title: Sympathetic and baroreflex cardiovascular control in hypertension-related left ventricular dysfunction.
abstract: The sympathetic overdrive that characterizes essential hypertension is potentiated when left ventricular hypertrophy or congestive heart failure is detected. No information exists, however, on whether this is the case also for left ventricular diastolic dysfunction. In 17 untreated hypertensive subjects with left ventricular diastolic dysfunction (age: 47.7+/-2.9 years, mean+/-SEM), we measured sympathetic nerve traffic (microneurography), heart rate (ECG), and beat-to-beat arterial blood pressure (Finapres) at rest and during baroreceptor deactivation and stimulation. Data were compared with those collected in 20 age-matched normotensive and 20 hypertensive subjects without a diastolic function impairment. Muscle sympathetic nerve traffic values were markedly and significantly greater in the 2 hypertensive groups than in the normotensive one (55.3+/-1.2 and 71.2+/-1.6 versus 41.7+/-1.0 bursts per 100 heartbeats, respectively; P<0.01 for both). For a similar blood pressure elevation, however, the sympathetic nerve traffic increase was significantly greater in patients with than without left ventricular diastolic dysfunction (+28.9%; P<0.05). In the population as a whole, muscle sympathetic nerve traffic was significantly and inversely related to various echocardiographic indices of diastolic function. Although baroreflex-heart rate control was significantly attenuated in the 2 hypertensive groups, baroreflex-sympathetic modulation was impaired only in those with diastolic dysfunction. These data provide the first evidence that, in hypertension, activation of the sympathetic nervous system may contribute not only at the blood pressure elevation but also at the development of left ventricular diastolic dysfunction. The sympathetic overactivity, which is likely to be related to the baroreflex impairment, may account for the increased cardiovascular risk characterizing diastolic dysfunction.
authors.affiliation: Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy. guido.grassi@unimib.it
authors.forename: Guido
authors.initials: G
authors.lastname: Grassi
authors.forename: Gino
authors.initials: G
authors.lastname: Seravalle
authors.forename: Fosca
authors.initials: F
authors.lastname: Quarti-Trevano
authors.forename: Raffaella
authors.initials: R
authors.lastname: Dell'Oro
authors.forename: Francesca
authors.initials: F
authors.lastname: Arenare
authors.forename: Domenico
authors.initials: D
authors.lastname: Spaziani
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000328:Adult; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena; D016022:Case-Control Studies; D015150:Echocardiography, Doppler; D006339:Heart Rate / Q000502:physiology; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D013318:Stroke Volume / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*