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 ± 54 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.