A Novel Noninvasive Device to Assess Sympathetic Nervous System Function in Patients With Heart Failure.

BACKGROUND: Heart failure is a complex syndrome associated with sympathetic nervous system and renin-angiotensin-aldosterone system hyperactivity. Sympathoinhibition and downregulation of sympathetic activity using medications and exercise training improve outcomes in patients with heart failure. Impedance cardiography provides data on hemodynamic and autonomic function that may assist with safe medication, exercise monitoring, and titration. PURPOSE: The purpose of this pilot study was to evaluate the sensitivity of the Vrije Universiteit Ambulatory Monitoring System (VU-AMS) version 5fs to detect hemodynamic and sympathetic nervous system changes associated with postural shift in persons with heart failure with reduced ejection fraction. METHODS: In this descriptive study, participants (N = 28) were recruited from an outpatient device clinic at a tertiary care hospital in Ontario, Canada. They completed a sit-to-stand posture protocol wearing an ambulatory blood pressure (ABP) and a noninvasive VU-AMS version 5fs impedance cardiography system. RESULTS: Most (n = 18, 64%) participants were eliminated from the final analyses in this sample because of difficulty in Q-onset and B-point identification in peculiar electrocardiogram and impedance cardiogram waveforms. The remaining participants (n = 10) had a mean age of 69 years (SD = 10 years) and responses to a sit-to-stand posture protocol that included a 5% increase in heart rate (p = .001), an 18% decrease in stroke volume (p = .01), and an 8% decrease in left ventricular ejection time (p = .01). Participants had an increased preejection period (11%, p = .01), a drop in cardiac output of 13% (p = .02), and a reduced mean arterial pressure of approximately 4% (p = .09) with standing. DISCUSSION: Although the VU-AMS version 5fs system detected anticipated hemodynamic and sympathetic nervous system changes to postural shift in participants (n = 10), the elimination of 64% (n = 18) of the sample because of scoring difficulties limits the use of this impedance cardiography device using standard scoring algorithms in persons with heart failure with reduced ejection fraction.

Prostaglandins induce vasodilatation of the microvasculature during muscle contraction and induce vasodilatation independent of adenosine.

Blood flow data from contracting muscle in humans indicates that adenosine (ADO) stimulates the production of nitric oxide (NO) and vasodilating prostaglandins (PG) to produce arteriolar vasodilatation in a redundant fashion such that when one is inhibited the other can compensate. We sought to determine whether these redundant mechanisms are employed at the microvascular level. First, we determined whether PGs were involved in active hyperaemia at the microvascular level. We stimulated four to five skeletal muscle fibres in the anaesthetized hamster cremaster preparation in situ and measured the change in diameter of 2A arterioles (maximum diameter 40 µm, third arteriolar level up from the capillaries) at a site of overlap with the stimulated muscle fibres before and after 2 min of contraction [stimulus frequencies: 4, 20 and 60 Hz at 15 contractions per minute (CPM) or contraction frequencies of 6, 15 or 60 CPM at 20 Hz; 250 ms train duration]. Muscle fibres were stimulated in the absence and presence of the phospholipase A2 inhibitor quinacrine. Further, we applied a range of concentrations of ADO (10(-7)-10(-5) M) extraluminally, (to mimic muscle contraction) in the absence and presence of L-NAME (NO synthase inhibitor), indomethacin (INDO, cyclooxygenase inhibitor) and L-NAME + INDO and observed the response of 2A arterioles. We repeated the latter experiment on a different level of the cremaster microvasculature (1A arterioles) and on the microvasculature of a different skeletal muscle (gluteus maximus, 2A arterioles). We observed that quinacrine inhibited vasodilatation during muscle contraction at intermediate and high contraction frequencies (15 and 60 CPM). L-NAME, INDO and L-NAME + INDO were not effective at inhibiting vasodilatation induced by any concentration of ADO tested in 2A and 1A arterioles in the cremaster muscle or 2A arterioles in the gluteus maximus muscle. Our data show that PGs are involved in the vasodilatation of the microvasculature in response to muscle contraction but did not obtain evidence that extraluminal ADO causes vasodilatation through NO or PG or both. Thus, we propose that PG-induced microvascular vasodilation during exercise is independent of ADO.