u/Mountain_Shop_313

#AI-produced post that I thought was worth sharing:

I’ve been reading more about Long COVID recently because there seems to be quite a lot of symptom overlap with what some people experience after myocarditis/myopericarditis: exercise intolerance/PEM, brain fog, disturbed sleep, autonomic symptoms/tachycardia, fatigue and relapses after infections or stress.

Obviously these symptoms don’t mean the underlying biology is necessarily the same, but it made me wonder whether some cases of prolonged post-viral myocarditis/myopericarditis could involve a broader immune dysregulation rather than simply persistent IL-1-type inflammation.

One area that seems interesting is interferon/JAK-STAT signalling and T-cell dysfunction. Long COVID studies have reported persistent immune activation alongside altered/exhausted T-cell phenotypes, interferon signalling, IL-6 pathways, complement abnormalities etc. “T-cell exhaustion” doesn’t simply mean low immunity—it can occur after chronic antigenic stimulation, where T cells remain activated but become functionally altered.

That led me to baricitinib, a JAK1/JAK2 inhibitor. Rather than blocking one cytokine such as IL-1, it reduces intracellular signalling from several cytokine pathways, including interferon-related signalling. There is now a large trial investigating baricitinib specifically for Long COVID, including outcomes such as fatigue, cognition and PEM.

There is also at least some precedent for JAK inhibition in clearly immune-mediated myocarditis. JAK inhibitors have been used in severe immune-checkpoint-inhibitor myocarditis, where T-cell activation is unquestionably central. That is obviously a very different disease from ordinary viral myocarditis, so I’m not suggesting the evidence transfers directly.

But it raises an interesting question for people who have a pattern like:

viral illness → cardiac symptoms/troponin rise → ongoing fatigue/PEM/autonomic symptoms → recurrent post-viral flares,

particularly where CRP/ESR remain normal despite evidence of myocardial injury.

Could a subset have relatively local or interferon/T-cell-driven inflammation that doesn’t generate a big systemic CRP response? And could that explain why treatments aimed primarily at IL-1 or prostaglandins sometimes only partially help?

There are major caveats. Baricitinib is a real immunosuppressant with infection, blood-count, liver and thrombotic considerations, and it is not an established treatment for ordinary myocarditis or Long COVID at present. Persistent viral infection would also complicate the logic of suppressing antiviral immunity. So this definitely isn’t something to self-experiment with.

I’m mainly posting because I think the Long COVID ↔ post-viral myocarditis overlap may be worth more research, particularly around interferon/JAK signalling, T-cell phenotypes and dysautonomia.

Would be interested to know whether anyone here has had detailed immune testing, been treated by an immunologist/rheumatologist, or come across research on JAK inhibitors, hydroxychloroquine, azathioprine/MMF etc. in chronic or recurrent myocarditis rather than the usual acute presentation.

Has anyone used these for myocarditis or myopericarditis? I'm mainly being treated for pericarditis with colchicine and nsaids, but also bisoprolol and ivabradine. Also taking anakinra which seems to have minimal effect at the moment after 5 weeks. Only had mildly elevated troponin following post-viral flares. My capacity has progressively reduced with progressive flares over the last 3 years and I have a progression on MRIs of increasingly dilated ventricles, going from normal to now mildly dilated on both sides over 3 MRIs across 3 years. No scarring or other structural changes. EF preserved at 66%.

I am now wondering if I'm missing a key aspect of the illness and this is more 'myopericarditis' given the troponin elevation and ventricular dilatation.

Now considering whether remodelling meds would be a good idea, like an SGLT2 inhibitor? Does anyone have experience of these along with other medications where EF has been preserved but they have symptoms of myocarditis/myopericarditis?

I'm currently on anakinra once a day and don't feel it's working - at the very least my nights are really rough, even though I feel fairly able during the day and I wonder if it's because the med is wearing off.

I am hearing and seeing increasing number of cases of people not seeing enough of an effect with once a day dosing and changing to 2x daily and seeing significant results.

Does anyone have any experience of this?

Thank you!

a couple questions on anakinra for those on it:

- how long did it take to start working for non-crp elevated pericarditis types?

- injecting evening or morning?

- did anyone see a small effect but then noticed more benefit from doubling the dose and taking morning and evening?

I think I'm seeing some benefit but it has a short half-life so I think it's leaving my system in the evening, then I'm getting rough nights and waking up in pain before the next injection.

I've had myoperi for 2 years with around 4/5 flares always occurring after a virus, mildly elevated troponin with no other elevated markers at time of flare. I've never recovered close back to my baseline since September 24. I used to have elite athletic capacity with a vO2max of 54 at 93kg.

It's been a wild journey and since my most recent flare I'm on naproxen, ivabradine, bisoprolol and colchicine and struggling to wean off naproxen after 3 months. I'm waiting for a potential anakinra prescription with a private doctor in the UK. Colchicine seems to have a mild antiinflammatory effect as I can't wean off that either, while naproxen definitely helps with pain and the betablocker really helps with tachycardia.

Echos have always been fine but MRI's have progressively shown structural changes - my first MRI was pretty clean, second showed mildly dilated RV, and most recent now shows mild biventricular dilatation - my cardiologist has referred me to an inherited cardiac conditions team. Though I'm fairly convinced this is a product of the unresolved myocarditis, not a standalone cardiomyopathic condition.

I'm not the best at resting and have pushed a lot in the last few months and throughout the illness in ways I didn't used to pre-flare, both with work and socially - life has been stressful for a number of reasons and I wonder if this is contributing to the structural changes. I thought for a long time I just had peri but the recent progression in my MRI now point towards more myocardial involvement.

Any advice, particularly from anyone who has myo/peri but has also seen structural changes and how to address would be really helpful. Wondering if anakinra or another medical plan would be best.

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Has anyone has this show up on an MRI while they have peri?

Potentially related to myocardium swelling?

Anyone in the Ventyx Bio trials for this medicine? Oral NLRP3 inhibitor with a lot of promise - could be much cheaper and more convenient to take than an injectable biologic long term.

Hi all,

I'm in the process of obtaining an anakinra prescription within the next month following some blood tests.

Along with the obvious concerns about costs and regular injection, I'm wondering about how long I may have to take the drug for and if it does truly cause remission. I've seen successful remission off arcalyst is fairly common, but I haven't seen loads of stories about the same with Anakinra. Most end up reducing the med down to once every 3/5/7 days but still having to stay on it long term to prevent flares.

Thanks for your insights in advance!