ME/CFS and DCA/Meldonium Study (Glucose/Insuline, Brainblood flow)

[pattismith]

Trying to find the link between SFN and Ventricular Premature Heartbeat is not an easy task.
Here what I can say:

I have some anti-alpha1 adrenergic that are very high together with anti-AT1R and anti-ETAR. (alpha 2A and M3 are only modestly elevated). Some of these functional antibodies have already been associated to some Rheumatic Diseases and cardiac arrhythmia are known comorbidities with RDiseases.
SFN is also a comorbidity with some RDisease to make it more complicated!

Some association between anti-adrenergic and muscarinic auto-antibodies were also associated to cardiac arrhythmia, so it's very complexe and I don't have the knowledge needed to solve the equation.

The only thing I understand is that I have SFN and some auto-immune process at play, and that they are likely associated to my Ventricular Premature Contraction.

Do you have any auto-immune process that you already know is affecting you and showed up in your blood work ? (Hashimoto or Grave's or any rheumatic disease, or other)

 

[Hd-x]

Do you have any auto-immune process that you already know is affecting you and showed up in your blood work

I have MCAS + allergy + some (hot+cold nodes) thyriod trouble that are auto-immune diseases
showing up in my blood by increased IGG2, Tryptase, Leukotriene, TGF-ß, IL4, IL8, TNF-y, Zonulin and descreased CD8+ cell count, low TSH, high FT3 (both thyriod values sometimes within the ref. range, sometimes outside)
Immunological: TH1+TH2 increased, with TH2 dominance. However, I was able with the time to get ridd off the TH2 shift and doing so improved my CFS further to some degree.

Certainly the burning muscles + paresthesia are disturbing, but I had lots off other healthy trouble (sportman hernia, torn meniscus, Impingement, Hypogonadism, IBS w. leaky gut, lymphadenopathy, sleep apnoe) that had to be fixed first, so that FMS & SFN was for a while not on my priority list.
Well, obvisiously I should try to do a few things against SFN if you think there could be a crosslink.

 

[pattismith]

I have MCAS + allergy + some (hot+cold nodes) thyriod trouble that are auto-immune diseases
showing up in my blood by increased IGG2, Tryptase, Leukotriene, TGF-ß, IL4, IL8, TNF-y, Zonulin and descreased CD8+ cell count, low TSH, high FT3 (both thyriod values sometimes within the ref. range, sometimes outside)
Immunological: TH1+TH2 increased, with TH2 dominance. However, I was able with the time to get ridd off the TH2 shift and doing so improved my CFS further to some degree.

Certainly the burning muscles + paresthesia are disturbing, but I had lots off other healthy trouble (sportman hernia, torn meniscus, Impingement, Hypogonadism, IBS w. leaky gut, lymphadenopathy, sleep apnoe) that had to be fixed first, so that FMS & SFN was for a while not on my priority list.
Well, obvisiously I should try to do a few things against SFN if you think there could be a crosslink.

I had the low CD8+ as well.
Did they check your anti-thyroid antibodies (TG, TPO, TSHR)? You may have something wrong like I had myself….
SFN is not the root of thyroiditis (not that I know), it's a frequent comorbidity. I had hyperthyroiditis + obvious skin SFN last august and I became aware of my PVC at this time (high HR and acute sensitivity to heart beat, you can feel it much better with sensory SFN!)
I was not too much worried about skin SFN paresthesia/burning as I thought it was such a minor problem in front of all my other problems so I thought I had to adress thyroiditis first and that maybe SFN will improve.
SFN + hyperthyroidism were generating lot's of acute cervical pain at that time and I was convinced spine hernia had to be ruled out... I went to neurosurgeon but he was sure my stenosis wasn't significant. So my conclusion was to blame on SFN + hyperthyroidism for making my pain so bad.
Do you take any iodine supplement?
Do you take coffee?
How many PVC do you have per one or 5 min?

 

[Hd-x]

I was drinking coffee, but currently not anymore and will also not do anymore in future.
I also quit smoking and switched over to nicotine pouches - this helps me getting off the cigarettes without problems, with the times I will step by step also reduce the nicotine pouches to get fully ridd off any nicotine.

Dr prescribed Iodine, but since I take such a bunch off supplemente because off MCAS/CFS, sometimes I just forget to take the Iodine pills.

Did they check your anti-thyroid antibodies (TG, TPO, TSHR)?

I need to check out my blood works, but I guess Dr hadnt test this.

How many PVC do you have per one or 5 min?

During the last 14days I had up to 3 PVC per 30secound.
Today it looks a lot better, some hours I had some, some hours I was free off any PVC.

 

[pattismith]

if I understand, Meldonium decreases carnitine in blood is it?
Let's hope your VPC low count will remain good!
(I can count about 1-2 per min in the evening, less in the morning)

I was drinking coffee, but currently not anymore and will also not do anymore in future.
I also quit smoking and switched over to nicotine pouches - this helps me getting off the cigarettes without problems, with the times I will step by step also reduce the nicotine pouches to get fully ridd off any nicotine.

Dr prescribed Iodine, but since I take such a bunch off supplemente because off MCAS/CFS, sometimes I just forget to take the Iodine pills.

Supplementation with iodine/selenium during two years put me from low Thyroid Syndrome to Hyperthyroidism with auto-immune thyroiditis.
I wish I had checked more regularly my anti-thyroid auto-antibodies, if only I had known the existing risk for people who are predisposed to this kind of disease...
It was a hard work to reverse that!
I would advise you to stop any iodine supplementation until you check your A-Thyroid A-antibodies (selenium is safe)

Edit: I forgot to add about SFN that Dr Oaklander thinks it's the root of many cases of IBS. Lesions of small nerves fibers ( from autonomic nervous system) going to the digestive tract are involved in some kind of dysautonomia, delayed emptying of the stomach or early emptying, IBS...

 

[Hd-x]

@pattismith
Interestingly, I have similar isssues, less PVC in the morning and more in evening.
About minerals: Urine+blood tests showed a Iodine deficiency ( I guess due to MCAS malabsorbation + leaky gut, I had also K, P, Se, Cu, Cr, Fe deficiency)
Some supplementation is needed in my case to keep all those nutritions at last at normal levels.

Let's hope your VPC low count will remain good!

Thank you, I hope yours will also improve.
Well, even if the VPC/PVC are a lot better, they disturb me (mentally) much more then SFN or any muscle pain.
(I can handle any chronic pain much better then such strange "heart-beat" trouble)
I am now since 5days on Meldonium and if I would not have the PVC I would say I feel really good, my fatigue is less then usual, also my brain fogging is today better, the low Dose regime seems to work fine for me and will stay on that low dose as so long it works.
Once the VPC/PVC fade away I will try to go back to gym and then it will show if Meldonium also reduces the PEM after a work out. (I had some success with Inosine + EEAs as PEM buster, but didnt fully get ridd off PEM)

if I understand, Meldonium decreases carnitine in blood is it?

My english is not that good, so I quote the Meldonium mechanismn from a medical paper:
"L-carnitine transports activated long-chain fatty acids from the cytosol into the mitochondria, where a-oxidation and adenosine triphosphate (ATP) synthesis take place. Meldonium inhibits g-butyrobetaine hydroxylase and fatty acid transportation by L-carnitine, overall reducing L-carnitine levels in tissue and plasma. The reduction of L-carnitine causes energy synthesis to shift from highly oxygen consuming fatty acid oxidation, to increased glucose metabolism. Aerobic glucose oxidation is more efficient, consuming far less oxygen, and increases the effectiveness of ATP generation. It also appears to increase glucose uptake leading to speculation of a role in the management of diabetes mellitus.
Meldonium protects mitochondria from overload of free fatty acid (FFA) through reduction of longchain acylcarnitines, increasing mitochondrial FFA utilisation and the redirection of FFA metabolism from the mitochondria to the peroxisomes. In ischaemic conditions, meldonium appears to restore the balance between cellular oxygen supply and demand, and prevents impairment of ATP transport"

 

[pattismith]

@Hd-x

did you notice there is a link between PVC and your heart rate?
I noticed that when my HR is less than 65, PVC doesn't show up, and if my HR raise upon 75, PVC show up (with a frequency about 1 per minute).

 

[Hd-x]

@pattismith
I dont get my HR that low.
It is usually 80bpm@rest - what I noticed is still a very strange connection betwenn my bpm and doing exercises.
My bpm looks fine if exercising , but after exercising my bpm "stays+sticks" for hours@100bpm and it takes several hours untill it goes down to my "normal" 80bpm.
If I eat the wrong "things" my BP + HR also goes high, but this may be MCAS related.
I am currently on Lorsatane to get the BP permanently down, this may hopefully take "some stress" from my heart.

Another thing I notice that I can "controll" some (not all) arrythmia depending on "how I breath", so I guess few problems are RSA (respiratory sinus arrhythmia) related.
RSA usually dont occour in eldery and after I studied a whole paper bunch about Sportcardiology it seems there is one exception: RSA are very common in athletes and 40% show abnormal ECGs, still PVCs are not sooo common. Certainly I am far away from beeing an athlete, but lifting weights with CFS is a heavy task (not only physically it is also mentally "hard" to stay "focused" with the "Brain fogging") - so it is not any compareable how I was doing in past where I was healthy - and, who knows how the heart (or CNS) adepts doing sports with CFS?
The Sportcardiologists paper also mentioned that arrythmia are going worster if people suddenly stop doing sports, (they recommend to go "slowly off", otherwise it can take up to several months untill the arrythmia slowly fade away)
However with the exception off just 2 short BTN Press attemps - I had at last 6weeks not touched any barbell, and the arrythmia are not gone, but are meanwhile going weekly a little bit better & better.

I am not fully sure if it is exercise related - but obvisously it is (or CNS related). What i will try next to taper before + after exercising with a Benzo to rule out a CNS related problem because off doing sports.
If it would not be CNS related, it will getting more difficult because unfortunalty most anti arrythmia drugs can itself led to dangerous arrythmia.
So trying such drugs without knowing for sure, whats going on, sounds not like the best idea & deal in town.

A somewhat different novel drug is Ivabradine, because it is a Funny-Channel (If-Inhibitor) that just reduces the HR and it didnt have any rebound/Jojo-effect like ß-blockers, Calcium-Channelblockers or so, nor does it cause dangerous arrythmia as so long you dont go to low with the bpm under Ivabradine.
So I am considering to check out what happens under Ivabradine.

 

[pattismith]

@pattismith
I dont get my HR that low.
It is usually 80bpm@rest - what I noticed is still a very strange connection betwenn my bpm and doing exercises.
My bpm looks fine if exercising , but after exercising my bpm "stays+sticks" for hours@100bpm and it takes several hours untill it goes down to my "normal" 80bpm.
If I eat the wrong "things" my BP + HR also goes high, but this may be MCAS related.
I am currently on Lorsatane to get the BP permanently down, this may hopefully take "some stress" from my heart.

Another thing I notice that I can "controll" some (not all) arrythmia depending on "how I breath", so I guess few problems are RSA (respiratory sinus arrhythmia) related.
…….

A somewhat different novel drug is Ivabradine, because it is a Funny-Channel (If-Inhibitor) that just reduces the HR and it didnt have any rebound/Jojo-effect like ß-blockers, Calcium-Channelblockers or so, nor does it cause dangerous arrythmia as so long you dont go to low with the bpm under Ivabradine.
So I am considering to check out what happens under Ivabradine.

I don't have experience with Losartan but your HR is still high.
I experienced high HR above 80 when I was hyperthyroid. This was the time when I became aware of my arrhythmia.
(Respiration often have effects on arrhythmia as it goes with changes on pressure on heart with autonomic response)
I don't mean you are hyperthyroid, but you may have cardiovascular neuropathy, which can happen with parasympathetic (vagal) impairment (again SFN is the main causal process).
It is well known in diabetic people:
https://www.ahajournals.org/doi/full/10.1161/circulationaha.106.634949

I had experience with low dose Ivabradine when I was hyperthyroid, it was a very good experience. I could tolerate it much better than beta-blockers (could not tolerate them at all). Ivabradine was very efficient for me and a game changer, and had excellent effect on my pain! Many CFS patients had good experience with it and you will find reports on PR about it.
I had to stop it when my HR went lower.
I checked if Ivabradine is good for PVC but can't find any evidence it's doing any positive effect on it.

 

[Hd-x]

I checked if Ivabradine is good for PVC but can't find any evidence it's doing any positive effect on it.

There is this single case report:
https://bjcardio.co.uk/2019/01/sign...cs-with-ivabradine-in-dilated-cardiomyopathy/

I cant translate what DOB-induced VPC (aka. PVC?) are (my english is not that good enough),
interestingly both links are the same study with different conclusions:
https://www.ncbi.nlm.nih.gov/pubmed/28541596
http://www.onlinejacc.org/content/62/18_Supplement_2/C106.2
In the NCBI link ---> the autors claim it reduces VPC , whereas the same autors say on the Onlinejaac link the opposite. However so, if we compare the VPC numbers in the table, we can see Ivabradine reduces VPC to some degreee - it is just not really that effective like the ß-blocker.

I had experience with low dose Ivabradine when I was hyperthyroid, it was a very good experience. I could tolerate it much better than beta-blockers (could not tolerate them at all). Ivabradine was very efficient for me and a game changer, and had excellent effect on my pain! Many CFS patients had good experience with it and you will find reports on PR about it.
I had to stop it when my HR went lower.

This sound really great and very encouraging.
How much mg did you take in past and what was yours BPM when you decide to stop using Ivabradine?

It is well known in diabetic people:

My morning glucose is high, but my HbA1c is 0.2 under max allowed ref range that justifies to diagnose Diabetes II.
Ultrasonic showed a so called "Pancreaslipomatosis" (ICD10-Code: E88.2)
I wasnt able to find anything about this, but I guess it may have some influence that my glucose levels are bad and that the insuline pathway didnt work that well in my case.

 

[pattismith]

I stopped Ivabradine when my HR went back under 80/mn

My morning glucose is high, but my HbA1c is 0.2 under max allowed ref range that justifies to diagnose Diabetes II.
Ultrasonic showed a so called "Pancreaslipomatosis" (ICD10-Code: E88.2)
I wasnt able to find anything about this, but I guess it may have some influence that my glucose levels are bad and that the insuline pathway didnt work that well in my case.

I don't know much about Diabete, it's just the Diabetic peripheral neuropathy and CAN that I was interesting in, because they are well studyied. By the way, you can find these neuropathies in Sjogren or Lupus as well or on their own, it's not specific to diabete.

 

[Hd-x]

@pattismith

but you may have cardiovascular neuropathy, which can happen with parasympathetic (vagal) impairment (again SFN is the main causal process).
It is well known in diabetic people:
https://www.ahajournals.org/doi/full/10.1161/circulationaha.106.634949

Thank you for this very interesting link, as far I am able to translate it, the article links CAN with Diabetes.
As far as I understand you that you mean SNF could also be a CAN main cause?
If so, do you know any article/link about the FSN+CAN connection that I could show my Dr?

 

[pattismith]

@pattismith

Thank you for this very interesting link, as far I am able to translate it, the article links CAN with Diabetes.
As far as I understand you that you mean SNF could also be a CAN main cause?
If so, do you know any article/link about the FSN+CAN connection that I could show my Dr?

Not sure if your cardiologist will do autonomic testing nor SFN testing, maybe a neurologist specialist of Autonomic Nervous System would? Dysautonomia International gives some good specialists name around the world, which country are you from?
CAN is not specific to Diabete, nor SFN, but they are both well known in Diabete.
Here I posted an article making the link between CAN and SFN whatever the underlying disease:

https://forums.phoenixrising.me/threads/cardiovascular-autonomic-neuropathy-can.79812/#post-2269726

In any book about SFN you will find diseases associated to SFN (in some of these disease, the neuropathy involves small but also big nerve fibers)

https://www.ildcare.nl/wp-content/uploads/2019/10/Chapter-6-def-v2-MV.pdf

 

[Hd-x]

@pattismith
Thx for the linked tread, as far as I understand the links provide information how to diagnose CAN or did I miss a SFN/CAN link?
Yesterday I got a 24h ECG, was going shopping, did a little bit homework and after doings so I was running up stairs, got some really nasty PVC from doing so and feeled exhausted. So, I did some hours pacing and after pacing I went to barbells for few heavy lifts@low Reps that ramped up my HR a lot, curiously I didnt got any single PVC by doing so. 1hour later few PVCs came back, but faded away after a while for the whole day. Thats just ridiculous if heavy lifts didnt trigger PVC, but still running few stairs immediately triggered it.
As far as I remember the arrythmia hasssle started after I tried to switch over to more aerobic training routes, obviously with CFS no longer "born" to do any endurance tasks ??

However so, my theory by doing different demanding things was that it may give a better ECG overview what the heart is doing instead off just undergoing a short resistance ECG on a bike.
I hope that I get a full ECG report and that the electrode didnt lost contact because off all the movements + sweating.
Tomorrow I will start to supp Q10 + Taurine, usually it shouldnt happen, but in theory ß-Alanine can deplete Taurine levels and as far I know low Taurine can also led to arrythmia.

 

[Judee]

@Hd-x, I'm not sure how we stumbled upon taurine for my mom's arrythmias but just a pinch helps very quickly. Went searching for articles regarding taurine and arrythmias and found this one (there are others but they are more difficult to read):

https://nutritionreview.org/2013/04/drugfree-alternatives-arrhythmia/

For instance it says that:

Arrhythmias characteristic of acute myocardial ischemia may be due to loss of intracellular taurine. Researchers found that intravenous administration of taurine prevented arrhythmias caused by digitalis. Taurine also inhibited the drop in potassium levels inside heart cells that can cause electrical instability and arrhythmias.

That last sentence may also show why @Mary 's use of potassium is so helpful to her.

Just a note that both taurine and potassium can lower blood pressure so if you already have low blood pressure that could pose a problem. Also please clear it with your doctor before you try.

 

[pattismith]

@pattismith
Thx for the linked tread, as far as I understand the links provide information how to diagnose CAN or did I miss a SFN/CAN link?
.

The article makes the link between SFN/CAN yes: (keep in mind CAN is diagnosed with Cardiovascular Reflex Tests : CARTS)

Quantitative Scale for Grading of Cardiovascular Autonomic Reflex Tests and Small Fibers from Skin Biopsies (QASAT)
2015
Peter Novak* Department of Neurology, University of Massachusetts Medical School, University Campus, S4-810D, 55 Lake Avenue North Worcester, MA 01655, USA

Abstract

Background:
Orthostatic intolerance including dizziness and syncope is common and may reflect autonomic dysfunction.
Cardiovascular reflex tests (deep breathing, Valsalva maneuver and tilt test) are established diagnostic methods for evaluation of orthostatic and autonomic symptoms.
Small fiber neuropathy, a frequent underlying mechanism, is evaluated by the quantitative sudomotor axonal reflex test (QSART) and skin biopsies. A comprehensive quantitative scale to grade abnormalities in these tests is lacking.

Methods:
This study defines the QASAT - Quantitative scale for grading of cardiovascular reflex tests using heart rate, blood pressure, Transcranial Doppler, QSART and small fibers (intrapidermal sensory and sweat gland) densities from skin biopsies. The QASAT has three main categories: cardiovascular, cerebral blood flow (includes cerebral autoregulation/vasoreactivity score) and small fiber neuropathy. QASAT was validated in 612 participants with diabetes mellitus (92), Parkinson’s disease (88), multiple system atrophy (23) and other diagnoses (409). The QASAT was compared with the Composite Autonomic Severity Score using ANOVA, correlations and sensitivity/specificity analysis.

Results:
Scores of heart rate variability from deep breathing, orthostatic hypotension, orthostatic cerebral blood flow, sensory and sweat gland small fiber densities were disease specific (p<0.0001) and were correlated with the severity of autonomic failure (r=0.84, p<0.0001).
Autonomic, sensory and cerebral blood flow abnormalities coexist and are correlated. Initial response to slow and fast tilt, baroreflex gain, QT interval, catecholamines and spectral analysis of the heart rate failed to correlate with severity of autonomic failure and therefore were not included in QASAT.

Conclusion: QASAT is an objective and validated instrument for grading of dysautonomia, associated small fiber neuropathy and cerebral blood flow. QASAT quantifies both below (bradycardia, supine/orthostatic hypotension) and above (tachycardia, supine/orthostatic hypertension) normal values. Cardiovascular tests are enhanced by scoring the cerebral hypoperfusion which underlies orthostatic symptoms. Inclusion of epidermal and sweat gland fiber density scoring improves lesion localization.

RESULTS

Data from 612 patients were included in the analysis. The following diagnostic groups were represented: diabetes mellitus (n,age ± sd,f/m) (92, 61.6 ± 12.6, 42/50), Parkinson disease (88, 70.9 ± 10.8,36/52) and multiple system atrophy (23, 63.8 ± 11.4,10/13).
The remaining patients (n=409) represent a heterogenous group with history of other disorders (typically with n<15) than mentioned above; these disorders include migraine, hypertension, multiple sclerosis, atypical parkinsonism, coronary artery disease, unexplained dizziness, chronic fatigue syndrome and others.

This study provides strong evidence that sensory and autonomic abnormalities coexist.

Both sensory and sweat gland fiber densities were reduced in small fiber neuropathies.
The reduction of both types of fibers was disease dependent, being highest in diabetes followed by Parkinson disease.
Furthermore, the fibers reduction was proportional to the severity of autonomic failure.

Therefore inclusion of epidermal sensory and sweat gland fiber density evaluation enables more detailed grading of the severity of small fiber neuropathies and also helps to localize the lesion.





https://www.omicsonline.org/open-ac...iopsies-qasat-2329-6895-1000226.php?aid=50516

 

[Hd-x]

I'm not sure how we stumbled upon taurine for my mom's arrythmias but just a pinch helps very quickly. Went searching for articles regarding taurine and arrythmias and found this one (there are others but they are more difficult to read):

I am supplementing ß-alanine and there were some mice modells, but it didnt say much:
https://link.springer.com/article/10.1007/s00726-005-0282-x
As far as I know there where never any human study that confirmed Taurine depletation by ß-alanine supplementation, but since CFS disturbs the metabolism in many strange ways,
I should at last check out if the arrythmia improve under Taurine supplementation. Low BP is no problem, i am more on the high BP side.

 

[Marylib]

I just discovered this thread because of looking up the study involving meldonium - I hadn't known what it was either. I developed POTS a few years ago and was pretty much bedbound for a few years. Eventually I discovered my POTS doc, who is a nephrologist The only meds he gave me to try that I can tolerate are ivabradine and pyridostigmine (mestinon). IV saline too, but waiting on a referral to a cardiologist where I am living now to get going on that again - I got a chest port implanted for access. He likes a regular EKG to check the QT interval. I also take verapamil (from the ME specialist) for better blood flow. These three meds are great in my case. Adding the verapamil made a big difference for me. When I had tried it 15 years ago, I didn't notice the difference, but I didn't have POTS then, just the usual orthostatic intolerance. POTS doc says not to worry about the kidneys in any way in terms of the verapamil, which I need to tell the ME specialist, since she has been giving it for years as something for people to try, with supervision of course. The Australians are using it, too, and it's extra interesting since the studies have come out about the calcium ion channel defect, since verapamil increases the inter-cellular calcium.

 

[Hd-x]

@pattismith
I got today my 24/7 ECG results via phone,
they said 1095 Extra beat systoles/day, but still few off them PVCs, the majority SVTs.
This opens perhaps few other treatment options besides Ivabradine if it would be really primary SVTs.
(I am waiting for the printed ECG paper)

In the meantime I continued supping Taurine + mg + potassium + MSP
This reduces the extra beats, I also tried different Benzos and nearly all failure, interestingly still Klonopin was curiously able to reduce at a low dose further some extra beats, so it seems few off them might be CNS related at last.
Yesterday I had with Taurine + mg + potassium + MSP + LD Klonopin no extra beats.
Today with the same combination few came back, so dont know what to think about and was starting to look for more treatments options for the case if the above combination perhaps somedays didnt work stable anymore .

@Marylib
thank you for sharing yours experience with Verapramil.
My answer took some time, because I was doing some research about Verapramil + MCAS, since it seems to be a DAO blocker.
So I was looking further if there are some "softer" calciumchannel blockers availible.
Since I have CFS + MCAS, I usually try to find drugs that adresses more then 1 symptom - doing so reduces the amount off necessary drugs and after some good experience with Meldonium,
I came up to the conclusion to give another Russian drug a try: Phenkarol
It is an older H1 antihistaminika with some "soft" calcium channel features and thus it can reduce SVTs
Russian studies claim it has a very good safety profile and that the drug itself cant cause dangerous arrythmia (like sometimes other anti arrythmia drugs do)

Some quotes:
The drug was shown to possess the pronounced antiarrhythmic and protective properties on the models of calcium-chloride-, adrenaline- and strophanthine-induced arrhythmias and to exert no influence on aconitine-induced arrhythmia. Phencarol was demonstrated to have no cardiodepressive effect, without significant QT prolongation, or sinus node depression. Although, the H(1)-histamine receptor blocker is less potent than amiodarone, much better safety profile of Phenkarol is advantageous, especially in children. Phenkarol was mostly beneficial in children with supraventricular PB

Since I need to take Antihistaminika because off MCAS and if this stuff also has some antiarrhythmic features, it might be worth a try, if it works, I kill two Fly with one stone