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EDITORIALS: Richard P Steeds and Kevin S Channer Drug treatment in heart failure BMJ 1998; 316: 567-568 [Full text]

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The non compesatory mechanism

Elisabetta Fabris, Alberto Maestroni   (13 May 1998)

The non compesatory mechanism 13 May 1998
Elisabetta Fabris, Students University of Milan, Alberto Maestroni Send response to journal: Re: The non compesatory mechanism	We would like to offer an alternative interpretation of the sympathetic overdrive in heart failure. Malliani and Pagani (1) advanced the hypothesis that the augmented sympathetic outflow in this clinical syndrome could be produced by a "positive" (2) spinal feed back reflex: a sort of Bainbridge reflex. The afferent fibres start from the atrial volume-receptors stimulated by an high filling pressure; from the spinal cord arise the efferent sympathetic fibres directed again to the heart where they have an excitatory ("positive") effect: tachycardia. An increased heart rate can not work as a compensatory mechanism in a failed heart: this is particulary true in acute heart failure when the baroreflex can not play a role in sympathetic overdrive. This interpretation could furnish the basis to explain the effectivness of b-blockers in congestive heart disease: these drugs, infact, reduce the abnormal positive feedback and not only heart rate. References 1) Malliani A, Pagani M. Cardiovascular reflexes mediated by sympathetic afferent fibers. Eur Heart J 1983 Jan;4 Suppl A:49-54 2) Pagani M, Pizzinelli P, Bergamaschi M, Malliani A A positive feedback sympathetic pressor reflex during stretch of the thoracic aorta in conscious dogs. Circ Res 1982 Jan;50(1):125-132