Objective Hemodynamic Cardiovascular Autonomic Abnormalities in Post-Acute Sequelae of COVID-19 2022 Hira et al

ABSTRACT

Background
Many COVID-19 patients are left with symptoms several months after resolution of the acute illness (“Post-Acute Sequalae of COVID-19” [PASC]). We aimed to determine the prevalence of objective hemodynamic cardiovascular autonomic abnormalities (CAA), explore sex differences, and assess the prevalence of CAA among hospitalized vs non-hospitalized PASC patients.

Methods
Patients with PASC (n=70; F=56; 42 years 95% CI [40,48]) completed standard autonomic tests, including an active stand test 399 days [338,455] after their COVID-19 infection. Clinical autonomic abnormalities were evaluated.

Results
Most patients with PASC met the criteria for at least one CAA (51; 73%; F=43). The Postural Orthostatic Tachycardia Syndrome hemodynamic criterion (POTSHR) of a heart rate increase of >30bpm within 5-10mins of standing was seen in 21 patients (30%; F=20; p=0.037 [by sex]). The Initial Orthostatic Hypotension hemodynamic criterion (IOH40) of a transient SBP change of >40mmHg in the first 15s of standing was seen in 43 (61%) patients and equally among females and males (63% vs. 57%; p=0.7). Only 9 (13%) patients were hospitalized; hospitalized vs. non-hospitalized patients had similar frequencies of abnormalities (67% vs. 74%; p=0.7).

Conclusions
Patients with PASC have evidence of CAA, most commonly IOH40, which will be missed unless an active stand test is used. Females have increased frequency of POTSHR, but IOH40 is equally prevalent between sexes. Finally, even non-hospitalized “mild” infections can result in long-term CAA.

Open access, https://www.onlinecjc.ca/article/S0828-282X(22)01091-1/fulltext

 

Interesting. Mostly beyond my ability to understand but I did notice one thing:

The active stand test is better than nothing, but it can miss cases of Neurally Mediated Hypotension (aka, neurocardiogenic syncope, vasodepressor syncope, delayed orthostatic hypotension, or whatever name(s) are currently being used).

In those first few years after I got sick I "passed" several active stand tests. [I think they were only 4-5 minutes long? Does the time vary?]

I was uncomfortable, had symptoms, but my heart rate did not rise quite enough for POTS and I was able to do it, did not pass out. (probably caused PEM afterwards but I didn't make the connection between exertion and the delayed PEM until years later).

But on two separate tilt table tests my blood pressure plummeted after 20-30 minutes and I passed out (no isoproterenol, just from the tilt alone).

 

"Assessment of Hemodynamic Criteria for Cardiovascular Autonomic Abnormalities
Following a 10-minute baseline in the supine position, participants completed an active stand test15 where they were instructed to stand as quickly as possible, and remain standing for 10 minutes.

Hemodynamic criteria for cardiovascular autonomic disorders were determined using HR and BP changes during the active stand test. The hemodynamic criterion for orthostatic hypotension (OH) was defined as a systolic BP (SBP) drop ≥20mmHg within 3 minutes of standing (OH20)20, 21, 22. The hemodynamic criterion for postural orthostatic tachycardia syndrome (POTS) was defined as a HR increase ≥30 bpm within 10 minutes of standing in the absence of OH (POTSHR)21 ,23 . Initial orthostatic hypotension (IOH) was defined as a transient SBP drop ≥40mmHg within 15 seconds of standing with recovery within 45 seconds (IOH40)24 . Inappropriate sinus tachycardia (IST) was assessed as a resting supine HR >100bpm (IST100)25"
.

 

This graphic from the study is helpful.

Spoiler: large graphic