title: Excessive sympathetic activation in heart failure with obesity and metabolic syndrome: characteristics and mechanisms.
abstract: Congestive heart failure is characterized by sympathetic activation, which has also been described in the metabolic syndrome. No information exists, however, as to whether the sympathostimulating effects of these 2 conditions summate when heart failure is complicated by the metabolic syndrome, leading to an exceedingly high adrenergic drive. This is clinically relevant, because in heart failure sympathetic activation is closely related to mortality. We studied 48 control subjects (age: 58.4+/-1.6 years, mean+/-SEM) and 89 age-matched heart failure patients (New York Heart Association class II), of whom 47 were without and 42 were with metabolic syndrome. Measurements included blood pressure (Finapres), heart rate (ECG), and sympathetic nerve traffic (microneurography) at rest and during baroreceptor manipulation. Waist circumference, blood pressure, and metabolic variables were greater in heart failure with metabolic syndrome than in heart failure without metabolic syndrome and in control subjects. Left ventricular ejection fraction and end-diastolic diameter were similarly altered in the 2 heart failure groups. Compared with control subjects, sympathetic nerve activity was greater in heart failure patients without metabolic syndrome (64.7+/-3.2 versus 45.8+/-2.9 bursts/100 heartbeats; P<0.01), a further pronounced increase being detected in those with metabolic syndrome (80.9+/-3.2 bursts/100 heartbeats; P<0.01). In the multivariate analysis, waist circumference and body mass index were the variables most closely related to sympathetic activation. Compared with control subjects, baroreflex responses were significantly attenuated in the 2 heart failure groups, the impairment being more marked in the group with than without metabolic syndrome. Thus, obesity and metabolic syndrome potentiate the sympathetic activation characterizing heart failure. This potentiation is likely to mainly depend on metabolic and baroreflex mechanisms.
authors.affiliation: Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy. guido.grassi@unimib.it
authors.forename: Guido
authors.initials: G
authors.lastname: Grassi
authors.forename: Gino
authors.initials: G
authors.lastname: Seravalle
authors.forename: Fosca
authors.initials: F
authors.lastname: Quarti-Trevano
authors.forename: Francesco
authors.initials: F
authors.lastname: Scopelliti
authors.forename: Raffaella
authors.initials: R
authors.lastname: Dell'Oro
authors.forename: Gianbattista
authors.initials: G
authors.lastname: Bolla
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000209:etiology* / Q000503:physiopathology*; D017704:Baroreflex; D005260:Female; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000150:complications / Q000503:physiopathology*; D008875:Middle Aged; D009765:Obesity / Q000150:complications / Q000503:physiopathology*