Autonomic dysfunction post-acute COVID-19 infection, 2021, Desai et al

[ola_cohn]

Introduction
SARS-CoV-2 infection which causes the disease COVID-19 is most known for its severe respiratory complications. However, a variety of extrapulmonary effects have since been described, with cardiovascular complications being amongst the most common[1]. Those who recover from the acute phase of COVID-19 may be left with residual symptoms such as chest pain and dyspnea, resulting in a decreased quality of life and a syndrome sometimes described as “long COVID”[2]. Recent evidence suggests that survivors with some of these chronic symptoms may have autonomic dysfunction with features of postural orthostatic tachycardia syndrome (POTS) and/or inappropriate sinus tachycardia (IST)3,4. POTS is characterized by symptoms that occur with standing, an increase in heart rate of ≥30 beats per minute (or heart rate >120 bpm) when moving from a supine to a standing position, and the absence of orthostatic hypotension[5]. IST is defined as a sinus heart rate >100 beats per minute at rest without an identifiable cause of sinus tachycardia[6]. Cardiac manifestations of autonomic dysfunction lie on a wide spectrum and can therefore be classified as either POTS, IST, or other unspecified symptoms such as tachycardia and palpitations without a clear, single underlying pathological mechanism.[7] The treatment of these arrhythmias includes nonpharmacologic management, such as increasing salt and fluid intake, as well as the use of oral medications. Beta-blockers or off label use of ivabradine have used reported to be used in both syndromes with the goal of controlling heart rate to reduce the symptoms8,9. Other therapies more common in POTS include fludrocortisone, midodrine, pyridostigmine, and alpha-2 agonists[8].

There is a need to understand the patient characteristics and risk factors for developing AD as a sequela of COVID-19. Furthermore, there is limited management information specific to patients suffering from AD following COVID-19. It is unclear how treatment of these patients and their prognoses may differ from other cases of POTS or IST. In this study, we investigated a small cohort of patients diagnosed with suspected AD post SARS-CoV-2 infection to elucidate possible risk factors and treatment strategies in this population.

Key words
autonomic dysfunction, COVID-19, arrhythmia, long COVID-19, vaccines, postural orthostatic tachycardia syndrome, inappropriate sinus tachycardia

Open access full text
https://www.heartrhythmcasereports.com/article/S2214-0271(21)00223-2/fulltext

 

[rvallee]

It's a good thing that LC has brought dysautonomia and POTS off the blacklist but it's still almost entirely discussed as an elevated heart rate on standing/sitting up and nothing else. There is just no depth, no useful knowledge, in addition to this simple number. You have to cross that 30 (?) BPM in the right time span and nothing else happens, your heart beats faster and that's it, that's 100% of it. Everything else is just stuff to list without context or depth, too trivial to care about.

Very annoying that the exact same failure is being repeated. This obsession with reducing everything to a single thing and ignoring everything else is becoming a genuinely critical block on medical progress, because almost nothing that's left to figure out fits in that mold. Which is why it got denied in the first place. Past failure fueling ongoing and future failure in a runaway process.

Frankly this is a lot like physics dealing with quantum mechanics, it's a complete paradigm shift and it just doesn't compute. But there's no math or observational science that can untangle this mess. It's a far easier blocker to deal with, technically, but it's far more difficult because of politics and ideology. What a disaster.