Impaired parasympathetic function in long-COVID postural orthostatic tachycardia syndrome – a case-control study, 2023, Stefano Rigo et al

Abstract
Purpose
Eighty percent of patients infected by SARS-CoV-2 report persistence of one symptom beyond the 4-week convalescent period. Those with orthostatic tachycardia and orthostatic symptoms mimicking postural tachycardia syndrome, they are defined as Long-COVID POTS [LCP]. This case-control study investigated potential differences in autonomic cardiovascular regulation between LCP patients and healthy controls.

Methods
Thirteen LCP and 16 healthy controls, all female subjects, were studied without medications. Continuous blood pressure and ECG were recorded during orthostatic stress test, respiratory sinus arrhythmia, and Valsalva maneuver. Time domain and power spectral analysis of heart rate [HR] and systolic blood pressure [SBP] variability were computed characterizing cardiac autonomic control and sympathetic peripheral vasoconstriction.

Results
LCP had higher deltaHR (+ 40 ± 6 vs. + 21 ± 3 bpm, p = 0.004) and deltaSBP (+ 8 ± 4 vs. -1 ± 2 mmHg, p = 0.04) upon standing; 47% had impaired Valsalva maneuver ratio compared with 6.2% in controls (p = 0.01). Spectral analysis revealed that LCP had lower RMSSD (32.1 ± 4.6 vs. 48.9 ± 6.8 ms, p = 0.04) and HFRRI, both in absolute (349 ± 105 vs. 851 ± 253ms2, p = 0.03) and normalized units (32 ± 4 vs. 46 ± 4 n.u., p = 0.02). LFSBP was similar between groups.

Conclusions
LCP have reduced cardiovagal modulation, but normal sympathetic cardiac and vasoconstrictive functions. Impaired parasympathetic function may contribute to the pathogenesis of Long-COVID POTS syndrome.

https://bioelecmed.biomedcentral.com/articles/10.1186/s42234-023-00121-6

 

I had a brief look at this- full text is available online and it seems like a pretty decent study. A lot more research to be done in this area, but a good start here. There does appear to be significant parasympathetic deregulation and inappropriately unbalanced/unopposed sympathetic drive in LC/POTs depending on the subgroup. I'd be interested to see more in this area, especially more HRV and cerebral perfusion studies including the effects of v low dose beta blockade. Currently I'm n=1 for my teeny beta blocker case report, but I've found them helpful- at least on my HR, BP, HRV, especially overnight and for orthostatic autonomic dysregulation. I'd be interested in any of your big brain knowledge or experience here?

 

@Kiwipom I can't offer any big brain knowledge but can offer experience of taking low dose beta-blockers. I was initially on 10mg of propranolol tid but found that to have too many gastro side effects, I now take 10mg every morning and occasionally a second dose later in the day. I wouldn't say I notice it's specific effects on a day-to-day basis but when I stopped taking it to trial pyridostigmine I felt much worse overall and improved once I resumed it again.

My other observation is that when I was healthy I always had pronounced respiratory sinus arrhythmia, RSA, (maybe weird to be aware of this but I trained as a vet and it's important to know because in some species it's normal and others is pathological), and ever since my M.E. relapsed and I developed quite severe POTS I have no evidence of RSA at all. As far as I can tell there is no mention of the results of the RSA monitoring in the study but I wasn't capable of reading it too closely so I may have missed something. It's disappearance is always something that has felt very significant to me in my own illness.