Two Different Hemodynamic Responses in ME/CFS Patients with Postural Orthostatic Tachycardia Syndrome During Head-Up Tilt Testing.
van Campen, C Linda M C, Rowe, Peter C, Visser, Frans C · Journal of clinical medicine · 2024 · DOI
Quick Summary
This study looked at how the bodies of ME/CFS patients with POTS (a condition causing rapid heart rate when standing) respond to positional changes differently than healthy people. Researchers found that ME/CFS patients with POTS fall into two groups: those with a smaller heart rate increase appear to have blood pooling in their legs, while those with a larger heart rate increase seem to have an overactive stress response system. These two different patterns might benefit from different treatments.
Why It Matters
Understanding that POTS in ME/CFS patients has multiple underlying mechanisms rather than a single cause is crucial for developing targeted treatments. If some patients primarily have blood pooling while others have hyperadrenergic responses, they may benefit from fundamentally different therapeutic approaches, potentially improving outcomes and reducing treatment failures.
Observed Findings
All ME/CFS patients showed greater stroke volume decreases during tilt compared to healthy controls.
POTS patients with HR increase of 30-39 bpm demonstrated an inverse relationship between HR increase and SVI decrease, consistent with venous pooling.
POTS patients with HR increase ≥40 bpm showed significantly smaller SVI changes and loss of the inverse HR-SVI relationship.
ME/CFS patients with normal HR-BP response displayed a similar venous pooling pattern to the lower-HR-increase POTS group.
Inferred Conclusions
ME/CFS patients with POTS can be stratified into at least two distinct hemodynamic phenotypes based on magnitude of HR increase during tilt.
The limited-HR-increase POTS phenotype is primarily driven by increased venous pooling and reduced preload.
The large-HR-increase POTS phenotype appears to involve a hyperadrenergic mechanism with different hemodynamic characteristics.
These different pathophysiological mechanisms may warrant distinct therapeutic approaches.
Remaining Questions
Do these two hemodynamic profiles remain consistent in individual patients over time, or do patients transition between phenotypes?
What specific treatments are most effective for each hemodynamic profile, and do they differ from treatments for POTS in non-ME/CFS populations?
What This Study Does Not Prove
This study does not prove that these two hemodynamic profiles are the only subtypes of POTS in ME/CFS or that they are stable across time in individual patients. It also does not establish which treatments are most effective for each profile—that would require prospective intervention studies. The observational design means we cannot determine causation, only correlations between HR changes and stroke volume patterns.
Are there additional biological markers (catecholamine levels, autonomic function tests, genetic factors) that could better characterize and predict these POTS subtypes?
Do these hemodynamic profiles correlate with symptom severity, disease progression, or functional outcomes in ME/CFS patients?