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Query: UMLS:C0028754 (obesity)
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The OSA syndrome, described over 100 years ago, was rediscovered in 1966. It is a common disorder, especially among fat, middle-aged men. Stentorian snoring and diurnal somnolence are the cardinal manifestations and should always lead to an examination during sleep. That examination (polysomnography) can demonstrate the pathognomonic events--repetitive apneas occurring in sleep--which signal the failure of the sleeping brain to maintain the patency of the supraglottic airway. All evidence points to the problem being an abnormal pharyngeal airway, one which has a shape or size or compliance that allows inspiratory collapse as the normal loss of pharyngeal dilator muscle tone occurs with sleep. The apneas are asphyxic events terminated by arousals which fragment sleep continuity and lead to the daytime sleepiness. Because the snoring occurs during sleep, the arousals are unremembered, and the sleepiness can develop so gradually that the patient may forget what normal alertness is like. It is important to interview the patient's spouse or partner. Besides obesity and maleness, other risk factors for OSA are diseases that have an impact on the configuration or effective compliance of the pharyngeal passageway. Recent studies support the clinical intuition that sleep apnea is undesirable. Sleepiness leads to accidents. The hypoxemia occurring during apnea can lead to potentially fatal cardiac dysrhythmias. A number of reports suggest that snoring and sleep apnea are associated with an increased risk of stroke, myocardial ischemia, and infarction. Finally, there are now two papers showing a significantly decreased probability of 5-year survival in patients with symptomatic sleep apnea. The good news is that treatment with tracheostomy or NCPAP improves mortality rates to normal. Approximately 90 per cent of patients can tolerate a night's initial trial with CPAP. Long-term acceptance of CPAP has now been reviewed in a number of studies, and it appears to be about 65 to 70 per cent.
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PMID:Sleep disorders and upper airway obstruction in adults. 219 4

Systolic or diastolic hypertension, cigarette smoking, diabetes mellitus, left ventricular hypertrophy, age, prior stroke, transient cerebral ischemic attack, extracranial arterial disease, and coronary heart disease are risk factors for the most common type of geriatric stroke, atherothrombotic brain infarction (ABI). Also, by contributing to hypertension and diabetes mellitus, obesity predisposes to ABI. The relationship of abnormal serum lipids and of physical inactivity to ABI is unclear. Antihypertensive treatment decreases the incidence of fatal and nonfatal stroke in patients with systolic and diastolic hypertension. Cessation of smoking also decreases risk.
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PMID:Risk factors for geriatric stroke: identification and follow-up. 220 86

Central fat distribution may be more closely associated with stroke risk than relative weight or body mass index, although both are associated with hypertension. Some of this association may reflect the fact that central obesity reflects adult weight gain, which may be more relevant to stroke risk than weight in old age. Three attributes associated with central obesity, hypertension and stroke risk deserve further exploration as a possible explanatory variables for the central obesity-stroke risk association. They are cigarette smoking, heavy alcohol intake and diabetes. Prevention of smoking and excess alcohol intake would be consistent with general public health guidelines and might be more relevant to stroke prevention than caloric reduction and management of general overweight.
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PMID:Obesity, hypertension and stroke. 220 49

Cardiac function of 30 patients who were morbidly obese was studied before bariatric surgery. Twelve patients were studied 13 +/- 4 months after surgery. These patients had a mean age of 37.1 +/- 2.9 years and a body mass index of 50.0 +/- 1.4 kg/m2. Cardiac function was measured by echocardiography, radionuclide angiography scanning, and right heart catheterization. To determine the degree of cardiac dysfunction, the patients were studied with exercise and intravenous fluid challenges. Ultrasonography produced evidence of myocardial thickening with an increased interventricular septum in eight patients (32%) and increased left ventricular mass in 17 patients (53%). The radionuclide scan suggested that morbid obesity was associated with a significantly (p less than 0.05) increased end-diastolic volume and decreased left ventricular ejection fraction as compared with patients who were of normal weight. With exercise the patient who was of normal weight had an increase in the end-diastolic volume, stroke volume, and heart rate, but the patient who was morbidly obese only increased heart rate to produce the necessary increase in cardiac output. Right heart catheterization indicated that the relationship of the pulmonary wedge pressure and the left ventricular stroke work index was abnormal in 14 of 29 patients (48.3%) and depressed in six of 29 patients (20.7%) with exercise. One liter of fluid caused an abnormal relationship of the pulmonary wedge pressure and the left ventricular stroke work index in 12 of 30 patients (40%) and a depressed response in 10 of 30 patients (33.3%). Cardiac studies were repeated in 12 patients after a 54.8 +/- 1.9 kg weight loss. Echocardiography indicated a decrease in dilatation (27.3% to 9.1%) and a significant (p less than 0.05) decrease in hypertrophy (45.5% to 0%). After the weight loss, radionuclide and right heart catheterization studies indicated improved cardiac function with reduced filling pressures and increased left ventricular work during fluid and exercise challenges. These results support the presence of obesity-related cardiomyopathy with ventricular dysfunction, which appears to be caused by a noncompliant ventricle. Significant weight loss achieved with gastroplasty results in increased ventricular compliance and improved cardiac function.
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PMID:Assessment of cardiac function in patients who were morbidly obese. 221 95

Diabetes mellitus is one of the most common chronic diseases affecting the elderly in the United States. It has been diagnosed in 9.6% of people 65 years of age and older, and an additional 9.3% meet oral glucose tolerance test criteria for the disease but have not been diagnosed. Taken together, diagnosed and undiagnosed diabetes affects almost one in every five people 65 years of age and older. An additional 23% of the elderly meet diagnostic criteria for impaired glucose tolerance, a condition that conveys excess risk for macrovascular disease. Prevalence of diagnosed diabetes in the elderly is expected to increase 44% in the next 20 years, to an estimated population of 3.9 million people. Elderly people with diabetes make an average of 3.7 visits per year to physicians specifically for care of their diabetes. Over 80% of this care is delivered by general and family physicians and internists. About 30% of diabetics 65 to 74 years of age are hospitalized each year, a rate that is almost twice that of elderly people without diabetes. Cardiovascular and peripheral vascular complications are often twice as prevalent as among people without diabetes. Risk factors for macrovascular disease are also highly prevalent among the elderly, including obesity, hypertension, and hypercholesterolemia. Three fourths of deaths of diabetic patients 65 years of age and older are caused by diseases of the circulatory system, primarily ischemic heart disease and stroke. The death rate from cardiovascular disease among elderly diabetic patients is twice that of people without diabetes in the same age range.
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PMID:Epidemiology of diabetes mellitus among the elderly in the United States. 222 42

We investigated the prevalence of carotid atherosclerosis, including mild early lesions, and its association with cervical bruits and various risk factors (age, male sex, hypertension, hyperlipidemia, diabetes mellitus, obesity, and cigarette smoking) in 232 consecutive Japanese patients. High-resolution real-time B-mode ultrasonography was performed to determine the extent of atherosclerosis, and it was quantified by using a scoring system. The prevalence of carotid atherosclerosis was 49%, 59%, and 41% in all 232 patients, the 100 symptomatic patients, and the 132 asymptomatic patients, respectively. Although carotid lesions were detected frequently (87%) in the 30 patients with cervical bruits, bruits were noted in only 30% of the 88 examined patients with carotid atherosclerosis. Independent risk factors for carotid atherosclerosis in these patients were found to be age, male sex, and hyperlipidemia; diabetes mellitus was a possible risk factor for carotid atherosclerosis. Our study did not show a close association between hypertension and carotid atherosclerosis, and this might be caused by the high prevalence of hypertension in our patients. Our findings suggest an increasing prevalence of carotid atherosclerosis in the Japanese, though this should be confirmed in a population-based study. Our study demonstrates the clinical usefulness of high-resolution B-mode ultrasonography for the evaluation of early carotid atherosclerosis.
Stroke 1990 Nov
PMID:Ultrasonic evaluation of early carotid atherosclerosis. 223 50

The hypothesis that obesity-related hypertension is relatively innocuous was explored by an examination of cardiovascular events over 34 years of follow-up when related to biennially measured weights and blood pressures using time-dependent covariate proportional hazards analysis. The 5209 participants were also classified by age, cigarette smoking, and antihypertensive treatment at each of four baseline examinations with 8-year follow-up periods. Over the period of follow-up, there were 978 cardiovascular events in men and 836 in women. Risk of cardiovascular morbidity and mortality in general and of CHD in particular was as strongly related to hypertension at all levels of body mass index. This was also found to apply when adjustment was made for possible confounding by cigarette smoking. Age and smoking-adjusted absolute risks of cardiovascular events were found to be higher in hypertensive individuals with high than with low BMIs. Furthermore, the relative risk of cardiovascular disease did not vary significantly with BMI. Thus hypertension is at least as dangerous in obese as in lean persons at all ages in either sex, providing no support for the hypothesis that hypertension in the obese is more benign. This is important, since obesity predisposes to hypertension and most who have hypertension are obese. This report examines the hypothesis for CVD outcomes considered by previous reports and also the subcategories of CVD disease such as myocardial infarction and stroke, and includes data on both men and women and on young and old.
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PMID:Is obesity-related hypertension less of a cardiovascular risk? The Framingham Study. 223 71

A large proportion of hypertensive men and women in Europe and North America are overweight. In obesity, the expanded blood volume increases cardiopulmonary volume, cardiac filling, left ventricular preload, stroke volume and, thereby, left ventricular work. Given enough exposure time, it is probable that all obese persons in the Western hemisphere would become hypertensive unless they succumb to competing causes of death. A postulated causal role of obesity in hypertension is based on epidemiological observations. In prospective studies weight gainers in adolescence are more often hypertensive than weight stable individuals. In the lower socio-economic strata of industrialized countries there is a higher prevalence of obesity and hypertension. Persons with high body weight show the greatest rise of BP with age. More relevant demonstration of a causal relationship is weight reduction in hypertensive patients. The evidence from a variety of sources, a) risk factor reduction and enhanced BP reduction in the Hypertension Detection and Follow-up Program patients on antihypertensive medication who experienced modest weight loss, b) clinical observations of formerly obese hypertensives who can forego BP lowering drugs, and c) the reversibility of haemodynamic change found in many overweight hypertensive patients after losing 10 kg, strongly suggests that the impact of obesity on hypertension is considerable.
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PMID:Obesity and hypertension: epidemiological aspects of the relationship. 225 90

Standardised data on blood pressure, 24 h urinary electrolyte excretion, body mass index (BMI) and alcohol intake were collected as part of the INTERSALT study in 598 men and women aged 20-59 years, selected randomly from three population groups in the United Kingdom. For the three centres combined, mean systolic blood pressure was 121.4 mm Hg and diastolic pressure 72.1 mm Hg, urinary sodium excretion 152.1 mmol/24 h, urinary potassium excretion 61.0 mmol/24 h, urinary sodium/potassium ratio 2.64 and BMI 25.2 kg/m2. Prevalence of heavy alcohol drinking in men (greater than or equal to 300 ml/week) was 27.5 per cent. Applying overall INTERSALT regression coefficients to the United Kingdom data suggested that modest changes in average sodium and potassium intakes, together with reductions in the prevalence of obesity and (in men) of heavy alcohol drinking could lead to important reductions in average population blood pressures and the prevalence of hypertension. The potential of this multifactorial approach to blood pressure control was illustrated by stratifying individuals within each of the United Kingdom centres by sodium and potassium excretion, BMI and alcohol intake. The 20 (out of 299) men considered at 'lower risk' for high blood pressure with respect to the above variables had systolic pressure lower by 11 mm Hg (P less than 0.01); for the 27 (out of 299) 'lower risk' women, systolic pressure was lower by 5 mm Hg (P = 0.06). These non-pharmacological approaches towards more favourable blood pressure levels could be accompanied by reductions in mortality from stroke and coronary heart disease.
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PMID:Sodium, potassium, body mass, alcohol and blood pressure in three United Kingdom centres (the INTERSALT study). 226 96

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


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