RESUMEN
A case of a 22-year-old young pregnant woman with palpitations and near syncope is presented. Holter monitoring showed very frequent premature beats and runs of wide complex tachycardia, refractory to antiarrhythmic drugs. Electrophysiologic evaluation disclosed spontaneous automatism arising in an atriofascicular pathway. Differential diagnosis is discussed.
Asunto(s)
Fascículo Atrioventricular Accesorio , Técnicas Electrofisiológicas Cardíacas , Frecuencia Cardíaca , Complicaciones del Embarazo/diagnóstico , Taquicardia Ventricular/diagnóstico , Complejos Prematuros Ventriculares/diagnóstico , Potenciales de Acción , Antiarrítmicos/uso terapéutico , Resistencia a Medicamentos , Electrocardiografía Ambulatoria , Femenino , Frecuencia Cardíaca/efectos de los fármacos , Humanos , Valor Predictivo de las Pruebas , Embarazo , Complicaciones del Embarazo/tratamiento farmacológico , Complicaciones del Embarazo/fisiopatología , Tercer Trimestre del Embarazo , Taquicardia Ventricular/tratamiento farmacológico , Taquicardia Ventricular/fisiopatología , Factores de Tiempo , Complejos Prematuros Ventriculares/tratamiento farmacológico , Complejos Prematuros Ventriculares/fisiopatología , Adulto JovenRESUMEN
Despite significant advances in our understanding of the biology determining systemic energy homeostasis, the treatment of obesity remains a medical challenge. Activation of AMP-activated protein kinase (AMPK) has been proposed as an attractive strategy for the treatment of obesity and its complications. AMPK is a conserved, ubiquitously expressed, heterotrimeric serine/threonine kinase whose short-term activation has multiple beneficial metabolic effects. Whether these translate into long-term benefits for obesity and its complications is unknown. Here, we observe that mice with chronic AMPK activation, resulting from mutation of the AMPK γ2 subunit, exhibit ghrelin signaling-dependent hyperphagia, obesity, and impaired pancreatic islet insulin secretion. Humans bearing the homologous mutation manifest a congruent phenotype. Our studies highlight that long-term AMPK activation throughout all tissues can have adverse metabolic consequences, with implications for pharmacological strategies seeking to chronically activate AMPK systemically to treat metabolic disease.