Hi Guys

I'm wondering if anyone can give me some info or has had any personal experience with heart problems.

On Monday I suddenly got intense chest pains that didn't die down for almost ten minutes. It wasn't like any lung problem I've had, I felt it was a heart problem. For the rest of the day, I felt my heart palpatate like crazy and kept getting flushed in the face. My husband even noticed my skin went all red and blotchy when I got flushed.

At the hospital a few hours later, my heart rate was at 120. Normally I have a very low heart rate and low blood pressure. They did an EKG which was ok, blood tests showed no blood clot in my heart or lung and a chest x-ray was clear.

The Dr that saw me had no idea what RSD is, so I couldn't really ask them if it may be linked to my rsd.

I went to my regular doctor on tuesday morning, who noted my heart rate was still over 100, but couldn't work out why. I was meant to get a holter monitor on for 24 hours but all the places nearby have them booked out, the earliest I can get one is next THursday, which is no help!

I'm still getting chest tightness today and my heart has been irregular and pretty jumpy still. I can feel it racing.

So I'm wondering, seeing as the tests for other causes were clear, if this could be caused in some way by my RSD? My rsd affects my central nervous system now and other internal organs. And I know heart rate etc come under the autonomic nervous system.

Has anyone else experienced anything similar? Should I be worried that a heart attack may be around the corner? I know I'm only 31, and that's why the emergency doctors weren't too worried, but rsd puts us in a whole other category and age is irrelevant. What should we do from here, seeing as it's been three days since the sudden chest pain happened and my heart is still not back to normal?

Any info or advice in this area would be great.

x Kate

Dear Kate -

Hi'ya. And sorry to meet up again under scary circumstances. This is however a subject I take quite seriously, having had a "nontransmural" (meaning the heart didn't stop) myocardial infarction three years into my RSD: a 100% occlusion of the mid Left Anterior Descending Artery. I survived only because I was in relatively decent shape (RSD notwithstanding) and had good "collateral blood flow" across the heart. And by the way, my EKG was normal at the time too.

That aside, it sounds like you are experiencing an arrhythmia, which I had once secondary to medication a year before I got RSD. I know that in Australia there is a state run health system, but is there anyway you could possibly be seen by a cardiologist, without waiting over a week for a halter monitor? Ideally, you would want to see an electo-cardologist, but I realize that may be asking to much.

Could it be related to RSD (which was understood not that long ago to be essentially a disorder of the sympathetic nervous system)? Check these out:

New aspects for the treatment of cardiac diseases based on the diversity of functional controls on cardiac muscles: the regulatory mechanisms of cardiac innervation and their critical roles in cardiac performance, Ieda M, Fukuda K, J Pharmacol Sci. 2009 Mar;109(3):348-53. Epub 2009 Mar 7, free full text at http://www.jstage.jst.go.jp/article/jphs/109/3/348/_pdf

Department of Regenerative Medicine and Advanced Cardiac Therapeutics, Keio University School of Medicine, Japan.

The heart is abundantly innervated, and the nervous system precisely controls the function of this organ. The density of cardiac innervation is altered in diseased hearts, which can lead to unbalanced neural activation and lethal arrhythmia. For example, diabetic sensory neuropathy causes silent myocardial ischemia, characterized by loss of pain perception during myocardial ischemia, and it is a major cause of sudden cardiac death in diabetes mellitus. Despite the clinical importance of cardiac innervation, the mechanisms underlying the control of this process remain poorly understood. We demonstrate that cardiac innervation is determined by the balance between neural chemoattractants and chemorepellents within the heart. Nerve growth factor (NGF), a potent chemoattractant, is synthesized abundantly by cardiomyocytes, and is induced by the upregulation of endothelin-1 during development. By comparison, the neural chemorepellent Sema3a is expressed at high levels in the subendocardium in the early stage of embryogenesis and is downregulated as development progresses, leading to epicardial-to-endocardial transmural sympathetic innervation patterning. We also show that the downregulation of cardiac NGF is a cause of diabetic neuropathy and that NGF supplementation prevents silent myocardial ischemia in diabetes mellitus. Both Sema3a-targeted and Sema3a-overexpressing mice display sudden cardiac death or lethal arrhythmias due to disruption of innervation patterning. The present review focuses on the regulatory mechanisms controlling cardiac innervation and the critical roles of these processes in cardiac performance.

PMID: 19270423 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...um&log$=freejr

OR THIS:

Neuropeptides in neurogenic disorders of the cardiovascular control, Szczepańska-Sadowska E, J Physiol Pharmacol. 2006 Nov;57 Suppl 11:31-53, free full text at http://www.jpp.krakow.pl/journal/arc...11_article.pdf.

Department of Experimental and Clinical Physiology, Medical University of Warsaw, Warsaw, Poland. eszs@amwaw.edu.pl

Growing number of studies reveal that the brain neural network plays significant role in the short-term and long-term regulation of the cardiovascular functions. The neurons involved in the complex neurogenic control of the cardiovascular system use classical neurotransmitters and nonconventional mediators such as peptides (angiotensin II, vasopressin, natriuretic peptides, endothelins, opioids, cytokines), steroids, ouabain-like factors and gaseous compounds. Among them the neuropeptides form a group of substances arising significant interest. Thanks to wide distribution of peptidergic neurons in the central nervous system, location of peptide receptors on neurons and glial cells, versatile but frequently overlapping mechanisms of activation of the intracellular processes the neuropeptides play significant role in short-term and long-term regulation of excitability and remodeling of the neurons. In several instances they modulate effects of the classical transmitting systems involved in regulation blood pressure, heart rate, water-electrolyte balance, metabolism, stress, pain, mood and memory. Prolonged activation or inhibition of specific neuropeptide pathways frequently results in long-lasting disorders of several regulatory systems. In this review this is exemplified by overactivity of angiotensin II, vasopressin and cytokines in the brain during hypertension, heart failure and stress. Multifarious actions of angiotensin II and vasopressin, and their mutual interaction with cytokines make of these neuropeptides excellent candidates for the compounds responsible for long-term resetting of the central cardiovascular control, and forming a link between the cardiovascular diseases, stress and mood disorders.

PMID: 17244937 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...log$=freejrpmc

And speaking of neuropeptides and RSD/CRPS, we lots of this sort of stuff:

Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS), Birklein F, Schmelz M, Neurosci Lett. 2008 Jun 6;437(3):199-202. Epub 2008 Mar 30, free full text at http://www.rsds.org/2/library/articl...in_Schmelz.pdf

Department of Neurology, Pain Research Unit, University of Mainz, Langenbeckstrasse 1, 55101 Mainz, Germany. birklein@neurologie.klinik.uni-mainz.de <birklein@neurologie.klinik.uni-mainz.de>

This review explains symptoms and nature of neuropeptide signaling and its importance for clinical symptoms of CRPS. Neurogenic inflammation regularly accompanies excitation of primary afferent nociceptors. It has two major components-plasma extravasation and vasodilatation. The most important mediators are the calcitonin gene-related peptide (CGRP) and substance P (SP). After peripheral trauma immune reaction (e.g. cytokines) and the attempts of the tissue to regenerate (e.g. growth factors) sensitize nociceptors and amplify neurogenic inflammation. This cascade of events has been demonstrated in rat models of CRPS. Clinical findings in these animals strongly resemble clinical findings in CRPS, and can be prevented by anti-cytokine and anti-neuropeptide treatment. In CRPS patients, there is meanwhile also plenty of evidence that neurogenic inflammation contributes to clinical presentation. Increased cytokine production was demonstrated, as well as facilitated neurogenic inflammation. Very recently even "non-inflammatory" signs of CRPS (hyperhidrosis, cold skin) have been linked to neuropeptide signaling. Surprisingly, there was even moderately increased neurogenic inflammation in unaffected body regions. This favors the possibility that CRPS patients share genetic similarities. The future search for genetic commonalities will help us to further unravel the "mystery" CRPS.

PMID: 18423863 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/1...ubmed_RVDocSum

I would print out as much of this as you want - certainly the three downloadable articles - and get them to your doctor's attention at once. Failing that, the next time you have any discomfort, I would get yourself back to (the) hospital with the articles in your teeth!

Now, you've got me up past 3:30 my time, all concerned, and I still have to get the kitchen ready for the morning.

take good care,
Mike

Hi Kate,

RSD does affect the organs. For me it is my heart and lungs. When my heart started beating too fast the first time I thought it was a heart attack. I went to the ER and all test were normal. I went to a cardiologist and he put me on Atenole. My heart rate will go up when my pain if flaired. My cardiologist told me that a very small percentage of open heart patients will develope RSD.
Make an appointment with a cardiologist. If he/she doesn't know about RSD have them visit the RSDS.org web site or print some information from the site and take it with you.
Good luck and take care,
Sherrie

Funny that you should bring this up. I've noticed frequent palpitations (PVC's - "skipped" beats) in the last two months. I don't remember ever having these before, and have been digging for information to see if they can be caused by my meds (gabapentin & duloxetine). The little info I've been able to find suggest that both meds can cause arrhythmias in a small percentage of patients. The general info about PVC's suggest that they usually aren't a concern unless accompanied by dizziness and/or lightheadedness. However, I'm a bit concerned since it's a new thing for me.

I'm keeping track of their frequency (which turns out to be almost all the time) and will talk to my doc about them at the next appointment.

Yes, Unfortunately I was flushed real bad for the last off and on again for 5 months or so. Taking Atlenelol for high blood pressure 75 mg cymbalta 120 mg for Rsd nerve pain and Hydrocodone.. Took off workone day because didn't feel well and had 220/110 bp. Doc gave me a new bp to try benicar hct and so I took it and alternated the altenelol. Atenelol has controlled my bp for 12 to 15 years.. Until diagnosed with Rsd in OCt 2008/Now you make me wonder if more of the same will happen to me.?? Doc took me off cymbalta slwoly because it is know yo cause irradict changes in bp in a short time>> Please email me and we will talk more when I am not at work.. Thanks sunshine

I get "strange pains" on my left chest/center.
For years now, and only occasionally. But, more so recently..
I write this off to cramping, of TOS or something like that, something going on that "I don't know".
But, lately with the stress I've been under, I'm starting to wonder if it's got something to do with my heart.
I guess the next time I feel it, I'll try to keep the phone nearby...
(I've got two left side molars bottom, that are definitely infected.)
(It's not the "elephant on the chest" feeling that I've heard of, but just cramping over my heart.)
Who knows??
Tuff to take care of if you don't drive.

One day here, next day gone.
Problem solved.
(Now WHOA! don't take that as if I'm taking it lightly. I've got a LOT to live for, I'm going to speak to my doctor this week about it!) That's just my sense of humor, coming from a family of sicko polish folks who grew up in Bridesburg, Phila. PA. The "Hot Spot" for cancer, due to Rohm and Haas, and company...
I've lost an aunt or uncle to everything from Lou Gehrig's to Marily Monroe's....


love to all,

Pete

Thank you SO SO much for the replies. And to you, Mike, for staying up late to answer my questions!

I was kinda hoping it wasn't RSD related (and it still may not be, we have more test results to come yet) and that it was just a one-off- that way it doesn't become a daily/regular thing and ANOTHER part of me my RSD has taken over! But that would be too easy, right? And an RSD life is never easy!

What you've all written and the article links make sense.

It's now Thursday morning here, and it all started on Monday morning. My heart beat feels a bit more normal at the moment but my chest is very tight. This problem is definitely not going away in a hurry. I'm going to ring my pain specialist today and try and get an appt with him, to talk about what we can do, if it is my RSD causing this. I think I will also make an appt with a cardiologist (yep, we can do that for free here), but I'll wait for the other blood test results to come back first.

Thanks heaps guys. If anyone else would like to add anything, I'd appreciate it!

x Kate

I have heart problems...I was in the 1% of the patients who the cathader ablation didnt work on...an EP study...8 hours and they gave up. I have PVC's PAC's and POTS. In one holiter monitor test I had over 10 thousand extra beats...and I feel them all. I have tried meds but I am so medication sensitive, so I take nothing anymore. I have seen almost every heart doc in ohio...no luck. So, I feel your pain. I hope they can figure out what is causing it and get something to stop it from actin up.

Kate -

That was so nice, thank you.

I just wanted to bring to your attention that without changing the body of my post, I dropped the starred note at the end, which read as follows:

* And if anyone wants to seriously assert that chronic CRPS has nothing to do with the sympathetic nervous system, then how is one to explain edema? A condition which, according to everything I've read, is caused be the failure of the sypathetic nervous sytem to maintin the tone of the peripherical vascular system, on account of which "neurogenic vasodialation" sets in, the vessels become flaccid, and the first thing that happens is that water leaks out of the blood, causing edema, followed ultimately by the loss of some of the hemoglobin itself, causing explained brusing, especially in the most "dependant" parts of the body, i.e., the feet and ankles.

And the reason I did so was not because I believe it's wrong, but because there is an alternative theory of CRPS which Prof. Anne Louise Oaklander of Harvard has been advancing for the last couple of years, that gets us to the basically the same result as does the classic model based upon a dsyfunctional of the sympathetic nervous system. Instead, she suggests that all the the symptoms of CRPS are triggered by the small fiber neuropathy she discovered. See, Evidence of focal small-fiber axonal degeneration in complex regional pain syndrome-I (reflex sympathetic dystrophy), Oaklander AL, Rissmiller JG, Gelman LB, Zheng L, Chang Y, Gott R, Pain, 2006;120:235-243, free full text at http://www.rsds.org/2/library/articl..._pain_2006.pdf and RSD/CRPS: the end of the beginning, Oaklander AL, Pain, 2008 Oct 15;139(2):239-40. Epub 2008 Sep 13, free full text at http://www.rsds.org/2/library/articl..._editorial.pdf

Dr. Oaklander's has recently restated her views in somewhat greater detail in Is reflex sympathetic dystrophy/complex regional pain syndrome type I a small-fiber neuropathy? Oaklander AL, Fields HL, Ann Neurol. 2009 Mar 18;65(6):629-638. I have a copy of it, but it's too big to post here. If anyone wants to see it drop me a PM with your email address, and I'll send it out.

Dr. Oaklander's view that small fiber neuropathy can explain all of the symptoms of CRPS were initially questioned in an editorial in the same issue of Pain in which her study appeared. Is CRPS I a neuropathic pain syndrome? Jänig W, Baron R, Pain 2006 Feb;120(3):227-9, free full text at http://www.rsds.org/2/library/articl...ology%2006.pdf

And for what it's worth, I personally have a problem with Dr. Oaklander's approach, because in her most recent article, she sets forth on all of the symptoms of CRPS her theory can explain, but fails to mention a big one that it may not: the brains of chronic CRPS patients show anatomical changes from the norm that are different for those seen in people with either chronic low back pain or fibromyalgia. See, The Brain in Chronic CRPS Pain: Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions, Geha PY, Baliki MN, Harden RN, Bauer WR, Parrish TB, Apkarian AV, Neuron, 2008;60:570-581, 574- 575, free full text at http://www.rsds.org/2/library/articl...aliki_etal.pdf Which is to say, how can observed changes in the anatomical structures of the brain simply be an adaptive response to pain (as the small fiber theory holds) if patients with different pain conditions have completely different structural changes to their brains? (And not just as to matters of degree.)

But for purposes of this thread and the questions you raised, it doesn't matter if Dr. Oaklander is right or wrong. In either event, it appears to be the same neuropeptides that would be doing the dirty work:

Neurogenic edema, another facet of CRPS, can be caused by inappropriate release of peptides contained in somatic polymodal C-fibers, including those that innervate cutaneous venules. Denervated venules lose endothelial adhesion markers, permitting plasma leakage. [Oaklander and Fields, 2009 at 633.]

And one of the authorities that is cited for this proposition is Neuropeptides, neurogenic inflammation and complex regional pain syndrome (CRPS), Birklein F, Schmelz M, Neurosci Lett. 2008 Jun 6;437(3):199-202, for which the abstract and link to the full text were provided in my response last night to your initial posting. Oddly enough, Oaklander and Field don't mention that Birklein and Schmeltz posited an entirely different mechanism for the role of neuropeptides in CRPS:

Primary afferent nociceptors [peripheral receptors for pain] release a variety of neuropeptides . . . .

* * *

Cytokines also increase the neuropeptide content of primary afferent neurons. Activation of sensitized primary afferents then causes an increased release of neuropeptides into the affected body region. Chronic release of neuropeptides might be responsible for the above mentioned CRPS symptoms [basically everything, including edema]. [pp. 199, 201.]

So with that, the circle may be complete.

Good luck with all of this, not that you'll need it, you being the ultimate trooper and all.

Mike