Dissociation between reflex sympathetic and forearm vascular responses to lower body negative pressure in heart failure patients with coronary artery disease

Division of Cardiology, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada Submitted January 6, 2009 ; accepted in final form August 28, 2009 Many heart failure (HF) patients exhibit paradoxical forearm vasodilation when central blood volume is reduce...

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Published in:	American journal of physiology. Heart and circulatory physiology 2009-11, Vol.297 (5), p.H1760-H1766
Main Authors:	Notarius, Catherine F, Morris, Beverley L, Floras, John S
Format:	Article
Language:	eng
Subjects:	Action Potentials Arms Biomarkers - blood Blood Blood Volume Cardiomyopathy, Dilated - complications Cardiomyopathy, Dilated - physiopathology Case-Control Studies Cold Temperature Comparative analysis Coronary Artery Disease - blood Coronary Artery Disease - complications Coronary Artery Disease - physiopathology Electrocardiography Forearm - blood supply Heart failure Heart Failure - blood Heart Failure - etiology Heart Failure - physiopathology Heart Rate Humans Lower Body Negative Pressure Male Middle Aged Muscle, Skeletal - innervation Norepinephrine - blood Plethysmography Random Allocation Reflex Regional Blood Flow Stroke Volume Sympathetic Nervous System - metabolism Sympathetic Nervous System - physiopathology Vasoconstriction Vasodilation Ventricular Function, Left
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Summary:	Division of Cardiology, University Health Network and Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada Submitted January 6, 2009 ; accepted in final form August 28, 2009 Many heart failure (HF) patients exhibit paradoxical forearm vasodilation when central blood volume is reduced by lower body negative pressure (LBNP). We tested the hypothesis that this response results from reflex sympathetic withdrawal. We recorded simultaneously forearm blood flow, muscle sympathetic nerve activity (MSNA), and plasma norepinephrine (PNE) during four random applications of LBNP, –5, –10, –20, and –40 mmHg, in 12 men with HF (mean left ventricular ejection fraction = 24 ± 2%) and 10 healthy, normal, age-matched men (N). Compared with N, MSNA burst frequency ( P = 0.001) and PNE ( P = 0.005) were significantly higher in the HF group, both at rest and during LBNP. As anticipated in N, LBNP –40 mmHg significantly increased MSNA (+14.2 ± 2.5 bursts/min; P < 0.05) and PNE (+0.83 ± 0.22 nmol/l; P < 0.05) and decreased forearm vascular conductance (FVC) (–11.7 ± 3.2 ml·min –1 ·mmHg –1 ; P < 0.05). In the HF group, LBNP elicited similar increases in MSNA (+11.5 ± 2.0; P < 0.05) and PNE (+0.85 ± 0.12; P < 0.05), without affecting FVC significantly (–4.1 ± 2.4; P = 0.01 vs. N, interaction P = 0.03). However, within the HF group, responses were bimodal: LBNP –40 mmHg increased MSNA in all subjects ( P < 0.001), yet the six patients with nonischemic or dilated cardiomyopathy (DCM) exhibited significant vasoconstriction (decrease in FVC; P = 0.001), whereas the six patients with ischemic cardiomyopathy (ICM) exhibited significant vasodilation (increase in FVC; P < 0.02 vs. DCM and N; interaction P = 0.02). Cold pressor testing increased MSNA and decreased FVC in ICM ( n = 4). Thus paradoxical forearm vasodilator responses to LBNP in HF are not mediated by reflex sympathetic withdrawal. ICM and DCM patients differ qualitatively in their vascular responses to hypotensive LBNP. etiology; microneurography; muscle sympathetic nerve activity; vascular conductance Address for reprint requests and other correspondence: C. F. Notarius, 6ES:414, Toronto General Hospital, Univ. Health Network, 200 Elizabeth St., Toronto, Ontario, Canada M5G 2C4 (e-mail: c.notarius{at}utoronto.ca ).
ISSN:	0363-6135 1522-1539