title: Depressed arterial baroreflex sensitivity and not reduced heart rate variability identifies patients with chronic heart failure and nonsustained ventricular tachycardia: the effect of high ventricular filling pressure.
abstract: In chronic heart failure (CHF) the contributing role of increased sympathetic activity and hemodynamic dysfunction in the genesis of ventricular arrhythmias has not been well established. To assess the relation between severe ventricular arrhythmias, hemodynamic impairment, and autonomic nervous system derangement, 142 patients with CHF in sinus rhythm underwent 24-hour electrocardiographic recording, right-sided heart catheterization, and evaluation of sympathovagal balance by heart rate variability (HRV) and baroreflex sensitivity (BRS). Patients were grouped according to the absence (without nonsustained ventricular tachycardia [NSVT]; n = 87) or presence (with NSVT; n = 55) of NSVT. Patients with NSVT had higher pulmonary artery and capillary pressures and more pronounced signs of sympathetic activation and parasympathetic withdrawal compared with those without NSVT. However, logistic regression analysis revealed that depressed BRS but not reduced HRV was significantly associated with the presence of NSVT, at both univariate analysis and after adjustment for clinical and hemodynamic variables. Moreover, it was found that when depressed BRS was associated with high pulmonary capillary pressure, the odds ratio for having NSVT rose markedly from 3.8 to 6.5. In conclusion, this study indicates that in stable CHF the assessment of arterial baroreflex function, but not HRV analysis, allows identification of patients at high risk of NSVT. It is suggested that the effect of depressed BRS is strengthened by the simultaneous presence of increased myocardial wall stress. These data support the hypothesis of a contributory role of autonomic nervous system dysfunction as expressed by the inability to activate effective vagal reflexes and an indirect index of ventricular stretch in the genesis of life-threatening arrhythmias.
authors.affiliation: Divisione di Cardiologia Centro Medico di Montescano, Fondazione S. Maugeri, Instituto di Ricovero e Cura a Carattere Scientifico, Pavia, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Mortara
authors.forename: M T
authors.initials: MT
authors.lastname: La Rovere
authors.forename: G D
authors.initials: GD
authors.lastname: Pinna
authors.forename: P
authors.initials: P
authors.lastname: Parziale
authors.forename: R
authors.initials: R
authors.lastname: Maestri
authors.forename: S
authors.initials: S
authors.lastname: Capomolla
authors.forename: C
authors.initials: C
authors.lastname: Opasich
authors.forename: F
authors.initials: F
authors.lastname: Cobelli
authors.forename: L
authors.initials: L
authors.lastname: Tavazzi
mesh_terms: D001341:Autonomic Nervous System / Q000503:physiopathology; D017704:Baroreflex; D006328:Cardiac Catheterization; D002311:Cardiomyopathy, Dilated / Q000503:physiopathology; D002908:Chronic Disease; D015150:Echocardiography, Doppler; D015716:Electrocardiography, Ambulatory; D006321:Heart / Q000294:innervation; D006333:Heart Failure / Q000175:diagnosis / Q000503:physiopathology*; D006339:Heart Rate; D006801:Humans; D016015:Logistic Models; D008875:Middle Aged; D016017:Odds Ratio; D017180:Tachycardia, Ventricular / Q000175:diagnosis / Q000503:physiopathology*; D018754:Ventricular Dysfunction / Q000503:physiopathology