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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical coincidence of hypertension, obesity and non insulin diabetes mellitus (NIDDM) has long been recognized. Increasing interest has also been recently focused on the possible role of insulin and insulin resistance in mediating this association. There is also evidence that hyperglycemia per se may have a role in the pathogenesis of hypertension and atherosclerosis in NIDDM patients. Glucose is a determinant to cellular ion homeostasis, promoting an increase of intracellular calcium and suppressing intracellular free magnesium and pH. Moreover, hyperglycemia promotes glycosilation of proteins and the consequent accumulation of advanced glycosilation end products in tissues. It has recently been suggested that iter is a cellular ionic basis for the clinical and epidemiological linkage of hypertension, left ventricular hypertrophy (LVH), obesity and non insulin dependent diabetes mellitus (NIDDM). These clinical conditions may be different expressions of a common underlying defect in ion handling, displayed by elevated cytosolic free calcium and suppressed free magnesium levels. Therapeutically, reversal of this excess free calcium accumulation and/or free magnesium deficit with ion specific agents, such as calcium channel blocker drugs, may thus ameliorate not only the elevated blood pressure of hypertension but also the concurrent cardiac, vascular and metabolic aspects of the hypertensive states.
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PMID:Diabetes, hypertension and atherosclerosis: pathophysiological role of intracellular ions. 820 15

The cardio-respiratory complications of sleep apnea syndrome have been prospectively assessed in 60 patients with massive obesity and free of chronic obstructive lung disease while the associated cardiovascular diseases and the alterations of pulmonary function were taken into account. These cardio-respiratory complications were observed only in patients with a number of apneas per hour of sleep greater than 20. The sleep apneas induced nocturnal hypoxemia that is frequently severe and independently correlated to the apnea index, diurnal hypoxemia and hypercapnia that are usually moderate, and presumably left ventricular hypertrophy that is not related to the development of daytime hypertension. However the nocturnal apneas were not associated with the development of an impairment of right or left ventricular function, or with the occurrence of cardiac arrhythmias or conduction disturbances. The absence of severe cardiac complications in this study may be related to the fact that the patients were relatively young and that the sleep apnea syndrome was diagnosed at an early stage of evolution. The findings of this study could help to define a more rationale approach in several therapeutic indications of sleep apnea syndrome.
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PMID:[Cardio-respiratory complications of sleep apnea in obese patients]. 822 Nov 69

Congestive heart failure is a frequent complication of massive obesity and a major cause of death. Prior to the cardiac decompensation stage, infraclinical haemodynamic disturbances can be observed in obese subjects with normal blood pressure: the cardiac output and cardiac index increase, due to a rise in systolic ejection volume, the total peripheral resistance falls and the intravascular volume augments. Cardiac adjustment takes place in the form of excentric left ventricular hypertrophy. Ventricular extrasystoles, often associated with this hypertrophy, might be the cause of sudden death in some obese patients. Arterial hypertension is about 3 times more frequent in obese subjects than in subjects of normal weight, and even more frequent in those with massive obesity. To the high preload due to obesity hypertension adds an increased after-load. This results in augmentation of the mass and work of the left ventricle with progressive alteration of its function. The incidence of coronary disease is increased in obese subjects, notably those with abnormal adiposity. Finally, the return circulation is very often perturbed, notably in gynecoid obesity: there is venous insufficiency with a higher risk for thromboembolism, and lymphatic insufficiency or capillary permeability disorders. A low-calorie diet and a physical rehabilitation of sedentary obese subjects facilitate weight reduction and at the same time tend to correct the associated metabolic disturbances; they reduce blood pressure and also seem to reduce the left ventricular hypertrophy.
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PMID:[Hemodynamics of massive obesity]. 831 Feb 45

Atherosclerotic cardiovascular disease is a complex problem involving lipid deposition, pressure, rheologic forces, carbohydrate tolerance and thrombogenesis. The major contributors identified through epidemiologic research include atherogenic personal attributes, living habits which promote them, signs of a compromised coronary circulation and host susceptibility to these risk factors. Of the atherogenic risk attributes, such as blood lipids, blood pressure, glucose tolerance and fibrinogen, each independently contributes to risk, and the risk associated with any one is compounded by the presence of the others. The risk associated with hypertension, hyperlipidemia or diabetes varies widely depending on the level of associated risk factors. Also, at a given level of total cholesterol, risk is greatly affected by the total/HDL cholesterol ratio, which provides a practical means for assessing the two-way traffic of cholesterol. In addition, living habits, such as cigarette smoking or lack of exercise, can independently affect the risk associated with any of the atherogenic traits. These living habits, obesity and diet can also affect the level of atherogenic risk factors and must be taken into account in assessing risk and implementing preventive measures. Finally, preclinical indicators of silent myocardial ischemia greatly augment the risk associated with a poor cardiovascular risk profile. Hence, ECG left ventricular hypertrophy, blocked intraventricular conduction, repolarization abnormalities and abnormal response to exercise on monitoring must be taken into consideration. Optimal risk predictions require a quantitative synthesis of risk factors into a composite estimate. Handbooks, hand calculators and PC software have been devised for office use based on multiple logistic risk formulations. These have been shown to accurately predict disease risk in a variety of American population samples, in elderly as well as young coronary candidates. Preventive management as well as risk estimation should be multifactorial if optimal results are to be achieved. Preventive strategies should include public health measures to alter the ecology so as to shift the distribution of risk factors to a more favorable level, health education to enable people to protect their own health and preventive medicine for high-risk candidates. Greater skill must be developed to carry out such interventions. In selecting drugs to correct hypertension, diabetes and lipid disorders, it is important to choose agents which do not adversely affect the composite risk profile.
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PMID:Long-term epidemiologic prediction of coronary disease. The Framingham experience. 832 76

Left ventricular hypertrophy (LVH), defined as an abnormal increase in left ventricular mass (LVM), is detected by echocardiography in 16-19% of a general population. Its prevalence is strongly associated with age, systolic blood pressure and obesity. In addition to the assessment of LVM, echocardiography allows different forms of left ventricular remodelling in hypertension to be described: eccentric or concentric, and symmetric or asymmetric LVH. The significance of the different forms, however, is not yet well defined. Increased LVM is now recognized as a powerful, independent risk factor for all cardiovascular diseases. This observation is at variance with the general concept that LVH is a useful adaptation of the left ventricle to chronic overload. To explain this paradox, three hypotheses are proposed: LVH serves as a marker, a limited adaptative process, or a pathological process. Each hypothesis implies different therapeutic approaches; thus it is necessary to clarify the reasons why LVH is such an important risk factor.
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PMID:Left ventricular hypertrophy: epidemiological prognosis and associated critical factors. 837 Mar 74

Left ventricular hypertrophy (LVH) detected by electrocardiography (ECG) and, more recently, by echocardiography has been shown to be an extremely strong predictor of morbidity and mortality in patients with essential hypertension and in members of the general population. Increased left ventricular mass (LVM) is strongly related to both increased blood pressure and overweight. Indexation of LVM by body surface or height has advantages for the detection of LVH related to hypertension or obesity. Indexation of LVM for height to the power 2.7 revealed by analysis of growth (allometric) relations may accomplish both these goals. In validation studies, the sensitivity of echocardiography to detect LVH has been reasonably high (85-100%), whereas that of ECG has ranged from as high as 50% in severely diseased necropsy populations to as low as 6-17% in recent studies in Cornell and Framingham. ECG sensitivity can be improved by using Cornell multivariate regression equations or by consideration of the Cornell voltage-QRS duration product. Obesity dramatically decreases the sensitivity of the ECG for detection of LVH, and recent research suggests a lower specificity and a higher rate of false-positive ECG diagnoses of LVH in black than in white subjects. Standard criteria for ECG LVH are less useful than echocardiographic findings for stratifying populations into high- and low-risk subgroups because of lower sensitivity, but improved ECG criteria need further evaluation in this respect.
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PMID:Methods for detection of left ventricular hypertrophy: application to hypertensive heart disease. 837 Mar 76

We have evaluated in a case-control study the association of the main risk factors with cerebrovascular ischemic accidents in elderly patients. Two hundred and twenty patients aged 65 year or more (average age 77.3 +/- 7.3 yr, 93 males and 127 females) admitted to our Division for stroke (122) or transient ischemic attacks (TIA) (98) were enrolled: 220 hospitalized patients, age and sex-matched, without actual or previous cardiovascular clinical manifestations were the control group. Advanced senile decay, hepatic or renale failure and malignancies were considered exclusion criteria for both groups. The following risk factors have been considered: family history, obesity, cigarette smoking, diabetes, hypercholesterolemia, hypertriglyceridemia, atrial fibrillation, left ventricular hypertrophy, and related continuous variables. After logistic multiple regression analysis, atrial fibrillation, hypertension and blood cholesterol concentration above 240 mg/dl were significantly and independently associated with stroke, while only hypertension and hypercholesterolemia were associated with TIA. The unexpected finding of a significant association between hypercholesterolemia and cerebrovascular ischemia seems attributable to the choice of hospitalized patients as control group. These results indicate that hypertension and atrial fibrillation are independently associated with ischemic stroke even in advanced age.
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PMID:[Ischemic stroke and transient ischemic attacks: a case-control study of the risk factors in elderly hospitalized patients]. 848 30

Left-ventricular hypertrophy (LVH), the primary cardiac manifestation of hypertension, has been identified as the most powerful risk factor for future cardiovascular events causing morbidity and mortality, such as myocardial infarction, congestive heart failure, sudden death, and so forth. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left-ventricular filling and contractility. Besides hypertension, other risk factors such as obesity, advanced age, valvular heart disease, and other pathologic disorders can cause an increase in the hemodynamic burden and lead to LVH. Nonhemodynamic determinants of left-ventricular mass include dietary salt intake, alcohol, and neurohormones. LVH and its sequelae can be reduced by specific antihypertensive therapy, but despite these promising findings, future epidemiologic studies are necessary to document the clinical benefits of a reduction in LVH.
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PMID:Hypertension and left-ventricular hypertrophy. 856 18

Left ventricular hypertrophy (LVH) is both a target organ response to arterial hypertension and a disorder that may be responsible for increasing risk of cardiovascular events, including coronary artery disease (CAD) events, in the elderly population. Hypertension and obesity are the strongest risk factors for LVH, and both disorders are more likely to occur with age. Not surprisingly, the prevalence of LVH markedly increases with age. Although LVH may initially be a compensatory mechanism to reduce ventricular wall stress, substantial data indicate that as LVH progresses, coronary flow reserve is reduced, and CAD events are increased. Furthermore, LVH leads to systolic and particularly, diastolic ventricular dysfunction, and an increase in the prevalence and complexity of ventricular dysrhythmias. All types of cardiovascular morbidity and mortality also are increased in patients with LVH. Pharmacologic and nonpharmacologic strategies that may decrease LVH and potentially reduce cardiovascular morbidity and mortality in the elderly are reviewed.
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PMID:Prevention and reduction of left ventricular hypertrophy in the elderly. 865 63

Overweight and hypertension are considered to be independent contributors to the development of left ventricular hypertrophy (LVH). We investigated a selected subgroup (n = 520, aged 52 to 67 years) of participants from the MONICA Augsburg cohort to assess gender-specificity of left ventricular adaptation in response to increasing weight and blood pressure degrees. M-mode-echocardiographic measurements were made and calculated according to the Penn-convention in 293 women and 227 men. LVH was defined as left ventricular mass indexed to height (LVMIm) > 143 g/m in men and > 102 g/m in women (Framingham criteria). Men and women were comparable with regard to increase in LVMIm from the lowest weight and blood pressure group to the highest groups, respectively. In men the increase in LVMIm was 31% from lean to severely obese subjects (111 vs. 145 g/m, p < 0.003) and 25% from normotensive to treated hypertensive subjects (116 vs. 145 g/m, p < 0.0001); in women respective values were 36% (83 vs. 113 g/m, p < 0.0001) and 27% (88 vs. 112 g/m, p < 0.0001). The combined occurrence of obesity and hypertension had an additional effect on left ventricular mass, which was much more pronounced in women than in men. In particular, the increase in LVMIm from the group of lean normotensives to the group of severely obese treated hypertensives was 85% (72 g/m vs. 133 g/m, p < 0.0001) in women and 49% (96 g/m vs. 144 g/m, p < 0.002) in men (p-value for the gender-interaction term < 0.05). The odds ratio for the LVH-prevalence in hypertensive obese subjects as opposed to normal weight normotensive subjects were 11.9 (p < 0.0001) in women and 4.9 (p < 0.0004) in men. In conclusion, we observed for both genders independently and similarly pronounced effects of hypertension and obesity. The combined occurrence of hypertension and obesity had an additional impact on left ventricular mass and hypertrophy, however, in women the effects were significantly more pronounced than in men. The data underscore the effects of hypertension and obesity in the development of LVH. In addition, gender specific factors seem to modulate the effects of these risk factors on left ventricular mass.
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PMID:[Sex differences in the correlation between obesity and hypertension with left ventricular mass and hypertrophy]. 871 46


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