Obesity increases cardiovascular risk through multiple mechanisms. Abdominal (visceral) adiposity is metabolically active and is largely responsible for the atherogenic dyslipidemia, hyperinsulinemia, hypertension, chronic inflammatory state, and prothrombotic state that constitute the metabolic syndrome, and the subsequent increased risk for cardiovascular disease and acute coronary events. Cholesterol guidelines for assessing cardiovascular risk have traditionally focused on low-density lipoprotein (LDL) levels, and reduction of plasma LDL has been shown to reduce cardiovascular events and total mortality. However, the cardiovascular risks associated with the dyslipidemia of obesity--characterized by low levels of high-density lipoprotein; increased triglycerides; increased subfractions of small, dense LDL; and increased levels of apolipoprotein B-100--are also now well recognized.

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Obesity is currently an epidemic, and the prevalence of cardiovascular risk factors is increasing dramatically as a result. Visceral adiposity is correlated with a proinflammatory and prothrombotic state that is believed to promote atherosclerosis and acute coronary syndromes. This article will review clinical trials on the effects of weight loss and pharmacotherapy on obesity associated inflammatory and thrombotic markers linked with cardiovascular disease.

Lower esophageal sphincter pressure, length of sphincter, and contraction of the crural diaphragm are determinants of esophageal function. Mean pressure manometrics in modified rapid pull-through reflects these three factors. Reproducibility and interobserver variability were studied to assess this method's efficacy and were compared with the maximum expiratory pressure in station pull-through in 44 individuals divided into three groups: achalasia, gastroesophageal reflux, and healthy volunteers. Mean pressure in rapid pull-through showed high reproducibility, no significant differences (14.4 +/- 8.4 vs 12.6 +/- 8.2 mm Hg) between two measurements, and a high correlation coefficient (r = 0.9). Interobserver variability was lower than that seen for maximum expiratory pressure (P < 0.001). Mean pressure was lower than maximum expiratory pressure in patients with achalasia (21.1 +/- 7 vs 30.7 +/- 8.6 mm Hg). Both methods showed identical sensitivity to establish a hypotensive sphincter in patients with reflux (73%). We think that mean pressure obtained by rapid pull-through is a good methodology to assess lower esophageal sphincter competence. It is rapid, simple, shows good reproducibility and low interobserver variability, and is clinically valid.