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Heart Failure/Cardiac Transplantation/Artificial Heart DiseaseDiurnal Variation in Blood Pressure in Patients With Biventricular Assist Devices and Retained, Nonpumping Native Hearts

 

作者: Jens Sehested,   Egbert Happe,   Kozo Ishino,   Roland Hetzer,   Ulf Schiessler,   Soren Schifter,  

 

期刊: Circulation  (OVID Available online 1994)
卷期: Volume 89, issue 6  

页码: 2601-2604

 

ISSN:0009-7322

 

年代: 1994

 

出版商: OVID

 

数据来源: OVID

 

摘要:

Background Studies indicate that centrally mediated rhythms in sympathetic tone play a prominent role in diurnal cardiovascular variability. Recent evidence from heart transplant recipients, in whom blood pressure does not decline during sleep despite normal variability in plasma norepinephrine, however, suggests that afferent cardiac nervous traffic is necessary for the generation of diurnal variability. This implies that in the presence of an innervated heart excluded from the systemic circulation, blood pressure would still decrease during sleep. To assess this hypothesis, we studied 24-hour blood pressure, heart rate, and neuroendocrine variability in patients with biventricular assist devices in whom the retained native hearts had ceased to pump.Methods and Results Eight patients were free of medication and were studied every 3 hours. Pump rates and output were kept constant throughout the study. Blood pressure showed a significant decline during sleep, as did norepinephrine and epinephrine (all P<.05). Atrial natriuretic factor showed a significant increase around midnight (P<.01). Significantly elevated levels were found for all hormones studied except for aldosterone and endothelin.Conclusions Our results suggest that diurnal variations in cardiac function or in catecholamine levels (indicative of sympathetic activity) as found in cardiac transplant recipients alone are not responsible or sufficient for producing a nocturnal drop in blood pressure. The presence of an innervated heart appears crucial in this respect. This could be of importance for the understanding of circadian cardiovascular pathophysiology. (Circulation. 1994;89:2601-2604.)

 



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