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Indeed, high blood pressure prevalence may vary from 3. One potential link between insulin resistance and an increase in blood pressure is the sympathetic nervous system. Thus, obesity is somewhat similar to a low-grade systemic inflammation. Low-grade inflammation may play a role in increasing blood pressure.

Elevated plasma IL-6 levels were significantly associated with systolic and diastolic blood pressures in women, whereas in men, IL-6 was associated with fasting insulin and fasting insulin resistance index. The physician who evaluates a referred patient for hypertension should be very concerned about obese patients who admit habitual snoring, nocturnal gasping or choking, witnessed episodes of apnea, and daytime sleepiness and should consider sleep-disordered breathing.

Numerous respiratory complications are associated with obesity. Obese individuals have an increased demand for ventilation and breathing workload, respiratory muscle inefficiency, decreased functional reserve capacity and expiratory reserve volume, and closure of peripheral lung units. These often result in a ventilation—perfusion mismatch, especially in the supine position. Obesity is a classic cause of alveolar hypoventilation. Accordingly, obesity could represent a major cause of respiratory insufficiency and pulmonary hypertension in patients with obstructive sleep apnea. Sleep apnea is defined as repeated episodes of obstructive apnea and hypopnea during sleep, together with daytime sleepiness or altered cardiopulmonary function.

It was considered that obesity might be a confounding factor, given the strong association of obesity with sleep apnea. However, sleep apnea might be one of the intermediary mechanisms by which overweight is causally related to hypertension. Interestingly, sleep apnea is associated with increased levels of CRP. Thus, obesity may influence many processes that are linked—for example, sleep apnea, hypertension, and atherosclerosis. It is important to remember, however, that the clinical and electrocardiographic signs of cor pulmonale appear later than those of pulmonary hypertension assessed by right heart catheterization.

From a cardiology viewpoint, patients with sleep apnea have an increased risk of diurnal hypertension, nocturnal dysrhythmias, pulmonary hypertension, right and left ventricular failure, myocardial infarction, and stroke, as well as increased mortality rates. Similarly, this degree of pulmonary hypertension is often observed in patients with chronic obstructive pulmonary disease.

Interestingly, in the latter population, a high prevalence of MetS was recently reported. Numerous studies have reported an association between BMI and waist-to-hip ratio and stroke. However, stroke severity for ischemic stroke was not associated with BMI.

Atherosclerosis begins in childhood 5 to 10 years as deposits of cholesterol esters in monocyte-derived macrophage foam cells in the intima of large muscular arteries fatty streaks. In the setting of the insulin resistance of obesity, coronary endothelial dysfunction is seen at the level of the resistance vessels. However, in older individuals, the effect of adiposity and body fat distribution on endothelial dysfunction may be less important than in young subjects.

Despite its limitations, , carotid IMT among adults is associated with obesity and other CHD risk factors and cardiovascular events. As individuals age, the atherosclerotic lesion becomes more complex. Indeed, postmortem examination of arteries from individuals 15 to 34 years of age Determinants of Atherosclerosis in Youth [PDAY] study who died from accidental injuries, homicides, or suicides revealed that the extent of fatty streaks and advanced lesions fibrous plaques and plaques with calcification or ulceration in the right coronary artery RCA and in the abdominal aorta were associated with obesity and with the size of the abdominal panniculus.

Black subjects had more extensive fatty streaks than did white subjects in all arterial segments examined, and men did have more extensive raised lesions in the RCA than did women. This has been reinforced in a younger cohort of men in whom the maximal density of macrophages per square millimeter in the lesions was associated with visceral obesity. Excluding diabetes and hypertension from the multivariate analysis did not change the findings.

This implies that the impact of obesity on all-cause mortality is mediated by mechanisms other than hypertension and diabetes. Assessing CHD with imaging techniques is important in obese patients. As discussed earlier, because baseline ECG may be influenced by the presence of obesity false-positive for inferior myocardial infarction, microvoltage, nonspecific ST-T changes and because obese patients may have impaired maximal exercise testing capacity dyspnea, orthopedic limitations, left ventricular diastolic dysfunction , other modalities may be of interest in the evaluation of CHD in this population.

Although attenuation correction has been developed for single-photon-emission computed tomography, attenuation artifacts, most commonly resulting from attenuation by the diaphragm or the breast, frequently can be seen in obesity. However, evaluation of significant clinical CHD may be adequately assessed in obese subjects through the use of nuclear cardiology imaging.

The specificity of single-photon-emission computed tomography may be slightly greater with technetium 99m rather than thallium, in part because of its higher energy versus 70 keV , but both isotopes continue to pose a problem of interpretation if accurate attenuation correction and gating are not performed. Although differences in tracer distribution may be seen, prolonged transmission scanning 5 versus 10 seconds per view with thallium is not mandatory for accurate clinical interpretation in obese as compared with lean patients after correction for the attenuation factor caused by obesity, and triple-head simultaneous emission transmission tomography with technetium 99m is also accurate in obesity.

Transesophageal echocardiography may be of diagnostic use in the evaluation of the presence of CHD in severely obese individuals. Transesophageal dobutamine stress echocardiography combines the advantages of pharmacological stress testing with superior-quality cardiac imaging, has been reported to be safe, and appears to be a good alternative to cardiac catheterization for assessing the presence of CHD and ischemic threshold in morbidly obese patients.

If cardiac catheterization is contemplated, femoral access may not be ideal, not only because of the volume of adipose tissue but also because of the presence of intertrigo. Nevertheless, the use of femoral closure devices may help decrease bleeding complications. Alternatively, the percutaneous radial approach has numerous advantages in the very obese patient because the frequency of complications with the use of this technique is very low. Cardiac surgeons often perceive obesity as a risk factor for perioperative adverse outcomes after coronary artery bypass grafting CABG. Obese patients have been shown to have a higher incidence of postoperative thromboembolic disease in noncardiac surgery, and their high risk of thromboembolic disease may necessitate an aggressive approach to deep venous thrombosis prophylaxis.

Congestive heart failure CHF is the only common cardiovascular condition that is increasing in incidence, prevalence, and mortality rates. Thus, the findings do not address the impact of weight loss or weight gain during the study period 37 months. The interrelation between sleep disorders and CVD is a topic of growing interest. Pulmonary hypertension and right heart disease are expected in obese patients with long-standing and moderately severe hypoxemia, which could be potentiated through CHF.

Although QT dispersion has been reported to be increased in obesity without improvement after weight loss, visceral obesity may be a better discriminate to evaluate the impact of weight loss on QT dispersion. The presence of late potentials may be facilitated by pathological myocardial changes associated with obesity myocyte hypertrophy, focal myocardial disarray, fibrosis, fat and mononuclear cell infiltration. The clinical significance of obesity-associated QT prolongation and the mechanisms involved remain speculative.

It is interesting to note, however, that elevated free fatty acids may affect cardiac repolarization. This may in part be secondary to increased plasma catecholamines. The autonomic nervous system is an important contributor to the regulation of both the cardiovascular system and energy expenditure, and it is assumed to play a role in the pathophysiology of obesity and related complications. This is of importance because higher heart rate is associated with increased mortality rates, , and decreased HRV is associated with increased cardiac mortality, independent of ejection fraction.

Intentional weight loss in obese patients can improve or prevent many of the obesity-related risk factors for CHD. Current therapies available for weight management that cause weight loss by inducing a negative energy balance include dietary intervention, physical activity, pharmacotherapy, and surgery. Behavior modification to enhance dietary and activity compliance is an important component of all of these treatments. Diverse modalities had been addressed lately by the AHA. Surgically induced weight loss produces a decrease in resting oxygen consumption and cardiac output that is proportional to the magnitude of weight loss.

Systemic arterial pressure declines, but systemic arterial resistance changes little if at all. Left ventricular stroke work diminishes. Pulmonary capillary wedge pressure tends to decrease but may still remain higher in relation to cardiac output as compared with normal-weight subjects. Left ventricular dysfunction may persist most strikingly during exercise.

TABLE 3. Benefits of Weight Reduction on the Cardiovascular System. Sympathetic mechanisms have been implicated in the development of LVH, and weight reduction in obese subjects reduces the indices of sympathetic activity such as plasma norepinephrine levels and urinary norepinephrine excretion. The renin-angiotensin system may also be involved in the pathogenesis of LVH, and weight reduction may decrease plasma renin activity and aldosterone levels. A reduction in angiotensin-converting enzyme activity after weight reduction could also be important.

Weight loss through different modalities, for example, starvation, , liquid protein diets, , very-low-calorie diets, and even obesity surgery, 81 has been associated with prolongation of the QT c interval. The prolongation of the QT c interval is independent of the biological and nutritional value of the constituent protein or the addition of mineral and trace supplements in the diet.

Accordingly, more care is now taken to ensure micronutrient supplementation and to monitor for adverse effects. Fenfluramine and dexfenfluramine, which reduce appetite by enhancing serotonin at nerve terminals in the hypothalamus, were removed from the marketplace in the United States in after reports of cardiac valve disorders, particularly aortic and mitral insufficiency.

Valve involvement in these patients was histopathologically similar to that noted in the carcinoid syndrome or ergotamine-induced valve disease. Sibutramine hydrochloride and orlistat are the latest drugs available on the market for the treatment of obesity and have been shown to be effective in the treatment of obesity and associated comorbidities.

Health service use and medical costs associated with obesity and related diseases have increased and will increase dramatically. Waist circumference may be a better predictor of healthcare costs than the widely used BMI. Nevertheless, this recommendation needs to be heeded with advice from an experienced clinician in exercise therapeutics. It is very important to inform patients about the results to be expected to avoid unrealistic weight loss expectations. The primary target should not be body weight normalization, but rather some weight loss, which can lead to substantial improvements in risk factors.

Of interest, even if weight loss is minimal, obese individuals with a good level of cardiorespiratory fitness show a reduced risk for cardiovascular mortality as compared with lean, poorly fit subjects. Obesity is a chronic metabolic disorder associated with CVD and increased morbidity and mortality rates. To meet increased metabolic needs, circulating blood volume, plasma volume, and cardiac output all increase.

The increase in blood volume in turn increases venous return to the right and the left ventricles, eventually producing dilation of these cardiac cavities, increasing wall tension. This leads to LVH, which is accompanied by a decrease in diastolic chamber compliance, eventually resulting in an increase in left ventricular filling pressure and left ventricular enlargement. As long as LVH adapts to left ventricular chamber enlargement, systolic function is preserved.

When LVH fails to keep pace with progressive left ventricular dilation, wall tension increases even more and systolic dysfunction may ensue. Systemic hypertension, pulmonary hypertension left ventricular failure, chronic hypoxia , and CHD all occur with disproportionately high frequency in obese individuals and may cause or contribute to alterations in cardiac structure and function.

The risk of sudden cardiac death is also increased in obesity. Although no prospective studies to date demonstrate that intentional weight loss increases survival, strong evidence indicates that weight loss in overweight and obese individuals reduces risk factors for diabetes and CVD. Until then, we hope that a favorable result will ensue through the clinical approach. Identification of genetic determinants or biomarkers that predict which obese individuals are at highest risk for heart failure;.

Fundamental studies attempting to understand the basis for heart failure in the obese and insulin-resistant individual; and. The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel.

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The Obesity Epidemic

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Alterations in left ventricular structure and function in young healthy obese women: assessment by echocardiography and tissue Doppler imaging. Left ventricular mass and body size in normotensive children and adults: assessment of allometric relations and impact of overweight. A new method for indexing left ventricular mass for differences in body size. Effect of lean body mass, fat mass, blood pressure, and sexual maturation on left ventricular mass in children and adolescents.

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Correlation of intraabdominal fat accumulation and left ventricular performance in obesity. Risks and benefits of gastric bypass in morbidly obese patients with severe venous stasis disease. Ann Surg. Cardiovascular risk factors and venous thromboembolism incidence: the longitudinal investigation of thromboembolism etiology. Chapter 6 Role of Neurotransmitters in Obesity Regulation. Chapter 7 Neurobiology of Obesity. A Review of the Literature. Chapter 24 The Atkins Paradigm. From the Biomedical Immune Viewpoint.

Link Between Metabolism and Vasculature. Role of DNA Methylation. Obesity and Degenerative Disease. Chapter 12 Obesity and Type 2 Diabetes. Novel Concept in Obesity Drug Development. Safety of Obesity Drugs. Chapter 16 Safety of Obesity Drugs. An Overview. Chapter 31 Laboratory and Clinical Studies of Chitosan. Chapter 32 Phaseolus vulgaris and Amylase Inhibition. A Review of the Evidence. Chapter 34 Role of Caralluma fimbriata in Weight Management. Chapter 36 AntiObesity by Marine Lipids.