Titre du document / Document title

Nonselective beta-adrenergic blocking agent, carvedilol, improves arterial baroflex gain and heart rate variability in patients with stable chronic heart failure

Auteur(s) / Author(s)

MORTARA Andrea ⁽¹⁾ ; LA ROVERE Maria Teresa ⁽¹⁾ ; PINNA Gian Domenico ⁽¹⁾ ; MAESTRI Roberto ⁽¹⁾ ; CAPOMOLLA Soccorso ⁽¹⁾ ; COBELLI Franco ⁽¹⁾ ;

Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)

⁽¹⁾ Department of Cardiology, Centro Medico di Montescano, S. Maugeri Foundation, IRCCS, Pavia, ITALIE

Résumé / Abstract

OBJECTIVES The purpose of this study was to investigate in a case-controlled study whether carvedilol increased baroreflex sensitivity and heart rate variability (HRV). BACKGROUND In chronic heart failure (CHF), beta-adrenergic blockade improves symptoms and ventricular function and may favorably affect prognosis. Although beta-blockade therapy is supposed to decrease myocardial adrenergic activity, data on restoration of autonomic balance to the heart and, particularly, on vagal reflexes are limited. METHODS Nineteen consecutive patients with moderate, stable CHF (age 54 ± 7 years, New York Heart Association [NYHA] class II to III, left ventricular ejection fraction [LVEF] 24 ± ± 6%), treated with optimized conventional medical therapy, received carvedilol treatment. Controls with CHF were selected from our database on the basis of the following matching criteria: age ± 3 years, same NYHA class, LVEF ± 3%, pulmonary wedge pressure ± ± 3 mm Hg, peak volume of oxygen ± 3 ml/kg/min, same therapy. All patients underwent analysis of baroreflex sensitivity (phenylephrine method) and of HRV (24-h Holter recording) at baseline and after six months. RESULTS Beta-blockade therapy was associated with a significant improvement in symptoms (NYHA class 2.1 ± 0.4 vs. 1.8 ± 0.5, p < 0.01), systolic and diastolic function (LVEF 23 ± 7 vs. 28 ± 9%, p < 0.01; pulmonary wedge pressure 17 ± 8 vs. 14 ± 7 mm Hg, p < 0.05) and mitral regurgitation area (7.0 ± 5.1 vs. 3.6 ± 3.0 cm², p < 0.01). No significant differences were observed in either clinical or hemodynamic indexes in control patients. Phenylephrine method increased significantly after carvedilol (from 3.7 ± 3.4 to 7.1 ± 4.9 ms/mm Hg, p < 0.01) as well as RR interval (from 791 ± 113 to 894 ± 110 ms, p < 0.001), 24-h standard deviation of normal RR interval and root mean square of successive differences (from 56 ± 17 to 80 ± 28 ms and from 12 ± 7 to 18 ± 9 ms, all p <0.05), while all parameters remained unmodified in controls. During a mean follow-up of 19 ± 8 months a reduced number of cardiac events (death plus heart transplantation, 58% vs. 31%) occurred in those patients receiving beta-blockade. CONCLUSIONS Besides the well-known effects on ventricular function, treatment with carvedilol in CHF restores both autonomic balance and the ability to increase reflex vagal activity. This protective mechanism may contribute to the beneficial effect of beta-blockade treatment on prognosis in CHF.

Revue / Journal Title

Journal of the American College of Cardiology   ISSN 0735-1097   CODEN JACCDI 

Source / Source

2000, vol. 36, n^o5, pp. 1612-1618 (40 ref.)

Langue / Language

Anglais

Editeur / Publisher

Elsevier, New York, NY, ETATS-UNIS  (1983) (Revue)

Mots-clés anglais / English Keywords

Heart failure ; Chronic ; Carvedilol ; Beta blocking agent ; Heart rate ; Variability ; Autonomic nervous system ; Hemodynamics ; Chemotherapy ; Treatment ; Mechanism of action ; Human ; Vasodilator agent ; Antiarrhythmic agent ; Cardiovascular disease ; Heart disease ;

Mots-clés français / French Keywords

Insuffisance cardiaque ; Chronique ; Carvédilol ; Bloquant β-adrénergique ; Rythme cardiaque ; Variabilité ; Système nerveux autonome ; Hémodynamique ; Chimiothérapie ; Traitement ; Mécanisme action ; Homme ; Vasodilatateur ; Antiarythmique ; Appareil circulatoire pathologie ; Cardiopathie ;

Mots-clés espagnols / Spanish Keywords

Insuficiencia cardíaca ; Crónico ; Carvedilol ; Bloqueador β-adrenérgico ; Ritmo cardíaco ; Variabilidad ; Sistema nervioso autónomo ; Hemodinámica ; Quimioterapia ; Tratamiento ; Mecanismo acción ; Hombre ; Vasodilatador ; Antiarrítmico ; Aparato circulatorio patología ; Cardiopatía ;

Localisation / Location

INIST-CNRS, Cote INIST : 20098, 35400009276347.0230