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Atrial Fibrillation Care: Put the Catheter (and Rx Pad) Down
Posted by jerrynmn1
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Re: Atrial Fibrillation Care: Put the Catheter (and Rx Pad) Down April 23, 2015 03:33PM |
Hi Tim - I agree with you about ablations not addressing the root cause of AF as I’ve been beating that drum for a very long time here on the forum since that was one of my initial concerns because I never, ever wanted an ablation. Being a gun-shy victim of unnecessary surgeries foist on me (the compliant, trusting, unsuspecting patient) in years prior to the onset of Afib compelled me to always learn viable options and core causes that might be remedies without resorting to drugs or surgery.
However, even though I was able to go from near permanent afib in 2003 to zero events (facilitated by natural interventions), maintained by only 50 mg of flecainide, I didn’t have enough time to wean more slowly off the drug and my insurance then was at risk of being cancelled due corporate change. So, I kept my Nov. 2003 date with Dr. Natale and I have been grateful for a mostly peaceful heart for 11 years. When we become virtually disabled from Afib for a prolonged period of time, a safe and successful ablation is a welcome change and I’ll readily be the first to acknowledge that.
However, as my response earlier in this thread and others indicates, there is a lot of investigatory work that could and should be ongoing such as studying the genetic links, dietary deficiencies and environmental influences but chances are that isn’t likely to happen given the standards of the current medical treatment model and that's truly unfortunate. Thus, Dr. Mandrola’s thinking is refreshing.
Before the 2003 ablation, I struggled for 8 years but never found much that made a difference until I was guided to this forum in 2002 (I think) and learned much more about natural interventions and focusing on the importance of optimizing magnesium and potassium that were never mentioned by the cardiologists I consulted up to that point. In fact, they still aren’t interested in testing properly for magnesium deficiency – one of the known causes of cardiac fibrosis which causes the electrical conduction interference in heart tissue.
Fibrosis is reversible over time and with intracellular magnesium repletion. This is of key importance to those of us (ablatees) because fibrosis formation is a natural body response and we need to be aware of why and what helps prevent the recurrence or face more ablations. As we age, it becomes even more critical.
The year after my ablation, it probably wasn’t by chance that I attended a Summit for Electrophysiologists on Atrial Fibrillation (2004) held here in Cleveland (Ohio) where I heard presenter David Van Wagoner, PhD discussing cardiac fibrosis and as a result, I wrote Conference Room 24 offering fundamental information that all afibbers… current or former…. need to keep foremost in their minds to help prevent recurrence.
Dr. Mandrola does us a favor to remind that the basics should be not only emphasized initially, but also never to become complacent and slack off because most likely and attributable to a genetic influence, we (afibbers) are prone to or are more susceptible to fibrosis formation than others who are less health-conscious than we, afibbers, tend to be (and we all know plenty of those examples). It likely is rooted in the inability to hang on to magnesium and probably potassium adequately and that very well could be genetic. But, that said and as we know… “we don’t have to be held hostage to our genes” because we do have control over genetic expression. (Thank you, Bruce Lipton, PhD)
Following are a few clips as samples from CR 24 as reminders about magnesium, oxidative stress damage and the fibrosis issue. If you haven’t read both CR 24 and 75, both are outstanding in relevant information that will help maintain NSR.
Happy reading and NSR to all,
Jackie
Cardiac Fibrotic Remodeling – The Role of Fibrosis in LAF
INTRODUCTION
Atrial fibrosis – is it simply the result of AF which then causes more episodes or might it be that fibrotic remodeling as a
result of aging leads to AF?
Or is the natural decline of fibrolytic enzymes at fault? Further, might we consider the oxidative stress connection? And
let’s also examine the evidence suggesting the pro-fibrotic effects of magnesium deficiency.
These questions were posed to me by Erling Waller ex-afibber (75) who thinks there may be a connection. His afib
began at 64 and then 10 years later, after some nutritional adjustments, his AF vanished. (See his story in Hans’ book.)
Erling has been a regular and prolific contributor of important information and was always generous with his time and
support to help others seeking answers. He continues to ponder the origin of AF and finds the fibrosis remodeling
connection not only intriguing but also plausible. Erling is tackling another remodeling project at the moment and asked
me to present this topic to the BB.
Interrelated factors in the “Fibrotic Remodeling Theory”
I. Fibrosis mechanism
II. Mechanisms of AF
III. Inflammation and C-reactive Protein
IV. Oxidative Stress and Nitric Oxide/Peroxynitrite production
V. Magnesium deficiency
II. MECHANISMS: ATRIAL FIBRILLATION
AF is a progressive disease; numerous lines of evidence suggest that disease progression results from cumulative
electrophysiological and structural remodeling of the atria.(5) Ongoing events coupled with fibrotic remodeling
perpetuate longer episodes. (4)
In many patients, AF begins with short episodes, typically characterized as "palpitations" (a fluttering sensation in the
chest), or "paroxysms."
Over time, there is a tendency for these episodes to become longer. Why does this happen? Once AF has been
initiated, the atria undergo a process known as "remodeling." (1)
Structural changes: (remodeling) In time, afib that persists for years, is also accompanied by significant degenerative
structural changes. (1)
• Individual muscle cells within the fibrillating atria tend to become elongated and sometimes wider. AF-induced atrial
remodeling causes both structural and electrical changes(1)
• Fibrosis: In addition, the space between individual myocytes typically becomes more fibrotic, with fatty infiltration, and
the atria is less able to contract. (1)
Electrical changes: (remodeling)
• Fibrillating atria tend to have more complicated patterns of electrical activity. This is due both to the increased fibrosis,
and to intrinsic changes in the electrical activity in the atrial myocytes. Research at the CCF has helped to characterize
the electrical remodeling process associated with long-standing AF. (1)
• The net result is that in patients with persistent AF, the atria are more able to sustain fibrillatory activity, due to the
combined effects of both structural and electrical remodeling. (1)
Atrial Electrical Remodeling (sustains afib) Refer to the video web page.
• The net result of the electrical and structural changes is that the enlarged atria are more likely to sustain fibrillatory
activity. Thus, AF can persist for a longer duration in the remodeled atria. (1)
• Calcium ions have an important role in both the electrical and contractile activity of the heart. Thus, calcium overload
is implicated as an early event in the electrical remodeling process. (1)
• Persistent AF results in further changes in protein expression, loss of myofibrillar structure, and eventually myocyte
death and replacement fibrosis. (1)
Atrial Structural Remodeling
The fibrillating atria are subjected to continuous, high rate electrical activity (with rates up to 500 per minute). This
results in impaired atrial contractility, and the initiation of structural changes. (Be sure to look at the picture of a heart
exhibiting AF-induced fibrosis and the stained fibrotic-tissue studies.) (1)
• At the macroscopic level, structural remodeling is frequently characterized by increased atrial fibrosis and fatty
infiltration, both on the endocardial surface, and between muscle bundles. (1)
• At the microscopic level, fibrosis can isolate muscle bundles. (1)
• (Key Point) It is evident that fibrosis can isolate muscle bundles and that this can alter the pathway of electrical
activation, creating a substrate that can promote the persistence of atrial fibrillation. (1)
Then... continue on to item V. Magnesium deficiency.
[www.afibbers.org]
In 2012, an outstanding elaboration on CR 24 was offered (CR 75). It’s worth going to both CR sessions and learning about cardiac fibrosis and related issues that can and do continue even after a successful ablation because fibrosis formation is part of a natural, protective process in the body and it’s good to understand that and the preventive measures that lower formation.
CONFERENCE ROOM Session 75
August 17 – December 2, 2012
Afib and Cardiac Fibrosis
Part 1 – Atrial Fibrosis and the Mechanism of Atrial Fibrillation
[www.nbi.nlm.nih.gov]
Heart Rhythm 2007 March; 4(3 Suppl): S24–S27.
Atrial Fibrosis and the Mechanisms of Atrial Fibrillation
Thomas H. Everett IV, PhD and Jeffrey E. Olgin, MD
From the Division of Cardiology and the Cardiovascular Research Institute University of California
San Franci sco, San Francisco, California
Abstract
Atrial fibrillation (AF) is so commonly associated with congestive heart failure (CHF), and CHF has been shown to be associated with atrial structural remodeling resulting in fibrosis. This atrial interstitial fibrosis has been seen in patients with CHF and animal models of pacing induced heart failure. With atrial fibrosis, conduction abnormalities result in an increase in AF vulnerability. The mechanisms of AF that is associated with CHF is still under debate as both focal and reentrant mechanisms have been observed in animal models of CHF. However, recent studies utilizing frequency domain analysis have shown that the AF within this model is characterized by discrete stable, high-frequency areas. The precise signaling processes involved in the development of atrial fibrosis are unknown. Angiotension appears to play some role, since inhibition of ACE (or AR
blunt atrial fibrosis in animal models of heart failure and decrease the incidence of AF in patients with heart failure. TGFβ1 also seems to play an important role. Mouse models that overexpress TGFβ1 have profound atrial fibrosis and atrial fibrillation (with normal ventricles. Heart failure in canine models is also produces increases in atrial TGFβ1 expression and inhibition of this prevents atrial fibrosis and the development of a substrate for atrial fibrillation. Atrial fibrosis appears to play a role in the development of a vulnerable substrate for AF, especially in the setting of CHF.
.
Erling
As has been reviewed in various posts, an abundance of science exists supporting the fact that cardiac fibrosis contributes to arrhythmia. If cardiac fibrosis forms in the ventricles, it can be lethal. The formation is probably not exclusively selective for atrial tissue so it's something not to be taken lightly. Science also supports that magnesium deficiency as well as excessive exposure to free-radical damage (ROS) is commonly associated with the genesis of fibrosis.
Fibrosis interference with electrical conduction is examined in numerous reports looking at gap-junction function and the cell-to-cell communication disrupted by the presence of fibrosis. Fibrotic interference in terms of electrical conduction (voltage) throughout the body is observed in various conditions involving the vast system of the fascia and connective tissue. Fibrotic connective tissue proliferation becomes part of the aging process. Tissues in some individuals age faster than in others.
While the etiology of fibrosis and understanding the fibrotic process, itself, is certainly important to understand, it’s also important to recognize the need for preventive measures so that fibrosis is less likely form in the first place. Preventive guidelines typically address antioxidant therapy as important but emphasis on magnesium optimization is not common advice.
While not in this review, consideration should also be given to the extensive findings relating fibrotic formations, hypertension and kidney function involvement with aldosterone or angiotension II and the malfunction of the matrix-metallo protein (MMP) system which impacts multiple organ function including the heart. Also not in this review is the impact of oxidative stress injury and resultant cardiac fibrosis in endurance athletes. Many facets of fibrosis to consider.
Recognition that cardiac fibrosis is not something to be ignored is supported in a recent study published in the American Journal of Cardiovascular Disease (2011)
Targeting cardiac fibrosis: a new frontier in antiarrhythmic therapy?
Key-point review follows. This report indicates a need to address fibrosis accumulations as a preventive treatment for arrhythmia and suggests that pharmaceuticals should be developed in addition to those currently available.
While we wait for various new pharmaceutical interventions that inhibit fibrosis formation to be formulated, tested, and receive FDA approval, it makes sense to consider the potential for preventing fibrosis formation in the first place by making sure that our intracellular stores of magnesium are optimal as verified by Exatest, evaluation of existing oxidative stress values and evaluation of critical antioxidants levels that, when missing, allow for inflammation and fibrotic accumulations. Example: deficiency of (antioxidant) glutathione allows for increased lung inflammation and resultant fibrosis.
Additionally, those of us who like to take an active-participation role in personal health management aimed at prevention can consider the use of proteolytic and fibrinolytic enzymes to help break up and dispose of fibrin deposits. Since we have the study showing that Nattokinase degrades Amyloid plaques in brain tissue of Alzheimer patients, those of us using NK and other systemic enzymes such as serrapeptase or the stronger, lumbrokinase, can take comfort in knowing that we are doing good things for our brain, heart, cardiovascular system and undoubtedly, many other organs prone to fibrosis as well if we choose to be our own health advocates and experiment.
What can be more significant than degrading brain plaque? If our hearts happen to benefit as well, it’s a win/win all around.
Jackie
(continue at the CR 75 )
However, even though I was able to go from near permanent afib in 2003 to zero events (facilitated by natural interventions), maintained by only 50 mg of flecainide, I didn’t have enough time to wean more slowly off the drug and my insurance then was at risk of being cancelled due corporate change. So, I kept my Nov. 2003 date with Dr. Natale and I have been grateful for a mostly peaceful heart for 11 years. When we become virtually disabled from Afib for a prolonged period of time, a safe and successful ablation is a welcome change and I’ll readily be the first to acknowledge that.
However, as my response earlier in this thread and others indicates, there is a lot of investigatory work that could and should be ongoing such as studying the genetic links, dietary deficiencies and environmental influences but chances are that isn’t likely to happen given the standards of the current medical treatment model and that's truly unfortunate. Thus, Dr. Mandrola’s thinking is refreshing.
Before the 2003 ablation, I struggled for 8 years but never found much that made a difference until I was guided to this forum in 2002 (I think) and learned much more about natural interventions and focusing on the importance of optimizing magnesium and potassium that were never mentioned by the cardiologists I consulted up to that point. In fact, they still aren’t interested in testing properly for magnesium deficiency – one of the known causes of cardiac fibrosis which causes the electrical conduction interference in heart tissue.
Fibrosis is reversible over time and with intracellular magnesium repletion. This is of key importance to those of us (ablatees) because fibrosis formation is a natural body response and we need to be aware of why and what helps prevent the recurrence or face more ablations. As we age, it becomes even more critical.
The year after my ablation, it probably wasn’t by chance that I attended a Summit for Electrophysiologists on Atrial Fibrillation (2004) held here in Cleveland (Ohio) where I heard presenter David Van Wagoner, PhD discussing cardiac fibrosis and as a result, I wrote Conference Room 24 offering fundamental information that all afibbers… current or former…. need to keep foremost in their minds to help prevent recurrence.
Dr. Mandrola does us a favor to remind that the basics should be not only emphasized initially, but also never to become complacent and slack off because most likely and attributable to a genetic influence, we (afibbers) are prone to or are more susceptible to fibrosis formation than others who are less health-conscious than we, afibbers, tend to be (and we all know plenty of those examples). It likely is rooted in the inability to hang on to magnesium and probably potassium adequately and that very well could be genetic. But, that said and as we know… “we don’t have to be held hostage to our genes” because we do have control over genetic expression. (Thank you, Bruce Lipton, PhD)
Following are a few clips as samples from CR 24 as reminders about magnesium, oxidative stress damage and the fibrosis issue. If you haven’t read both CR 24 and 75, both are outstanding in relevant information that will help maintain NSR.
Happy reading and NSR to all,
Jackie
Cardiac Fibrotic Remodeling – The Role of Fibrosis in LAF
INTRODUCTION
Atrial fibrosis – is it simply the result of AF which then causes more episodes or might it be that fibrotic remodeling as a
result of aging leads to AF?
Or is the natural decline of fibrolytic enzymes at fault? Further, might we consider the oxidative stress connection? And
let’s also examine the evidence suggesting the pro-fibrotic effects of magnesium deficiency.
These questions were posed to me by Erling Waller ex-afibber (75) who thinks there may be a connection. His afib
began at 64 and then 10 years later, after some nutritional adjustments, his AF vanished. (See his story in Hans’ book.)
Erling has been a regular and prolific contributor of important information and was always generous with his time and
support to help others seeking answers. He continues to ponder the origin of AF and finds the fibrosis remodeling
connection not only intriguing but also plausible. Erling is tackling another remodeling project at the moment and asked
me to present this topic to the BB.
Interrelated factors in the “Fibrotic Remodeling Theory”
I. Fibrosis mechanism
II. Mechanisms of AF
III. Inflammation and C-reactive Protein
IV. Oxidative Stress and Nitric Oxide/Peroxynitrite production
V. Magnesium deficiency
II. MECHANISMS: ATRIAL FIBRILLATION
AF is a progressive disease; numerous lines of evidence suggest that disease progression results from cumulative
electrophysiological and structural remodeling of the atria.(5) Ongoing events coupled with fibrotic remodeling
perpetuate longer episodes. (4)
In many patients, AF begins with short episodes, typically characterized as "palpitations" (a fluttering sensation in the
chest), or "paroxysms."
Over time, there is a tendency for these episodes to become longer. Why does this happen? Once AF has been
initiated, the atria undergo a process known as "remodeling." (1)
Structural changes: (remodeling) In time, afib that persists for years, is also accompanied by significant degenerative
structural changes. (1)
• Individual muscle cells within the fibrillating atria tend to become elongated and sometimes wider. AF-induced atrial
remodeling causes both structural and electrical changes(1)
• Fibrosis: In addition, the space between individual myocytes typically becomes more fibrotic, with fatty infiltration, and
the atria is less able to contract. (1)
Electrical changes: (remodeling)
• Fibrillating atria tend to have more complicated patterns of electrical activity. This is due both to the increased fibrosis,
and to intrinsic changes in the electrical activity in the atrial myocytes. Research at the CCF has helped to characterize
the electrical remodeling process associated with long-standing AF. (1)
• The net result is that in patients with persistent AF, the atria are more able to sustain fibrillatory activity, due to the
combined effects of both structural and electrical remodeling. (1)
Atrial Electrical Remodeling (sustains afib) Refer to the video web page.
• The net result of the electrical and structural changes is that the enlarged atria are more likely to sustain fibrillatory
activity. Thus, AF can persist for a longer duration in the remodeled atria. (1)
• Calcium ions have an important role in both the electrical and contractile activity of the heart. Thus, calcium overload
is implicated as an early event in the electrical remodeling process. (1)
• Persistent AF results in further changes in protein expression, loss of myofibrillar structure, and eventually myocyte
death and replacement fibrosis. (1)
Atrial Structural Remodeling
The fibrillating atria are subjected to continuous, high rate electrical activity (with rates up to 500 per minute). This
results in impaired atrial contractility, and the initiation of structural changes. (Be sure to look at the picture of a heart
exhibiting AF-induced fibrosis and the stained fibrotic-tissue studies.) (1)
• At the macroscopic level, structural remodeling is frequently characterized by increased atrial fibrosis and fatty
infiltration, both on the endocardial surface, and between muscle bundles. (1)
• At the microscopic level, fibrosis can isolate muscle bundles. (1)
• (Key Point) It is evident that fibrosis can isolate muscle bundles and that this can alter the pathway of electrical
activation, creating a substrate that can promote the persistence of atrial fibrillation. (1)
Then... continue on to item V. Magnesium deficiency.
[www.afibbers.org]
In 2012, an outstanding elaboration on CR 24 was offered (CR 75). It’s worth going to both CR sessions and learning about cardiac fibrosis and related issues that can and do continue even after a successful ablation because fibrosis formation is part of a natural, protective process in the body and it’s good to understand that and the preventive measures that lower formation.
CONFERENCE ROOM Session 75
August 17 – December 2, 2012
Afib and Cardiac Fibrosis
Part 1 – Atrial Fibrosis and the Mechanism of Atrial Fibrillation
[www.nbi.nlm.nih.gov]
Heart Rhythm 2007 March; 4(3 Suppl): S24–S27.
Atrial Fibrosis and the Mechanisms of Atrial Fibrillation
Thomas H. Everett IV, PhD and Jeffrey E. Olgin, MD
From the Division of Cardiology and the Cardiovascular Research Institute University of California
San Franci sco, San Francisco, California
Abstract
Atrial fibrillation (AF) is so commonly associated with congestive heart failure (CHF), and CHF has been shown to be associated with atrial structural remodeling resulting in fibrosis. This atrial interstitial fibrosis has been seen in patients with CHF and animal models of pacing induced heart failure. With atrial fibrosis, conduction abnormalities result in an increase in AF vulnerability. The mechanisms of AF that is associated with CHF is still under debate as both focal and reentrant mechanisms have been observed in animal models of CHF. However, recent studies utilizing frequency domain analysis have shown that the AF within this model is characterized by discrete stable, high-frequency areas. The precise signaling processes involved in the development of atrial fibrosis are unknown. Angiotension appears to play some role, since inhibition of ACE (or AR
blunt atrial fibrosis in animal models of heart failure and decrease the incidence of AF in patients with heart failure. TGFβ1 also seems to play an important role. Mouse models that overexpress TGFβ1 have profound atrial fibrosis and atrial fibrillation (with normal ventricles. Heart failure in canine models is also produces increases in atrial TGFβ1 expression and inhibition of this prevents atrial fibrosis and the development of a substrate for atrial fibrillation. Atrial fibrosis appears to play a role in the development of a vulnerable substrate for AF, especially in the setting of CHF.
.
Erling
As has been reviewed in various posts, an abundance of science exists supporting the fact that cardiac fibrosis contributes to arrhythmia. If cardiac fibrosis forms in the ventricles, it can be lethal. The formation is probably not exclusively selective for atrial tissue so it's something not to be taken lightly. Science also supports that magnesium deficiency as well as excessive exposure to free-radical damage (ROS) is commonly associated with the genesis of fibrosis.
Fibrosis interference with electrical conduction is examined in numerous reports looking at gap-junction function and the cell-to-cell communication disrupted by the presence of fibrosis. Fibrotic interference in terms of electrical conduction (voltage) throughout the body is observed in various conditions involving the vast system of the fascia and connective tissue. Fibrotic connective tissue proliferation becomes part of the aging process. Tissues in some individuals age faster than in others.
While the etiology of fibrosis and understanding the fibrotic process, itself, is certainly important to understand, it’s also important to recognize the need for preventive measures so that fibrosis is less likely form in the first place. Preventive guidelines typically address antioxidant therapy as important but emphasis on magnesium optimization is not common advice.
While not in this review, consideration should also be given to the extensive findings relating fibrotic formations, hypertension and kidney function involvement with aldosterone or angiotension II and the malfunction of the matrix-metallo protein (MMP) system which impacts multiple organ function including the heart. Also not in this review is the impact of oxidative stress injury and resultant cardiac fibrosis in endurance athletes. Many facets of fibrosis to consider.
Recognition that cardiac fibrosis is not something to be ignored is supported in a recent study published in the American Journal of Cardiovascular Disease (2011)
Targeting cardiac fibrosis: a new frontier in antiarrhythmic therapy?
Key-point review follows. This report indicates a need to address fibrosis accumulations as a preventive treatment for arrhythmia and suggests that pharmaceuticals should be developed in addition to those currently available.
While we wait for various new pharmaceutical interventions that inhibit fibrosis formation to be formulated, tested, and receive FDA approval, it makes sense to consider the potential for preventing fibrosis formation in the first place by making sure that our intracellular stores of magnesium are optimal as verified by Exatest, evaluation of existing oxidative stress values and evaluation of critical antioxidants levels that, when missing, allow for inflammation and fibrotic accumulations. Example: deficiency of (antioxidant) glutathione allows for increased lung inflammation and resultant fibrosis.
Additionally, those of us who like to take an active-participation role in personal health management aimed at prevention can consider the use of proteolytic and fibrinolytic enzymes to help break up and dispose of fibrin deposits. Since we have the study showing that Nattokinase degrades Amyloid plaques in brain tissue of Alzheimer patients, those of us using NK and other systemic enzymes such as serrapeptase or the stronger, lumbrokinase, can take comfort in knowing that we are doing good things for our brain, heart, cardiovascular system and undoubtedly, many other organs prone to fibrosis as well if we choose to be our own health advocates and experiment.
What can be more significant than degrading brain plaque? If our hearts happen to benefit as well, it’s a win/win all around.
Jackie
(continue at the CR 75 )
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