Discordance between microneurographic and heart-rate spectral indices of sympathetic activity in pulmonary arterial hypertension.

OBJECTIVES: To determine, in patients with pulmonary arterial hypertension (PAH), whether there is a relationship: (1) between sympathetic nerve firing rate and spectral indices of sympathetic neural heart rate modulation; and (2) between heart rate variability (HRV) and right atrial pressure, a stimulus to sinoatrial node stretch. DESIGN: Characterisation of patients and healthy controls. SETTING: Teaching hospital-based study. PATIENTS: 9 PAH patients without elevated pulmonary capillary wedge pressure and nine age-matched control subjects. INTERVENTIONS: Heart rate (HR) and muscle sympathetic nerve activity (MSNA) were recorded during 10 min of supine rest in both PAH patients studied after right heart catheterisation, and healthy volunteers. Coarse-graining spectral analysis determined HR spectral power. MAIN OUTCOME MEASURES: (1) Low-frequency (PL) spectral component of HRV; (2) MSNA burst frequency; and in PAH patients: (3) right atrial pressure. RESULTS: MSNA burst frequency was higher in PAH patients (48 (24) and 29 (11) bursts/min, respectively; mean (SD); p = 0.05), whereas total power (p = 0.01), its fractal (p<0.01) and harmonic (p = 0.04) components, and PL (p = 0.01) were all reduced. PL related inversely to both MSNA burst frequency (r = -0.86, p = 0.005) and right atrial systolic pressure (r = -0.77, p = 0.04). CONCLUSIONS: Thus, in PAH (as in patients with left ventricular systolic dysfunction) loss of PL relates inversely to gain in MSNA burst frequency. Diminished sympathetic neural heart rate modulation and increased right atrial stretch may combine to attenuate HRV, an adverse prognostic marker.

Auditory steady-state responses to tones amplitude-modulated at 80-110 Hz.

Steady-state responses can be recorded from the human scalp in response to tones that are sinusoidally modulated in amplitude at rates between 60 and 120 Hz. For 60 dB SPL 1000-Hz tones the maximum baseline-to-peak amplitude of about 0.06 microV occurs for modulation rates between 80 and 95 Hz. The phase of the response does not change with modulation depths greater than 25% and the amplitude saturates at modulation depths greater than 50%. The presence or absence of a response can be accurately determined by frequency-domain statistics and the response becomes clearly recognizable at intensities that are 16 +/- 8 dB above behavioral thresholds. With increasing intensity the response increases in amplitude at 1.9 nV/dB until an intensity of 70 dB SPL. As the intensity increases above 70 dB SPL the response increases in amplitude more rapidly at 7.8 nV/dB (at 1000 Hz) and contains significant energy at harmonics of the modulation frequency. This second stage of the intensity function is more prominent for stimuli with lower carrier frequencies (500 more than 1000 more than 2000 Hz) and is attenuated by high-pass masking. These steady-state responses should be helpful in evaluating human auditory physiology and in objective audiometry.