Sympathetic and baroreflex function in hypertensive or heart failure patients with ventricular arrhythmias

Objective To determine whether in hypertension and in heart failure the occurrence of ventricular arrhythmias is associated with alterations in sympathetic drive and baroreflex function. Design and methods We studied 28 untreated essential hypertensives (age, 53.0 +/- 1.1 years, mean standard error of the mean), 15 without and 13 with monofocal premature ventricular contractions (PVCs) in Lown class I, and 30 heart failure patients (age, 53.8 +/- 1.3 years) in New York Health Association class II-III,17 without and 13 with PVCs also in Lown class I. In each patient we measured, along with echocardiographic variables, the beat-to-beat mean blood pressure (Finapress), heart rate (HR) (EKG), muscle sympathetic nerve traffic (MSNA) (microneurography), venous plasma norepinephrine and renin activity (high-pressure liquid chromatography and radioimmunoassay, respectively). Measurements were performed at rest and during arterial baroreceptor stimulation and deactivation via stepwise intravenous infusion of phenylephrine and nitroprusside, respectively. Results The mean blood pressure, HR and MSNA were similar in hypertensive patients without and with PVCs. However, compared with non-arrhythmic patients, hypertensives with PVCs displayed a baroreflex-HR and baroreflex-MSNA modulation reduced by 27.7 +/- 4.2 and 17.9 +/- 2.8%, respectively (P < 0.05). Heart failure patients with PVCs showed haemodynamic and echocardiographic variables superimposable to those without PVCs. Compared with these patients, however, they exibited a significant increase in MSNA values (75.8 +/- 3.0 versus 63.6 +/- 2.8 bs/100 hb, P < 0.05), coupled with a significant impairment in baroreflex-HR and baroreflex-MSNA control (-52.5 +/- 5.4 and -37.5 +/- 3.6%, P < 0.01). Conclusions These data provide evidence that in both hypertension and heart failure, sympathetic and baroreflex mechanisms exert a pro-arrhythmogenic role. This role, however, appears to be more pronounced in heart failure than in hypertension, in which the impaired vagal function may exert a concomitant favouring effect. (C) 2004 Lippincott Williams Wilkins.