Journal of Cardiac Failure
Volume 13, Issue 6 , Pages 470-475, August 2007

Comparison of Muscle Sympathetic Activity in Ischemic and Nonischemic Heart Failure

  • Catherine F. Notarius, PhD

      Affiliations

    • From the Toronto General Research Institute, Toronto, Ontario
    • Division of Cardiology, University Health Network
    • Corresponding Author InformationReprint requests: Catherine F. Notarius, PhD, 6ES:414, Toronto General Hospital, University Health Network, 200 Elizabeth Street, Toronto, Ontario; Canada, M5G 2C4.
  • ,
  • Jonas Spaak, MD, PhD

      Affiliations

    • Current affiliation: Division of Cardiology, Department of Clinical Sciences at Danderyd University Hospital, Karolinska Institutet, Stockholm, Sweden.
    • Division of Cardiology, University Health Network
  • ,
  • Beverley L. Morris, RN

      Affiliations

    • Division of Cardiology, University Health Network
  • ,
  • John S. Floras, MD, DPhil

      Affiliations

    • From the Toronto General Research Institute, Toronto, Ontario
    • Division of Cardiology, University Health Network

Received 7 February 2007; received in revised form 22 March 2007; accepted 29 March 2007.

Toronto, Ontario, Canada

Abstract 

Background

The magnitude of sympathetic activation in chronic heart failure is assumed to be independent of its cause. However, because a higher sympathetic component of heart rate variability (HRV) in patients with ischemic cardiomyopathy (ICM) has been reported, we hypothesized that patients with ICM would have a higher resting muscle sympathetic nerve activity (MSNA) than patients with nonischemic dilated cardiomyopathy (DCM).

Methods and Results

Resting MSNA was assessed by microneurography and HRV concurrently by coarse-graining spectral analysis in 30 treated normotensive patients with chronic heart failure (12 with ICM and 18 with DCM), matched for age and left ventricular ejection fraction, and 23 healthy normal control subjects, matched for age and blood pressure. Peak oxygen uptake was determined during graded cycling (17 W/min) to maximum effort. MSNA was significantly different between groups (P < .001; ICM 60 ± 3; DCM 47 ± 3; control subjects 35 ± 3 bursts/min). Compared with control subjects, the total spectral power and the high-frequency component of HRV were lower in both ICM and DCM groups, but fractal and low-frequency power were lower only in the ICM group (P < .05). Peak oxygen uptake (milliliters per kilogram of body weight per minute) was significantly less in the ICM group than in the DCM group (P = .04) and lower in both groups than in the control subjects (P < .001).

Conclusions

These observations suggest an additional ischemic stimulus to sympathetic activation in heart failure, which may impair exercise capacity reflexively.

Key Words: Etiology, Peak exercise capacity, Microneurography, Left ventricular systolic dysfunction

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 This study was supported by a Heart and Stroke Foundation of Ontario Grant in Aid (T4938). Dr. Floras is a Career Investigator of the Heart and Stroke Foundation of Ontario and holds the Canada Research Chair in Cardiovascular Integrative Biology.

PII: S1071-9164(07)00119-4

doi:10.1016/j.cardfail.2007.03.014

Journal of Cardiac Failure
Volume 13, Issue 6 , Pages 470-475, August 2007