, and impaired kidney function.
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PMID:Epidemiology and risk factors of macrovascular disease in diabetes mellitus. 220 34

The Framingham study on coronary heart disease (CHD) has shown that life-style, particularly diet, smoking, and alcohol consumption, has a great impact on the incidence of CHD. Blood lipoproteins, rather than total blood cholesterol, have been found to be more accurate predictors of CHD risk. Blood triglyceride, previously considered to have little bearing on CHD risk, was found to have a negative impact in many cases. A population subgroup with high triglyceride greater than or equal to 1.7 mmol/L (greater than or equal to 150 mg/dL), low high-density lipoprotein less than or equal to 1.04 mmol/L (less than or equal to 40 mg/dL), increased insulin resistance, and a higher incidence of diabetes mellitus has been found to be at increased risk for CHD. Diet intervention trials have shown that a reduction in total cholesterol and saturated fat consumption produced reduction in CHD incidence proportionate to the fall in cholesterol. Cigarette smoking increased CHD risk moderately; those who smoked one pack per day had twice the risk of nonsmokers. Alcohol consumption actually lowered CHD incidence in the Framingham study; however, when alcohol consumption was greater than two drinks per day, a rise in mortality from cancer and stroke was observed.
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PMID:Diet, smoking, and alcohol: influence on coronary heart disease risk. 222 Aug

Sudden fissuring of an atherosclerotic plaque has been suggested as the primary trigger of transient spontaneous ischemia in both the coronary and cerebral circulation. Measurements of urinary 11-dehydro-TXB2 and 2,3-dinor-TXB2, as well as results of Aspirin trials, have suggested that episodic platelet activation at the site of this acute vascular lesion is mediated, at least partly, by enhanced thromboxane (TX) A2 biosynthesis. Thus, episodic increases in metabolite excretion have been detected in unstable angina. Aspirin (75-325 mg/day) prevents about one third of all fatal and nonfatal thrombotic events in this setting. That a similar "dynamic" thrombotic process occurs during the early phase of acute myocardial infarction is suggested by thromboxane metabolite measurements and by the results of the ISIS-2 trial showing a similar impact of short-term Aspirin therapy to that seen in unstable angina. Percutaneous transluminal coronary angioplasty is associated with transiently enhanced TXA2 biosynthesis and Aspirin-suppressable periprocedural thrombotic complications. On the other hand, both non-insulin-dependent diabetes mellitus and type IIa hypercholesterolemia are associated with a relatively reproducible and persisting abnormality of TXA2-dependent platelet function. This association is likely to reflect a systemic rather than localized stimulus to platelet activation and a continuous rather than episodic alteration. Low-dose (50 mg/day) Aspirin can largely suppress thromboxane metabolite excretion in both diseases. Thus, low-dose Aspirin and/or selective prostaglandin H2/TXA2-receptor antagonists may be important tools to test the hypothesis that TXA2-dependent platelet activation represents an important transducer of the enhanced thrombotic risk associated with these metabolic abnormalities.
Stroke 1990 Dec
PMID:Thromboxane biosynthesis in cardiovascular diseases. 226 Jan 37

Available data indicate that cardiovascular disease has become the leading cause of death in American Indians. However, limited information is available on cardiovascular disease incidence, prevalence, and risk factors in this population. Reported cardiovascular disease rates vary greatly among groups in different geographic areas. These rates have been obtained from studies of varying sizes and different methodologies. The Strong Heart Study, which uses standardized methodology, is designed to estimate cardiovascular disease mortality and morbidity rates and the prevalence of known and suspected cardiovascular disease risk factors in American Indians. The study population consists of 12 tribes in three geographic areas: an area near Phoenix, Arizona, the southwestern area of Oklahoma, and the Aberdeen area of North and South Dakota. The study includes three components. The first is a mortality survey to estimate cardiovascular disease mortality rates for 1984-1988 among tribal members aged 35-74 years, and the second is a morbidity survey to estimate incidence of both first and first or recurrent hospitalized myocardial infarction and stroke (cerebrovascular disease) among tribal members aged 45-74 years in 1984-1988, and the third is a clinical examination of 4,500 tribal members aged 45-74 years in order to estimate the prevalence of cardiovascular disease and its associations with risk factors. Family history, diet, alcohol and tobacco consumption, physical activity, degree of acculturation, and socioeconomic status are assessed in personal interviews. The physical examination includes measurements of body fat, body circumferences, and blood pressure, an examination of the heart and lungs, an evaluation of peripheral vascular disease, and a 12-lead electrocardiogram. Laboratory measurements include fasting and postload glucose, insulin, fasting lipids, apoproteins, fibrinogen, and glycated hemoglobin. Also measured are serum and urine creatinine and urinary albumin. DNA from lymphocytes is isolated and stored for future genetic studies.
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PMID:The Strong Heart Study. A study of cardiovascular disease in American Indians: design and methods. 226 May 46

There is evidence from in vitro systems that the extent of neuronal loss in acute central nervous system ischaemia can be reduced by manoeuvres which restrict availability of glucose to the ischaemic area. Experiments were designed to test whether hypoglycaemia induced with insulin is associated with improved behavioural outcome in a recovery model of stroke. Rats learned a maze task as a test of working memory, believed to be subserved by the hippocampus, and then had a period of cerebral ischaemia, followed by reperfusion. After an interval of 14 days they were tested on the same maze, where lesioned animals had very significant (p less than 0.0001) impairment of working memory, whereas lesioned and treated (2.0 u/kg-1 insulin, minimum single plasma glucose value: 3.1 mmol/l-1) animals were indistinguishable from control animals. It is concluded that a striking degree of protection can be obtained with levels of mild hypoglycaemia which may be acceptable and practicable for use in humans.
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PMID:Insulin protects cognitive function in experimental stroke. 226 64

The effects of insulin treatment on the pathophysiology of non-insulin-dependent diabetes mellitus (NIDDM) are reviewed herein. Short-term studies indicate variable and partial reduction in excessive hepatic glucose output, decrease in insulin resistance, and enhancement of beta-cell function. These beneficial actions may be due to a decrease in secondary glucose toxicity rather than a direct attack on the primary abnormality. Insulin should be used as initial treatment of new-onset NIDDM in the presence of ketosis, significant diabetes-induced weight loss (despite residual obesity), and severe hyperglycemic symptoms. In diet-failure patients, prospective randomized studies comparing insulin to sulfonylurea treatment show approximately equal glycemic outcomes or a slight advantage to insulin. A key goal of insulin therapy is to normalize the fasting plasma glucose level. In contrast to the conventional use of morning injections of intermediate- and long-acting insulin, preliminary studies suggest potential advantages of administering the same insulins only at bedtime. Obese patients may require several hundred units of insulin daily and still not achieve satisfactory control. In some, addition of a sulfonylurea to insulin may reduce hyperglycemia, the insulin dose, or both. However, long-term benefits from such combination therapy remain to be demonstrated conclusively. Established adverse effects of insulin treatment in NIDDM are hypoglycemia, particularly in the elderly, and weight gain. Self-monitoring of blood glucose can identify patients in whom excessive weight gain is caused by subtle hypoglycemia. Whether insulin causes weight gain by direct effects on appetite or energy utilization remains controversial. A potential adverse effect of insulin has been suggested by epidemiological studies showing associations between hyperinsulinemia or insulin resistance and increased risk for coronary artery disease, stroke, and hypertension. Although potential mechanisms for an atherogenic action of insulin exist, current evidence does not prove cause and effect and does not warrant withholding insulin therapy (or compromising on dosage) when it is needed.
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PMID:Insulin use in NIDDM. 227 9

Pituitary apoplexy is characterized by a wide spectrum of clinical features. A quite rare case of painless thyroiditis, hypopituitarism and central diabetes insipidus (DI) followed by pituitary apoplexy was presented. A 61-year-old woman was admitted to our hospital in May, 1986 because of marked general malaise, polydipsia and weight loss which became progressively worse. Four months earlier she had experienced episodes of abrupt onset of severe headache associated with nausea and blurring vision. Physical examinations revealed a fine tremor, dry skin and nervousness. The thyroid gland was not palpable. Visual fields were intact. Her blood pressure was 105/64 mmHg with variable tachycardia. The routine laboratory studies were normal or negative except for hypoalbuminemia, hypocholesterolemia and hypernatremia. Erythrocyte sedimentation rate was 12 mm/hr. An impairment in corticotropin secretion was suspected from the low plasma cortisol and the low urinary excretion of 17-OHCS and the sufficient response to ACTH. Basal levels of GH and gonadotropin were also low, and responses to the stimulation tests (Insulin-stress, L-DOPA, and LH-RH) were all blunted. Brain computed tomographic scan and magnetic resonance imaging demonstrated a suprasellar mass that, after infusion, developed peripheral ring-like enhancement and large hyperintense pituitary mass, respectively. A diagnosis of pituitary apoplexy with anterior pituitary failure was made. However, the initial levels of thyroid hormones showed elevated as follows: Free T3 7.6 pg/ml, Free T4 3.3 ng/dl and T3-resin uptake 41.1%. TSH responses to TRH were all suppressed. TSH receptor antibody (TBII) was negative. Both antithyroglobulin and antimicrosomal antibodies were repeatedly positive. A thyroid scan with 99mTc revealed no uptake in the thyroid area. These findings led us to the diagnosis of "painless autoimmune thyroiditis". She had become hypothyroid without any medication. At that time radioactive 99mTc and 123I uptakes increased significantly. When hydrocortisone was substituted, daily urine output abruptly increased to about 10 liters with low osmolality, and the presence of DI was suspected. This diagnosis was confirmed by water deprivation and hypertonic saline infusion tests and subsequent pitressin test. She is currently quite well on L-thyroxine, hydrocortisone and desmopressin (1988). This association with pituitary apoplexy must be a rare occurrence, as a literature search has failed to find a similar case. The pathogenetic trigger of "painless thyroiditis" in this case may be responsible for some immunological change due to secondary adrenal insufficiency after pituitary apoplexy.
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PMID:[An unusual association of transient resolving thyrotoxicosis due to painless thyroiditis, hypopituitarism and central diabetes insipidus associated with spontaneous pituitary apoplexy]. 230 57

Cohorts of diabetic (n = 121) and non-diabetic (n = 584) patients were prospectively followed for up to ten years after having suffered from a stroke. All but six of the diabetic patients had Type 2 (non-insulin-dependent) diabetes mellitus. The diabetic patients had more risk factors associated with stroke: heart failure (p less than 0.001) and angina pectoris (p less than 0.001), than the non-diabetic patients. Neither body mass index nor blood pressure levels differed between the groups at admission. Haematocrit levels were higher in the diabetic group (p less than 0.01). The diabetic patients were more commonly afflicted by cerebral embolism and to a lesser extent by transient ischaemic attacks than the non-diabetic patients. When calculated by log-rank tests, the diabetic group had an increased risk of death (p less than 0.001), recurrent stroke (p = 0.001), and of myocardial infarction (p = 0.001) after the initial stroke. Autopsy-verified causes of death between the groups did not differ significantly, although half of all deaths during the period one to six months after stroke were caused by pulmonary embolism in the diabetic group. Thus, diabetes increases the risk of death after a stroke, and it also increases among stroke survivors the risk of recurrent stroke and myocardial infarction.
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PMID:Prognosis after stroke in diabetic patients. A controlled prospective study. 234 37


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