Deconditioning in patients with orthostatic intolerance
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Abstract
Objective: To study the frequency and degree of deconditioning, clinical features, and relationship between deconditioning and autonomic parameters in patients with orthostatic intolerance.
Methods: We retrospectively studied all patients seen for orthostatic intolerance at Mayo Clinic between January 2006 and June 2011, who underwent both standardized autonomic and exercise testing.
Results: A total of 184 patients (84 with postural orthostatic tachycardia syndrome [POTS] and 100 without orthostatic tachycardia) fulfilled the inclusion criteria. Of these, 89% were women, and median age was 27.5 years (interquartile range [IQR] 22–37 years). Symptom duration was 4 years (IQR 2–7.8). Of the patients, 90% had deconditioning (reduced maximum oxygen uptake [VO2max%] <85%) during exercise. This finding was unrelated to age, gender, or duration of illness. The prevalence of deconditioning was similar between those with POTS (95%) and those with orthostatic intolerance (91%). VO2max% had a weak correlation with a few autonomic and laboratory parameters but adequate predictors of VO2max% could not be identified.
Conclusion: Reduced VO2max% consistent with deconditioning is present in almost all patients with orthostatic intolerance and may play a central role in pathophysiology. This finding provides a strong rationale for retraining in the treatment of orthostatic intolerance. None of the autonomic indices are reliable predictors of deconditioning.
GLOSSARY
- BP=
- blood pressure;
- DBP=
- diastolic blood pressure;
- HR=
- heart rate;
- HUT=
- head-up tilt;
- IIE=
- early phase II;
- IIL=
- late phase II;
- MET=
- metabolic equivalent;
- OI=
- orthostatic intolerance;
- POTS=
- postural orthostatic tachycardia syndrome;
- PP=
- pulse pressure;
- RER=
- respiratory exchange ratio;
- SBP=
- systolic blood pressure;
- TST=
- thermoregulatory sweat test;
- VM=
- Valsalva maneuver;
- VO2max=
- maximum oxygen uptake;
- VR=
- Valsalva ratio
Footnotes
Study funding: Supported in part by the NIH (NS32352 Autonomic Disorders Program Project; NS44233 Pathogenesis and Diagnosis of Multiple System Atrophy, and U54 NS065736 Autonomic Rare Disease Clinical Consortium), Mayo CTSA (UL1 RR24150), and Mayo funds. The Autonomic Diseases Consortium is a part of the NIH Rare Diseases Clinical Research Network (RDCRN). Funding and/or programmatic support for this project has been provided by U54 NS065736 from the National Institute of Neurological Diseases and Stroke (NINDS) and the NIH Office of Rare Diseases Research (ORDR). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute of Neurological Disorders and Stroke or the NIH.
Supplemental data at www.neurology.org
- Received February 20, 2012.
- Accepted May 22, 2012.
- Copyright © 2012 by AAN Enterprises, Inc.
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