title: Sympathetic and reflex abnormalities in heart failure secondary to ischaemic or idiopathic dilated cardiomyopathy.
abstract: Congestive heart failure (CHF) is characterized by a sympathetic activation and a baroreflex impairment whose degree is directly related to the clinical severity of the disease. However, whether these abnormalities vary according to the ischaemic or idiopathic dilated nature of the CHF state has not been conclusively documented. In patients with a clinically stable, chronic CHF state in New York Heart Association functional class II and III, due either to ischaemic heart disease (IHD; n=22, age 60.3+/-2.4 years, means+/-S.E.M.) or to idiopathic dilated cardiomyopathy (IDC; n=20, age 58.9+/-2.8 years), and in 30 age-matched controls, we measured arterial blood pressure (using a Finapres device), heart rate (by electrocardiogram) and postganglionic muscle sympathetic nerve traffic (by microneurography) at rest and during baroreceptor manipulation induced by the vasoactive drug-infusion technique. Blood pressure values were not significantly different in CHF patients and controls. Compared with controls, heart rate was similarly increased and left ventricular ejection fraction (by echocardiography) similarly reduced in CHF patients with IHD or IDC. Muscle sympathetic nerve traffic was significantly greater in CHF patients than in controls, and did not differ between patients with IHD or IDC (67.3+/-4.2 and 67.8+/-3.8 bursts/100 heart beats respectively). This was also the case for the degree of baroreflex impairment. These data show that CHF states due to IHD or to IDC are characterized by a similar degree of peripheral sympathetic activation and by a similar impairment of the baroreflex function. Thus the neuroadrenergic and reflex abnormalities characterizing CHF are independent of its aetiology.
authors.affiliation: Clinica Medica, University of Milano-Bicocca, Ospedale San Gerardo dei Tintori, Via Donizetti 106, 20052 Monza-Milan, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Grassi
authors.forename: G
authors.initials: G
authors.lastname: Seravalle
authors.forename: G
authors.initials: G
authors.lastname: Bertinieri
authors.forename: C
authors.initials: C
authors.lastname: Turri
authors.forename: M L
authors.initials: ML
authors.lastname: Stella
authors.forename: F
authors.initials: F
authors.lastname: Scopelliti
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002311:Cardiomyopathy, Dilated / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D016022:Case-Control Studies; D002851:Chromatography, High Pressure Liquid; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D009599:Nitroprusside / Q000494:pharmacology; D009638:Norepinephrine / Q000097:blood; D010656:Phenylephrine / Q000494:pharmacology; D012083:Renin / Q000097:blood; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000503:physiopathology*; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D012083:Renin; D009638:Norepinephrine