Is it time to move beyond blood pressure and heart rate during head-up tilt testing?, 2024, Mitchell

Dolphin

Dolphin

Senior Member (Voting Rights)
written by: Mitchell G. Miglis, Noor Syed, Melissa M. Cortez, Frans C. Viser, C. Linda MC van Campen, Peter Novak

Unfortunately one can only see the references here:
https://link.springer.com/article/10.1007/s10286-024-01036-1

One can see the start of the letter here:
https://www.springermedizin.de/is-i...ood-pressure-and-heart-rate-during-h/27098904

Miglis, M.G., Syed, N., Cortez, M.M. et al. Is it time to move beyond blood pressure and heart rate during head-up tilt testing?. Clin Auton Res (2024). https://doi.org/10.1007/s10286-024-01036-1

Anyway given that Viser & van Campen are 2 of the most prominent orthostatic intolerance researchers in ME/CFS, I thought this might be of interest.
 
For a very quick precis, I've automagically clipped the text from what I highlighted on initial skim.

Is it time to move beyond blood pressure and heart rate during head-up tilt testing?
  • Autonomic specialists continue to rely on HUTT as the gold standard for obtaining the physiological criteria needed to support the diagnosis of neurally-mediated syncope, OH and POTS. However, there is a sizeable portion of patients with OI in whom BP and HR measurements on HUTT are either nondiagnostic or completely normal, including those who are severely symptomatic during the test.
  • patients are often dismissed without a clear diagnosis or treatment plan and can suffer significant disability
  • important questions: What physiological abnormalities are we missing by focusing on BP and HR alone?
Cerebral blood flow
  • There is accumulating evidence supporting the notion that measurements of cerebral blood flow (CBF) can advance the diagnostic utility of HUTT.
  • logical, as the cardinal symptoms of OI (i.e., lightheadedness, visual changes, presyncope) are fundamentally the result of cerebral hypoperfusion.
  • intracranial and extracranial techniques of CBF measurements have been explored. Intracranial CBF measurements are performed with transcutaneous Doppler (TCD) probes positioned over either one or both middle cerebral arteries using a specialized head set with a three-dimensional TCD positioner to maintain the proper angle of insonance during testing.
  • Extracranial techniques involve ultrasound positioning over extracranial vessels, such as the internal carotid (IC) and vertebral arteries (VA). This latter technique has the benefit of being able to control for vessel diameter, which can be affected by hypocapnea and gravitational fluid shifts during HUTT
  • measured simultaneously with HR, BP, and end-tidal CO 2(EtCO2), as all these variables affect CBF
  • EtCO2 is especially important to include to control for the effects of hypocapnea on intracranial vasoconstriction
  • Several studies have demonstrated that cerebral hypoperfusion in the absence of POTS, OH, or neurally mediated hypotension can occur in 8–13% of patients during HUTT, a condition categorized as orthostatic cerebral hypoperfusion syndrome (OCHOS), where the orthostatic hypocapnia is absent, or hypocapnic cerebral hypoperfusion (HYCH), where the orthostatic hypocapnia is present.
  • usually symptomatic, whereas not all patients with OH are
  • suggest that CBF may have a stronger correlation with orthostatic symptoms than BP or HR change
  • fundamental limitations of CBF measurements, which record blood flow velocity and not blood flow itself, in one or two vessels and not the entire cerebral circulation
  • standardized normative CBF data are lacking
  • In one elegant study, the authors measured CBF, EtCO2, muscle sympathetic nerve activity (MSNA), total peripheral resistance and cardiac output in 11 patients with POTS and 10 healthy controls undergoing HUTT. They found that reductions in CBF occurred first in patients with POTS, corresponding with initial OH and a large fall in central thoracic blood flow, followed by hyperpnea and hypocapnea, then an increase in MSNA. These abnormalities were absent in control participants. This led the authors to suggest that hyperpnea and hypocapnia increase brain-wide vasoconstriction and hypoxia–ischemia via the Bohr Effect, resulting in increased cerebral oxygen demand, neuronal excitability and continued sympathetic activation.
  • unclear if hypocapnia is a primary or secondary process in disorders of OI, capnography is an easy and affordable option to add to HUTT
Electroencephalography
  • utility of EEG during HUTT in distinguishing between disorders of orthostatic intolerance is debated
  • can be valuable in confirming psychogenic pseudosyncope and nonepileptic orthostatic spells
Near-infrared-spectroscopy
  • Near-infrared-spectroscopy (NIRS) is a noninvasive technique that uses near-infrared light wavelengths to estimate cerebral tissue oxygen saturation (SctO2) in a mix of arterial and venous blood, with sensors typically applied to the bilateral forehead. The main benefit of NIRS is its ease of use.
  • requires no training to administer or interpret.
Heart rate variability
  • While several studies have reported impaired HRV in the time domain in disorders of orthostatic intolerance, such as POTS, studies have reported inconsistent abnormalities in the frequency domain
Conclusion
  • As autonomic specialists we should all be aware that orthostatic changes in CBF, EtCO2, electrocortical activity, HRV, or oxygen extraction, among other physiological changes, can occur in the presence of a completely normal BP or HR response on HUTT, and that neglecting to measure such changes can be a missed opportunity, most importantly for some of our patients.
Click to expand...
 
Nothing scientific to say, just that this letter makes me and my daughter (who has OCHOS) very happy.

I also learned a few things, and it answers my question about the difference between transcranial and carotid/vertebral measurements (they are both valid, with a slight advantage to the non-transcranial option).

And I was pleased to see that the two groups of researchers – the Novak group in the US and the Visser et al group in the Netherlands – collaborate.

(I had noticed that the Visser group didn’t use the term OCHOS even when it seemed what they had identified was OCHOS, and was wondering why. Well, it’s obviously not anything acrimonious if they are publishing together. Probably just preferred terminology or related to the presence of ME/CFS in the Visser patients.)
 
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