Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension directly predisposes to all of the major atherosclerotic cardiovascular disease outcomes, including coronary artery disease, stroke, cardiac failure, and peripheral artery disease. Coronary artery disease deserves a high priority in treatment of hypertension because it is the most common and lethal sequela. However, reduction of blood pressure as the sole therapeutic goal of antihypertensive therapy is no longer appropriate. Hypertension tends to cluster with other atherogenic risk factors, including dyslipidemia, glucose intolerance, insulin resistance, obesity, and elevated uric acid. Hypertension is only one of the many risk factors for atherosclerotic cardiovascular disease and is variably hazardous, depending on the number and severity of these coexistent metabolically linked risk factors. The presence of coexistent, already overt cardiovascular disease and left ventricular hypertrophy also greatly influence the hazard and choice of therapy. The urgency for, and choice of, therapy should be based on the multivariate cardiovascular risk profile rather than relying solely on the character and severity of the blood pressure elevation. In this way at-risk hypertensive persons can be more appropriately targeted for treatment designed to improve their multivariate risk profile and to provide maximum benefit and cost effectiveness.
 ...
PMID:Cardioprotection and antihypertensive therapy: the key importance of addressing the associated coronary risk factors (the Framingham experience). 884 93

Several health hazards and social disabilities are associated with obesity. Increased mortality is associated with increased body weight. A high rate of mortality results from heart disease, diabetes mellitus, gallbladder disease, high blood pressure, and cancer. Physiologic cardiovascular changes occur, leading to left ventricular hypertrophy and lipid abnormalities. Hypertension, stroke, and venous stasis are increased. Pulmonary abnormalities include obstructive sleep apnea, which can be associated with secondary polycythemia and right ventricular hypertrophy. Gallstones, gallbladder disease, and accumulation of fat on the liver are significantly increased. Gout and reproductive abnormalities in women are common. Osteoarthritis of the knees and spine occur, although osteoporosis is rare. Risk for endometrial and breast cancer is increased, particularly in the presence of increased central fat. Changes in the skin include stretch marks, acanthosis negricans, hirsutism, intertrigo, and multiple papillomas. Impaired psychosocial function is manifested as social isolation, loss of job mobility, increased employee absenteeism, and economic and social discrimination.
 ...
PMID:Health hazards of obesity. 897 52

We reviewed clinical data, autopsy reports, and microscopic slides on 10 patients with sleep apnea/obesity hypoventilation syndrome (SA/OHS) to define the cardiopulmonary pathological features and establish clinicopathologic correlations. Ten obese (>136 kg) patients without SA/OHS were studied as controls. Patients with SA/OHS exhibited biventricular cardiac failure and pulmonary hypertension with a higher prevalence of moderate/severe pulmonary hemosiderosis (8 v 0 patients), alveolar hemorrhage (7 v 4 patients), capillary proliferation (4 v 0 patients), iron encrustation of elastica (1 v 0 patients) and medial hypertrophy of muscular pulmonary arteries (11.9 +/- 2.4 v 9.7 +/- 1.6%) (P < .05). In two patients capillary proliferation resembled capillary hemangiomatosis. Mean right ventricular thickness was higher in the SA/OHS group (0.71 +/- 0.17 v 0.42 +/- 0.1 cm) (P < .01). Four patients with SA/OHS and three controls had moderate/severe myocardial fibrosis. Biventricular cardiac failure caused death in seven patients with SA/OHS. Hypoxia is probably the most important cause of pulmonary hypertension, arterial muscularization, and right ventricular hypertrophy in SA/ OHS. Left ventricular failure in some SA/OHS patients may be the result of hypertensive cardiac disease. In others, the etiology of left ventricular failure was not determined morphologically, suggesting functional abnormalities related to obesity and/or apneic episodes.
 ...
PMID:Cardiopulmonary pathology in patients with sleep apnea/obesity hypoventilation syndrome. 938 47

Obesity is associated with the presence of left ventricular hypertrophy (LVH) and, conversely, with decreased sensitivity of the electrocardiogram (ECG) for LVH due to attenuating effects on QRS amplitudes. Although the Framingham-adjusted Cornell voltage, incorporating age, sex, and body mass index (BMI), was developed to correct for the effects of obesity on the accuracy of the ECG, the impact of body habitus on ECG detection of LVH for newer, more accurate ECG criteria based on the time-voltage area under the QRS complex has not been determined. The authors examined the test accuracy of the Sokolow-Lyon voltage, Cornell voltage, Cornell product (product of QRS duration and Cornell voltage), Framingham-adjusted Cornell voltage, and time-voltage area of the horizontal plane vector QRS for the detection of echocardiographic LVH in relation to body habitus in 250 patients. Normal-weight or overweight status was based on sex-specific population-based BMI partitions. Using partitions with a matched specificity of 98% in the overall population without LVH, the sensitivity of standard ECG criteria varied according to body habitus. Sensitivity of the Framingham-adjusted Cornell voltage was less in normal-weight than in overweight patients (49 vs 59%, P = .0004); there were also trends toward lower sensitivity in normal-weight patients for the Cornell voltage (40 vs 65%, P = .10) and the Cornell product (43 vs 65%, P = NS), but sensitivity of the Sokolow-Lyon voltage was lower in obese than in nonobese patients (18 vs 50%, P = .025). In contrast, the horizontal plane vector area had similar sensitivity in obese and normal-weight patients (76 vs 74%, P = NS). Specificity varied with body habitus only for the Framingham-adjusted Cornell voltage: 100% in normal-weight vs 95% in overweight patients (P < .05). Thus, accuracy of the Framingham-adjusted Cornell voltage and Sokolow-Lyon voltage varies significantly with body habitus. In contrast, accuracy of the Cornell voltage and the Cornell product appears less dependent on BMI, and the time-voltage area of the QRS minimizes the effects of obesity on the accuracy of the ECG for LVH.
 ...
PMID:ECG identification of left ventricular hypertrophy. Relationship of test performance to body habitus. 923 9

Considerable efforts have been invested recently to improve electrocardiographic (ECG) classification accuracy for left ventricular hypertrophy (LVH). This study examines how LVH classification accuracy is influenced by (1) the selection of an echocardiographic standard for LVH, (2) LVH severity level in the test groups, and (3) the adjustment of LVH criteria for obesity and age. Using data obtained from large, community-based populations, this study explores prospects for improving ECG models for LVH classification and examines some of the general characteristics of newer ECG models for estimating left ventricular mass (LVM) on a continuous scale. The results indicate that the apparent ECG classification accuracy for LVH is substantially influenced by echocardiographic standards and criteria for LVH, LVH severity level, and selection criteria for test populations, and these differences explain some of the often substantial differences in test results from clinical versus community-based evaluation studies. The low reproducibility of echocardiographic LVM as the standard is a limiting factor in attempts to improve ECG criteria for LVH and LVM prediction models. Adjustment of ECG amplitudes to anthropometric factors that simultaneously influence LVM may result in confounding effects and may lead to the development of inappropriate models. The performance of ECG models for LVM prediction improved substantially by the inclusion of body weight as a covariate with ECG variables. The addition of standing height and various covariates reflecting obesity did not improve LVM prediction accuracy. Compared to the older LVM prediction models of the Novacode ECG program, the correlation between echocardiographic and ECG estimates of LVM increased sufficiently (from 0.33 to 0.54 in women and from 0.46 to 0.62 in men) to suggest that these improved ECG models are suitable for monitoring LVH progression/ regression in study groups participating in hypertension intervention trials.
 ...
PMID:Improved ECG models for left ventricular mass adjusted for body size, with specific algorithms for normal conduction, bundle branch blocks, and old myocardial infarction. 923 10

The effects of obesity on target organ injuries and cardiovascular risk factors were examined in hypertensive subjects. The subjects were 22 obese (OB-HT) and 54 nonobese (NO-HT) men with never-treated essential hypertension, and 37 obese (OB-NT) and 50 nonobese (NO-NT) normotensive men. In these 4 groups with the average age of about 50 years, we evaluated serum lipids, glucose tolerance, and hypertensive organ injuries in the heart, kidney, and optic fundus. Although the fasting blood glucose levels were similar in the 4 groups, the area under the blood glucose curve after 75 g glucose ingestion (NO-NT 15.6, OB-NT 17.5, NO-HT 15.8, OB-HT 17.6 x 10(3) mg/dl.min; p < 0.02) and the fast serum insulin level (NO-NT 7.3, OB-NT 10.1, NO-HT 7.7, OB-HT 12.2 mU/l; p < 0.001) were increased in obese men. In OB-HT, serum HDL-cholesterol was decreased (-11%, p < 0.05) and triglycerides were increased (+ 58%, p < 0.01) comparing with NO-NT. The incidence of electrocardiographic left ventricular hypertrophy was not significantly different among the 4 groups, however, urinary albumin excretion was increased in OB-HT (NO-NT 3.0, OB-NT 3.4, NO-HT 3.6, OB-HT 4.3 mg/g creatinine; p < 0.05) and sclerotic lesions of the retinal arteries were observed even in normotensive OB-NT. These data suggest that obesity unfavorably alters lipid and glucose metabolism, and facilitates organ injuries such as arteriosclerosis and renal dysfunction in hypertensive subjects.
 ...
PMID:[Implications of obesity for target organ injuries and cardiovascular risk factors in hypertensive subjects]. 939 43

LVH AND RISK: Left ventricular hypertrophy (LVH) is a powerful predictor of cardiovascular morbidity and mortality, independent from blood pressure and other cardiovascular risk factors. Available data indicate that patients who fail to achieve a reduction in LVH are much more likely to suffer cardiovascular events than those in whom LVH is reduced or even normalized using antihypertensive treatment. Reversal of LVH, therefore, represents a major goal in the treatment of hypertensive patients. REGRESSION OF LVH: Since obesity and dietary sodium intake may modulate the degree of LVH, non-pharmacological intervention has achieved a successful reduction in left ventricular mass (LVM). LVM is more closely related to 24-h blood pressure values than to clinical blood pressure values. Recent evidence from the Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation has shown that the regression of cardiac hypertrophy is predicted to a greater degree by the effect of antihypertensive treatment on 24-h average blood pressure than by that on clinic or home blood pressure. The increase in blood pressure variability may also be an independent determinant of cardiovascular target-organ damage, particularly of cardiac hypertrophy. However, the effects of antihypertensive drugs on blood pressure variability can be difficult to determine, mainly because a correct measurement of variability requires a beat-to-beat measurement of ambulatory blood pressure; several measures have been proposed to evaluate the smoothness of blood pressure control during antihypertensive treatment. Other important determinants of LVH reduction are represented by baseline values of LVM, extent of blood pressure reduction and duration of treatment. Furthermore, the degree of cardiac hypertrophy reduction is not the same for the different classes of antihypertensive drugs because, beyond the control of blood pressure, they may interfere differently with several non-haemodynamic stimuli, including the renin-angiotensin-aldosterone and the adrenergic systems or other growth factors. A more pronounced reduction in LVM with angiotensin converting enzyme inhibitors and calcium antagonists has been demonstrated in several recent meta-analyses. The results of further multicenter on-going trials are awaited to evaluate definitely whether various antihypertensive strategies differ in their ability to reverse LVH and to adequately assess the relationship between changes in LVM and subsequent prognosis, with serial control of blood pressure values measured in the clinic and by ambulatory monitoring.
 ...
PMID:Left ventricular hypertrophy: how to influence an important risk factor in hypertension. 953 98

Assessment of cardiorespiratory consequences of sleep apnoea syndrome (SAS) is difficult owing to confounding factors, especially obesity, that are strongly associated with SAS. This study was designed to assess the cardiorespiratory consequences of SAS by comparing the results of a comprehensive cardiorespiratory evaluation in apnoeic and nonapnoeic patients with massive obesity. In a retrospective chart-review study, we studied 60 patients with massive obesity defined by a body mass index (BMI) >40 kg.m(-2), presenting no chronic respiratory disease, who underwent an extensive assessment of cardiorespiratory consequences of obesity, including overnight polysomnography, lung function tests, arterial blood gas analysis, evaluation of vascular risk factors, myocardial scintigraphy with dipyridamole stress-test, isotopic ventriculography, Doppler echocardiography and Holter electrocardiogram recording. SAS defined by an apnoea + hypopnoea index (AHI) > or = 10 was diagnosed in 42% of patients (25 out of 60). Mean+/-SD AHI of SAS-positive (SAS+) patients was 38+/-24. Age, BMI, ventilatory function parameters, prevalence of smoking history and diabetes mellitus did not differ significantly in SAS+ versus SAS-negative (SAS-) groups. The following complications were observed more frequently in SAS+ than in SAS- patients: daytime hypoxaemia (35 vs 9%, p<0.02), pulmonary arterial hypertension (36 vs 7%, p<0.05) and increased interventricular septal thickness (50 vs 15%, p<0.03). No association was found between SAS on the one hand and systemic arterial hypertension, coronary artery disease, left ventricular dysfunction and nocturnal cardiac arrhythmias on the other. Nocturnal apnoeas in massive obesity may thus be associated with moderate daytime hypoxaemia, mild pulmonary arterial hypertension and moderate left ventricular hypertrophy, but not with severe cardiorespiratory complications.
 ...
PMID:Cardiorespiratory consequences of sleep apnoea syndrome in patients with massive obesity. 954 65

Animal models have shown that hypertension may be accompanied by an increase in sympathetic activity. The findings of increased plasma norepinephrine or increased muscle sympathetic nerve traffic have now provided clear evidence, however, that sympathetic activity is increased in essential hypertension and that adrenergic neural mechanisms are already involved in the early phase of this condition. Furthermore, in the early and late phases of hypertension, the presence of other cardiovascular risk factors frequently accompanying hypertension such as obesity, insulin-resistance, and smoking, concomitant with hypertension, brings about sympathetic activation which may be superimposed on the activation resulting from the hypertensive state itself. Finally, sympathetic activation is directly involved in the progression of end-organ damage and plays a paramount role in the cardiovascular structural changes typical of the blood pressure elevation occurring in left ventricular hypertrophy, arteriolar remodeling, and atherosclerosis. These findings underscore the importance of aiming anti-hypertensive treatment at the reduction not only of blood pressure levels, but also of enhanced sympathetic cardiovascular drive.
 ...
PMID:[Sympathetic nervous factors, pressure variability and organ damage in arterial hypertension]. 977 76

Hypertension is defined as a disease of elevated systolic and diastolic blood pressure and consequently the goals of treating hypertension have been simply to normalize the blood pressure. However, effective blood pressure control has not resulted in the expected decreases in coronary artery disease. These findings have forced researchers to reexamine the importance of blood pressure in causing coronary artery disease, and to pose the question "Is there more to hypertension than high blood pressure?" Although there are probably several reasons for the poor reduction in the incidence of coronary artery disease in hypertensive patients, one of the most compelling appears to be the realization that hypertension is not simply a disease of numbers, but is a complex inherited syndrome of cardiovascular risk factors, all of which contribute to heart disease in these patients. Included in the hypertension syndrome are abnormalities of lipid profile, insulin resistance, changes in renal function, endocrine changes, obesity, abnormalities of coagulation factors, left ventricular hypertrophy and diastolic dysfunction, and abnormalities of vascular structure and compliance. In many patients, high blood pressure is a late manifestation of this disease process and is preceded by some or all of the associated cardiovascular risk factors. Perhaps where we have gone wrong in the management of hypertension is in the belief that this is simply a disease of numbers. To improve our management, we need to find methods to diagnose these patients early in the course of this disease process, and to treat it as a syndrome rather than as a number.
 ...
PMID:Hypertension: where have we gone wrong and how can we fix it? 979 49


<< Previous 1 2 3 4 5 6 7 8 9 10