V. Ilardo

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.

Behaviour of regional adrenergic outflow in mild-to-moderate renal failure

Objectives Chronic renal failure is characterized by a marked sympathetic activation. No information exists, however, as to whether the adrenergic overdrive is confined to selected vascular districts or is rather generalized to the whole cardiovascular system. Methods In 15 patients aged 60.5 ± 2.0 years (mean ± SEM) with stable chronic renal failure belonging to stage 2–3 of the Kidney Foundation classification and in 12 age-matched healthy controls, we measured arterial blood pressure (Finapres), heart rate (ECG), venous plasma norepinephrine (high-performance liquid chromatography) and postganglionic sympathetic nerve traffic in skeletal muscle and skin areas (microneurography). Muscle and skin nerve traffic measurements were made in a randomized sequence over two periods of 30 min each, spaced by a 20–30-min interval. Measurements also included evaluation of skin sympathetic responses to emotional stimuli. Results Muscle sympathetic nerve traffic was markedly and significantly greater in renal failure patients compared with controls (58.2 ± 3.6 vs. 36.8 ± 5.7 bursts/100 heart beats, P < 0.01), with this also being the case for plasma norepinephrine (380.6 ± 63 vs. 210.8 ± 29 pg/ml, P < 0.05). By contrast, skin sympathetic nerve traffic was superimposable in the two groups (11.5 ± 0.8 vs. 12.7 ± 1.7 bursts/minute, P = not significant), this being the case also for the responses to emotional arousal. Conclusion These data provide the first evidence that the sympathetic activation characterizing renal failure is not generalized to the entire cardiovascular system. This may depend on the fact that the two sympathetic districts are governed by mechanisms that are differently affected by the chronic uraemic state.