Abstract

Insulin resistance, metabolic syndrome, and adipokine dysregulation are now implicated in hypertensive pulmonary vascular disease (1–3). Even in nonobese humans with idiopathic pulmonary arterial hypertension (IPAH), the prevalence of insulin resistance is nearly 50% (1,2), suggesting a link between glucose dysregulation and IPAH. Additionally, IPAH develops spontaneously in animal models of obesity and adipokine alterations (4). The underlying mechanisms by which metabolic mediators exacerbate or cause pulmonary vascular disease are unknown. We tested the hypothesis that improvements in metabolic hormones are associated with amelioration of pulmonary hemodynamics in a 48-year-old morbidly obese female IPAH patient who underwent bariatric surgery. Despite no change in IPAH therapy, she had dramatic hemodynamic improvement coupled with reduced insulin resistance, plasma lipids, and cholesterol levels. The IPAH patient was New York Heart Association functional class III and desired bariatric surgery. After counseling about elevated …

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