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Discordance between microneurographic and heart rate spectral indices of sympathetic activity in pulmonary arterial hypertension
  1. Cheri L.M. McGowan (cmcgowan{at}uhnres.utoronto.ca)
  1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada
    1. John Swiston (swiston{at}interchange.ubc.ca)
    1. Department of Medicine, University of British Columbia, Canada
      1. Catherine F. Notarius (c.notarius{at}utoronto.ca)
      1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada
        1. Susanna Mak (smak{at}mtsinai.on.ca)
        1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada
          1. Beverley L. Morris (bmorris{at}uhnres.utoronto.ca)
          1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada
            1. Peter E. Picton (peter.picton{at}uhn.on.ca)
            1. University Health Network, Canada
              1. John T. Granton (dr.john.granton{at}uhn.on.ca)
              1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada
                1. John S Floras (john.floras{at}utoronto.ca)
                1. University Health Network and Mount Sinai Hospital Department of Medicine, Canada

                  Abstract

                  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 sino-atrial 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 9 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 neural heart rate modulation and increased right atrial stretch may combine to attenuate HRV, an adverse prognostic marker.

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