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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity has been identified as an independent risk factor for coronary heart disease and congestive heart failure. Although congestive heart failure can be secondary to coronary heart disease, in morbid obesity these conditions can be independent. Cardiac structure and function can be altered even in the absence of systemic hypertension and underlying organic heart disease. In obese patients total blood volume increases and creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The frequent coexistence of systemic hypertension in obese individuals facilitates development of left ventricular dilatation and hypertrophy. Congestive heart failure may occur and may be attributable to left ventricular diastolic dysfunction or to combined diastolic and systolic dysfunction. The risk of coronary heart disease seems to be more strictly correlated to central obesity than to increased body mass index. Insulin resistance seems to be the key factor that links obesity and ischaemic heart disease. In such a condition the so called Syndrome X appears. It is characterized by: obesity, systemic hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL cholesterol levels. Considering that left ventricular hypertrophy is often present, many risk factors coexist in obese patients. Weight loss is very useful in obese patients. It may reduce mortality and morbidity for coronary heart disease and delay or avoid the appearance of congestive heart failure. It is proved that after weight loss, blood pressure, glucose, cholesterol, triglycerides and left ventricular mass decrease.
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PMID:[Obesity and the heart]. 1649 82

The strong activation of the clotting cascade that occurs during total hip arthroplasty places patients at increased risk for venous thromboembolism. The risk is higher in those patients with the following predisposing factors, listed in approximate order of importance: hip fracture; malignancy, particularly if associated with chemotherapy; antiphospholipid syndrome; immobility; history of venous thromboemholism; administration of tamoxifen; raloxifene; oral contraceptives or estrogen; morbid obesity; stroke; atherosclerosis; and an American Society of Anesthesiologists physical status classification of 3 or greater. The following risk factors are weak or controversial: advanced age; diabetes mellitus; congestive heart disease; atrial fibrillation; varicose veins; and smoking. However, 50% of patients who develop thromboembolism after total hip arthroplasty have no clinical predisposing factors. In a matched, controlled study, we defined the major genetic predispositions that increase the risk of venous thromboembolism after total hip arthroplasty: deficiency of antithrombin III (< 75%) and protein C (< 70%), and prothrombin gene mutation. Preoperative genetic screening in conjunction with the recognized clinical risk factors can help categorize postoperative venous thromboembolism risk and differentiate patients who can be protected with milder and safer prophylaxis (eg, aspirin, intermittent pneumatic compression) compared with those at higher risk who need to be anticoagulated.
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PMID:Thromboembolic disease after total hip arthroplasty: who is at risk? 1700 73

Although tissue Doppler (TD) imaging of the left ventricle is now commonly used in clinical settings, TD imaging of the right ventricle (RV) is not routinely practiced. Yet, there are significant data on clinical uses of RV TD imaging, including established normal values using both color and spectral TD. In acute left ventricular (LV) inferior wall myocardial infarction, depressed RV TD velocities have been shown to correlate with the presence of RV impairment, and with patient outcome. In patients with LV heart failure, TD imaging has been correlated to RV ejection fraction by radionuclide angiography, and is an independent predictor of outcome. In patients with congenital heart disease, RV TD has been especially valuable for assessing RV function, and has been correlated to invasive hemodynamic indices, and RV ejection fraction by magnetic resonance imaging. The RV performance (Tei) index has been calculated and validated using TD-derived, rather than conventional pulsed Doppler time intervals. RV TD indices have been shown to be useful in the detection of subclinical and clinical disease in morbid obesity, chronic pulmonary, and systemic disease. TD-derived RV strain imaging can detect segmental myocardial dysfunction, overcoming limitations to conventional TD imaging resulting from tethering. For both TD velocity and strain imaging, however, appreciation of the limitations of these techniques is necessary for their appropriate use. Given its rapid acquisition times, reproducibility, and ease of addition to standard transthoracic echocardiographic protocols, RV TD and strain imaging are important additional modalities in the comprehensive echo-Doppler assessment of RV function.
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PMID:Right ventricular tissue Doppler and strain imaging: ready for clinical use? 1745 72

Abdominal -- and not peripheral -- obesity induces insulin resistance. Morbid obesity is not always accompanied by either diabetes mellitus or metabolic syndrome. Development of morbid obesity can require appropriate insulin secretion and recruitment of small insulin-sensitive adipocytes, able to store fatty acids. These fatty acids are therefore not stored in ectopic sites (muscle, liver, islets of Langerhans), and neither insulin resistance nor glucolipid toxicity develops and causes insulin deficiency. This explains the relative rarity of diabetes in morbid obesity. Patients with morbid obesity are at greater risk of developing mechanical complications (e.g. cardiac, pulmonary, or locomotor system, or sleep apnea) than metabolic complications or cardiovascular heart disease.
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PMID:[Obesity, immune resistance and metabolic complications: what morbid obesity can teach the doctor]. 1745 53

The incidence of obesity worldwide has increased markedly in the past 2 decades, with estimates of increases of 50% in the United States alone. Research indicates that weight loss produced by diet alone is not sustained and that 75% of dieters regain most of the weight lost within 1 year and 90% within 2 years. Morbid obesity is associated with comorbid conditions, including heart disease, hypertension, diabetes, mechanical arthropathy, sleep apnea, and numerous other serious disorders and a shortened life expectancy. Because of limited success with medical management, surgical treatment of morbid obesity has been used increasingly, especially with the development of laparoscopic procedures, including Roux-en-Y gastric bypass (RYGB). RYGB is associated with low surgical mortality, marked decreased food intake, and significant, sustained weight loss. However, in this emerging, unique population there is growing appreciation that these procedures may be associated with the development of bone loss and skeletal fragility because of altered nutrient metabolism. Despite the threat of skeletal fragility and fracture, there is limited data addressing the effects of bariatric surgery on bone metabolism and bone loss.
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PMID:Bone loss. An emerging problem following obesity surgery. 1792 86

Laparoscopic Roux-en-Y gastric bypass (LGB) is one of the most popular surgeries for morbid obesity. Robotic use is also on the rise. Data concerning outcomes is limited, hence the need for more information. The first 100 robotic-assisted bypasses by one surgeon in one institution were studied. Data obtained from clinic notes and hospital records included all who underwent the procedure. There were 79 females and 21 males. Mean age and body mass index were 42 years and 48 kg/m2, respectively. Comorbidities included diabetes, 22 per cent; hypertension, 47 per cent, gastroesophageal reflux disease, 40 per cent; obstructive sleep apnea, 53 per cent; dyslipidemia, 17 per cent; and heart disease, 8 per cent. Prior surgeries included cesarean -section, 26 per cent; cholecystectomy, 17 per cent; hysterectomy, 3 per cent; hernia, 1 per cent, and other abdominal surgery, 27 per cent. Intraoperatively procedures included adhesiolysis, 22 per cent; cholecystectomy, 16 per cent; and herniorrhaphy, 3 per cent. Average time was 177.7 minutes. Mean stay was 1.51 days. Thirty-day mortality was 0. Emergency department re-evaluations included 13. Most were minor problems. There was one gastrojejunal leak. Early complications included leak, thrombosis, and bleeding requiring transfusion in four patients. There were four strictures. Overall follow up was greater than 90 per cent. Average weight loss was 21.2 per cent of excess body weight by Month 1, 33.8 per cent by Month 3, and 50.7 per cent by Month 6. Learning curves for time and major complications were 30 and 50 cases, respectively (P = 0.03, 0.04). Robotic use in bariatrics is possible in community hospitals. Although technologies are still in their infancy, complication rates and weight loss are comparable to nonrobotic procedures.
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PMID:100 robotic-assisted laparoscopic gastric bypasses at a community hospital. 1894 36

Obesity is associated with comorbidities that may lead to disability and death. During the past 20 years, the number of individuals with a body mass index >30, 40, and 50 kg/m(2), respectively, has doubled, quadrupled, and quintupled in the United States. The risk of developing comorbid conditions rises with increasing body mass index. Possible cardiac symptoms such as exertional dyspnea and lower-extremity edema occur commonly and are nonspecific in obesity. The physical examination and electrocardiogram often underestimate cardiac dysfunction in obese patients. The risk of an adverse perioperative cardiac event in obese patients is related to the nature and severity of their underlying heart disease, associated comorbidities, and the type of surgery. Severe obesity has not been associated with increased mortality in patients undergoing cardiac surgery but has been associated with an increased length of hospital stay and with a greater likelihood of renal failure and prolonged assisted ventilation. Comorbidities that influence the preoperative cardiac risk assessment of severely obese patients include the presence of atherosclerotic cardiovascular disease, heart failure, systemic hypertension, pulmonary hypertension related to sleep apnea and hypoventilation, cardiac arrhythmias (primarily atrial fibrillation), and deep vein thrombosis. When preoperatively evaluating risk for surgery, the clinician should consider age, gender, cardiorespiratory fitness, electrolyte disorders, and heart failure as independent predictors for surgical morbidity and mortality. An obesity surgery mortality score for gastric bypass has also been proposed. Given the high prevalence of severely obese patients, this scientific advisory was developed to provide cardiologists, surgeons, anesthesiologists, and other healthcare professionals with recommendations for the preoperative cardiovascular evaluation, intraoperative and perioperative management, and postoperative cardiovascular care of this increasingly prevalent patient population.
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PMID:Cardiovascular evaluation and management of severely obese patients undergoing surgery: a science advisory from the American Heart Association. 1952 35

Obesity increases the likelihood of diseases like type 2 diabetes (T2D), heart disease, and cancer, and is one of the most serious public health problems of this century. In contrast to ineffectual prevention strategies, lifestyle modifications, and pharmacological therapies, bariatric surgery is a very effective treatment for morbid obesity and also markedly improves associated comorbidities like T2D. However, weight loss and resolution of T2D after bariatric surgery is heterogeneous and specific to type of bariatric procedure performed. Conventional mechanisms like intestinal malabsorption and gastric restriction do not fully explain this, and potent changes in appetite and the enteroinsular axis, as a result of anatomical reorganization and altered hormonal, neuronal, and nutrient signaling, are the portended cause. Uniquely these signaling changes appear to override vigorous homeostatic defenses of stable body weight and compelling self-gratifying motivations to eat and to reverse defects in beta-cell function and insulin sensitivity. Here we review mechanisms of weight loss and T2D resolution after Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy bariatric surgery, two markedly different procedures with robust clinical outcomes.
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PMID:Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: understanding weight loss and improvements in type 2 diabetes after bariatric surgery. 2147 29

Obesity is associated with an increased risk of death, and morbid obesity carries a significant risk of life-threatening complications such as heart disease, diabetes, and high blood pressure. Bariatric surgery is recognized as the only effective treatment of morbid obesity. The estimated number of bariatric operations performed in the United States in 2008 was more than 13 times the number performed in 1992. Despite this increase, only 1% of the eligible morbidly obese population are currently treated with bariatric surgery.
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PMID:Bariatric surgery outcomes. 2205 56

The monosomy 1p36 syndrome is a cause of syndromic obesity. It is characterised by psychomotor delay, hypotonia and typical craniofacial dysmorphism. Other features commonly associated are behavioural anomalies including hyperphagia and self-injuring, seizures, congenital heart disease and hypothyroidism. The authors report the case of a 9-year and 5-month-boy referred to the paediatric endocrinology clinics for morbid obesity. Clinical findings were generalised obesity with a body mass index >95th centile, acanthosis nigricans of the neck, arms with self inflicted lesions, deep-set eyes, straight eyebrows, broad nasal bridge and pointed chin. He was unable to walk and had no expressive language. Cytogenetic analysis identified 1p36.33-pter deletion (~139 Mb terminal deletion in chromosome 1 short arm) and Y chromosome duplication. The blood analysis showed insulin resistance and dyslipidaemia. The authors emphasise the need to consider monosomy 1p36 as a cause of severe psychomotor delay and obesity.
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PMID:Morbid obesity in a child with monosomy 1p36 syndrome. 2260 91


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