Hi again, Charlotte -
Cliche-> established truth-> official dogma. You'll hear the cliche 'AF begets AF', generally interpreted to mean that chaotic fibrillations alone cause pro-arrhythmic changes (remodeling) to the atria, according to which AF will inevitably become more frequent, perhaps even permanent. Rarely mentioned, if ever, is the likelihood that for the majority of cases pro-arrhythmic atrial remodeling preceded AF, and had for years been progressing slowly and silently setting the stage for AF, then continuing to worsen because of increasing fibrosis (independent of fibrillations) due to uncorrected magnesium deficiency. Amongst AFers there is near 100% certainty of long-standing intracellular deficiency of magnesium with pro-fibrotic, pro-arrhythmic consequences. These studies of Dr. K. Shivakumar, MD, et al make the point (there are numerous supporting studies):
==========
Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart. (http://www.ncbi.nlm.nih.gov/pubmed/11585706)
Kumar BP, Shivakumar K, Kartha CC.
Int J Biochem Cell Biol. 1997 Jan; 29(1):129-34.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis... Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of
==========
Model of cardiovascular injury in magnesium deficiency. (http://www.ncbi.nlm.nih.gov/pubmed/11133266)
Shivakumar K.
Med Hypotheses. 2001 Jan; 56(1):110-3.
Magnesium deficiency is known to produce cardiovascular lesions... This article cites evidence in support of a hypothesis that a fall in serum magnesium levels may trigger a temporal sequence of events involving vasoconstriction, hemodynamic alterations and vascular endothelial injury to produce pro-inflammatory, pro-oxidant and pro-fibrogenic effects, resulting in initial perivascular myocardial fibrosis which, in turn, would cause myocardial damage and replacement fibrosis.
==========
Superoxide-mediated activation of cardiac fibroblasts by serum factors in hypomagnesemia (http://www.ncbi.nlm.nih.gov/pubmed/11585706)
C. Kumaran and K. Shivakumar
Free Radical Biology and Medicine, Vol. 31(7) (2001) pp. 882-886
Magnesium deficiency is known to produce myocardial fibrosis in different animal models, but the underlying mechanisms are unclear. However, circulating levels of pro-oxidant and mitogenic factors are reported to be elevated in a rodent model of acute magnesium deficiency, suggesting a role for humoral factors in the pathogenesis of the cardiovascular lesions. ... The findings are consistent with the postulation that serum factors may activate cardiac fibroblasts via a superoxide-mediated mechanism and contribute to the fibrogenic response in the heart in magnesium deficiency.
==========
Pro-fibrogenic effects of magnesium deficiency in the cardiovascular system. (http://www.ncbi.nlm.nih.gov/pubmed/12635886)
Shivakumar K.
Magnes Res. 2002 Dec; 15(3-4):307-15.
Magnesium deficiency is known to produce cardiovascular injury. A large body of experimental evidence supports the postulation that an immuno-inflammatory reaction and increased oxidative stress may damage the myocardium and vasculature in magnesium deficiency. Reparative/reactive fibrosis in response to the injury has, however, received little attention. Recent evidence from a rodent model of acute magnesium deficiency suggests that humoral factors may activate cardiac fibroblasts by a free radical-mediated mechanism and contribute to cardiac fibrogenesis. A similar mechanism may also promote cellular hyperplasia and increased matrix synthesis in the vasculature.
==========
Clearly, termination of my 7 year AF stint came about by gaining magnesium
sufficiency along with sufficient "magnesium-dependent fibrinolytic enzymes" for removal of the scar tissue (fibrosis) that had developed over years of magnesium deficiency. From
The Magnesium Factor by Dr.s Seelig and Rosanoff (2003):
"Among the enzymes that have been studied intensively, over 350 need magnesium, directly, to do their work properly... indirectly it is involved in thousands of others."
The bottom line? You can assume, with near 100% certainty, that you are deficient in magnesium, and probably have been for a long time, ultimately resulting in AF (a possible 'canary in the coal mine' warning of worse things to come?). Your #1 priority is to create magnesium sufficiency. Magnesium is that important.
Some years ago Jackie authored the important CR Session 24,
Cardiac Fibrotic Remodeling (http://www.afibbers.org/conference/session24.pdf)
inevitably become more frequent, perhaps persistent, even permanent. Cliche-> revealed truth-> official dogma. Rarely mentioned is the likelihood that in the vast majority of cases pro-arrhythmic atrial remodeling was progressing slowly and silently for years prior to the first AF event, setting the stage for AF, and continuing to worsen because of increasing fibrosis (independent of fibrillation effects). There is near 100% certainty of long-standing intracellular deficiency of magnesium amongst AFers along with its pro-fibrotic, pro-arrhythmic consequences (over 80% of the general population is known to be deficient). These studies of K. Shivakumar, MD et al make the point (there are many other supporting studies):
==========
Magnesium deficiency-related changes in lipid peroxidation and collagen metabolism in vivo in rat heart.
Kumar BP, Shivakumar K, Kartha CC.
Int J Biochem Cell Biol. 1997 Jan; 29(1):129-34.
Magnesium deficiency is known to produce a cardiomyopathy, characterised by myocardial necrosis and fibrosis... Thus, the present study provides evidence of increased lipid peroxidation and net deposition of collagen in the myocardium in response to dietary deficiency of magnesium.
[
www.ncbi.nlm.nih.gov]
==========
Model of cardiovascular injury in magnesium deficiency.
Shivakumar K.
Med Hypotheses. 2001 Jan; 56(1):110-3.
Magnesium deficiency is known to produce cardiovascular lesions... This article cites evidence in support of a hypothesis that a fall in serum magnesium levels may trigger a temporal sequence of events involving vasoconstriction, hemodynamic alterations and vascular endothelial injury to produce pro-inflammatory, pro-oxidant and pro-fibrogenic effects, resulting in initial perivascular myocardial fibrosis which, in turn, would cause myocardial damage and replacement fibrosis.
[
www.ncbi.nlm.nih.gov]
==========
Superoxide-mediated activation of cardiac fibroblasts by serum factors in hypomagnesemia
C. Kumaran and K. Shivakumar
Free Radical Biology and Medicine, Vol. 31(7) (2001) pp. 882-886
Magnesium deficiency is known to produce myocardial fibrosis in different animal models, but the underlying mechanisms are unclear. However, circulating levels of pro-oxidant and mitogenic factors are reported to be elevated in a rodent model of acute magnesium deficiency, suggesting a role for humoral factors in the pathogenesis of the cardiovascular lesions. ... The findings are consistent with the postulation that serum factors may activate cardiac fibroblasts via a superoxide-mediated mechanism and contribute to the fibrogenic response in the heart in magnesium deficiency.
[
www.ncbi.nlm.nih.gov]
==========
Pro-fibrogenic effects of magnesium deficiency in the cardiovascular system.
Shivakumar K.
Magnes Res. 2002 Dec; 15(3-4):307-15.
Magnesium deficiency is known to produce cardiovascular injury. A large body of experimental evidence supports the postulation that an immuno-inflammatory reaction and increased oxidative stress may damage the myocardium and vasculature in magnesium deficiency. Reparative/reactive fibrosis in response to the injury has, however, received little attention. Recent evidence from a rodent model of acute magnesium deficiency suggests that humoral factors may activate cardiac fibroblasts by a free radical-mediated mechanism and contribute to cardiac fibrogenesis. A similar mechanism may also promote cellular hyperplasia and increased matrix synthesis in the vasculature.
[
www.ncbi.nlm.nih.gov]
==========
Clearly, termination of my 7 year AF stint came about by gaining magnesium
sufficiency along with sufficient "magnesium-dependent fibrinolytic enzymes" to remove the scar tissue (fibrosis) accumulated over years of magnesium deficiency. From
The Magnesium Factor by Dr.s Seelig and Rosanoff (2003)*:
"Among the enzymes that have been studied intensively, over 350 need magnesium, directly, to do their work properly... indirectly it is involved in thousands of others."
The bottom line: Since you have come down with a case of the AFs you can assume, with near 100% certainty, that you are deficient in magnesium, and likely have been for a long time, ultimately resulting in AF (it's the canary in the coal mine warning of worse things). Your #1 priority is to develop magnesium sufficiency. Magnesium is that important.
Some years ago Jackie authored the important CR Session 24,
Cardiac Fibrotic Remodeling (http://www.afibbers.org/conference/session24.pdf)
Be well!
Erling
*[
www.amazon.com]