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(Hypertension. 2004;44:727.)
© 2004 American Heart Association, Inc.

Scientific Contributions

Sustained Sympathoinhibitory Effects of Cardiac Resynchronization Therapy in Severe Heart Failure

Guido Grassi; Antonio Vincenti; Roberta Brambilla; Fosca Quarti Trevano; Raffaella Dell’Oro; Antonio Cirò; Giuseppe Trocino; Antonella Vincenzi; Giuseppe Mancia

From the Clinica Medica (G.G., F.Q.T., R.D.’O., G.M.), Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca; and Centro Interuniversitario di Fisiologia Clinica e Ipertensione (G.G., R.D.’O., G.M.), Centro Auxologico Italiano (G.G., G.M.), and Divisione di Cardiologia (A.V., R.B., A.C., G.T., A.V.), Ospedale San Gerardo, Milan, Italy.

Correspondence to Prof Giuseppe Mancia, Clinica Medica, Ospedale S. Gerardo, Via Donizetti 106, 20052 Monza (Milano), Italy. E-mail giuseppe.mancia{at}unimib.it

Evidence is available that in heart failure, cardiac resynchronization therapy by biventricular pacing improves myocardial function and exercise capacity. Whether this is accompanied by a sustained inhibition of heart failure–dependent sympathoexcitation is uncertain. In 11 heart failure patients (mean±SEM age, 68.4±1.5 years) in New York Heart Association (NYHA) class III and IV under medical treatment with an intraventricular conduction delay (QRS duration 130 ms), with a markedly depressed left ventricular ejection fraction, and undergoing implantation of a biventricular pacemaker, we measured beat-to-beat blood pressure and muscle sympathetic nerve traffic. Measurements, which also included echocardiographic and clinical variables, were performed before and 10 weeks after successful resynchronization therapy. Ten age- and NYHA class–matched heart failure patients who were under medical treatment for the same time period served as controls. Long-term resynchronization therapy improved cardiac function and caused a significant increase in systolic blood pressure coupled with an improvement in maximal oxygen consumption and exercise capacity. These effects were coupled with a significant and marked reduction in sympathetic nerve traffic when expressed both as burst frequency over time (44.1±3.6 vs 30.7±3.0 bs/min, –30.5%, P<0.02) and as burst frequency corrected for heart rate (68.3±5.9 vs 47.3±4.3 bs/100 beats, –32.1%, P<0.02). No significant change in the aforementioned parameters was seen in the control group. These data provide the first direct evidence that in severe heart failure, resynchronization therapy exerts a marked and sustained sympathoinhibition. Because in heart failure sympathetic overactivity adversely affects prognosis, this may have important clinical implications.

Key Words: electrical stimulation • heart failure • sympathetic nervous system • autonomic nervous system

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