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