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CREATINE - I think you may all want to read this link
Posted by Richard
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Richard
CREATINE - I think you may all want to read this link November 22, 2003 04:38AM |
Hello All,
I'm running out of time, as we are having a birthday party for my daughter today, but I found this research to be very important, and wanted to share.
Here's a few excerpts to peak your interest: Cr is Creatine.
Cr has been found to be neuroprotective against N-methyl-D-aspartate and malonate excitotoxicity following a 1% (w/w) diet for 1 week in rats (Malcon et al., 2000). These investigators did not find protection against -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or kainic toxicity. In either case, no dose-response relationship was established. Cr has been shown to protect hippocampal neurons from glutamate toxicity and partially protect embryonic neurons from -amyloid toxicity (Brewer and Wallimann, 2000). This protection against -amyloid was also seen in adult and aged neurons and therefore may attenuate the formation of senile plaques seen in Alzheimer's disease. In both cases, intracellular Cr and PCr were elevated when compared with toxin-treated neurons not supplemented with Cr.
Because Cr is involved in energy production and acts as a shuttle of ATP from the inner mitochondria to the cytosol, Cr was theorized to be useful in diseases of mitochondria where energy production is altered. Cr supplementation has been shown to be beneficial in diseases in which there is mitochondrial dysfunction such as Parkinson's, Huntington's, and myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
Anything that helps with ATP production and transportation, has to be good in my opinion.
[pharmrev.aspetjournals.org]
I hope you all read, and if anyone's taking this supplement, could you pls. comment and let me know your dosage. Thank you.
Richard
I'm running out of time, as we are having a birthday party for my daughter today, but I found this research to be very important, and wanted to share.
Here's a few excerpts to peak your interest: Cr is Creatine.
Cr has been found to be neuroprotective against N-methyl-D-aspartate and malonate excitotoxicity following a 1% (w/w) diet for 1 week in rats (Malcon et al., 2000). These investigators did not find protection against -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid or kainic toxicity. In either case, no dose-response relationship was established. Cr has been shown to protect hippocampal neurons from glutamate toxicity and partially protect embryonic neurons from -amyloid toxicity (Brewer and Wallimann, 2000). This protection against -amyloid was also seen in adult and aged neurons and therefore may attenuate the formation of senile plaques seen in Alzheimer's disease. In both cases, intracellular Cr and PCr were elevated when compared with toxin-treated neurons not supplemented with Cr.
Because Cr is involved in energy production and acts as a shuttle of ATP from the inner mitochondria to the cytosol, Cr was theorized to be useful in diseases of mitochondria where energy production is altered. Cr supplementation has been shown to be beneficial in diseases in which there is mitochondrial dysfunction such as Parkinson's, Huntington's, and myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
Anything that helps with ATP production and transportation, has to be good in my opinion.
[pharmrev.aspetjournals.org]
I hope you all read, and if anyone's taking this supplement, could you pls. comment and let me know your dosage. Thank you.
Richard
|
J. Pisano
Re: CREATINE - I think you may all want to read this link November 22, 2003 12:27PM |
Richard,
Hope all is well at your party!
Just some information for you to run through your mind blender....
Animal studies have shown that atrial myocardium is as rich a source of creatine kinase MB as is ventricular myocardium. Atrial myocardium has a lactate dehydrogenase1/lactate dehydrogenase2 ratio less than 1.00, whereas in ventricular myocardium the ratio is greater than 1.00. (1)
Kinase is an enzyme that can transfer a phosphate from a high energy phosphate such as ATP, to an organic molecule. Incidently, I have begun to wonder weather or not people are really getting enough phosphorus in their diets. After analyzing my own diet, I find that I am perhaps somewhat deficient in this. The conventional wisdom dotes that since people drink so much carbonated beverages they get an overaboundance of this. If you are on a lower carbohydrate diet or avoiding dairy and or breads, you may very well be low in this essential mineral. Brewer's Yeast is a good source.... I digress..
In a recent article by the CCF, David Van Wagoner says this:
We have recently found that atrial tissue
specimens from patients with persistent atrial fibrillation had decreased creatine kinase activity (and
thus decreased ATP) at the level of the myofibril. Further we found evidence of increased protein
nitration, suggesting an important role for oxidative stress in the pathophysiology of atrial
fibrillation [2]. It is intriguing to note that, in isolated rat atrial myocytes, mechanosensitive
modulation of ATP-sensitive K+ channels was enhanced when the ATP concentration was
reduced [3]. The relevance of mechanosensitive modulation of these surface-membrane channels to
the physiology of the intact myocyte (and atria) still remains to be established. While the
repolarizing outward currents tend to be reduced in atrial fibrillation, we and others have found that
the inward rectifier current (IK1) is increased, perhaps reflecting a compensatory attempt to maintain
an adequate resting potential in the presence of frequent depolarization [1,4].
I have copied the link below, with references. This article talks about the mechansisms of AFIB, which, you, Hans and PC, have been talking about in the CR.
[mef.physiol.ox.ac.uk]
Joe
1. J Thorac Cardiovasc Surg. 1986 Jul;92(1):63-72.
Changes in serum creatine kinase and lactate dehydrogenase caused by acute perioperative myocardial infarction and by transatrial cardiac surgical procedures.
Hope all is well at your party!
Just some information for you to run through your mind blender....
Animal studies have shown that atrial myocardium is as rich a source of creatine kinase MB as is ventricular myocardium. Atrial myocardium has a lactate dehydrogenase1/lactate dehydrogenase2 ratio less than 1.00, whereas in ventricular myocardium the ratio is greater than 1.00. (1)
Kinase is an enzyme that can transfer a phosphate from a high energy phosphate such as ATP, to an organic molecule. Incidently, I have begun to wonder weather or not people are really getting enough phosphorus in their diets. After analyzing my own diet, I find that I am perhaps somewhat deficient in this. The conventional wisdom dotes that since people drink so much carbonated beverages they get an overaboundance of this. If you are on a lower carbohydrate diet or avoiding dairy and or breads, you may very well be low in this essential mineral. Brewer's Yeast is a good source.... I digress..
In a recent article by the CCF, David Van Wagoner says this:
We have recently found that atrial tissue
specimens from patients with persistent atrial fibrillation had decreased creatine kinase activity (and
thus decreased ATP) at the level of the myofibril. Further we found evidence of increased protein
nitration, suggesting an important role for oxidative stress in the pathophysiology of atrial
fibrillation [2]. It is intriguing to note that, in isolated rat atrial myocytes, mechanosensitive
modulation of ATP-sensitive K+ channels was enhanced when the ATP concentration was
reduced [3]. The relevance of mechanosensitive modulation of these surface-membrane channels to
the physiology of the intact myocyte (and atria) still remains to be established. While the
repolarizing outward currents tend to be reduced in atrial fibrillation, we and others have found that
the inward rectifier current (IK1) is increased, perhaps reflecting a compensatory attempt to maintain
an adequate resting potential in the presence of frequent depolarization [1,4].
I have copied the link below, with references. This article talks about the mechansisms of AFIB, which, you, Hans and PC, have been talking about in the CR.
[mef.physiol.ox.ac.uk]
Joe
1. J Thorac Cardiovasc Surg. 1986 Jul;92(1):63-72.
Changes in serum creatine kinase and lactate dehydrogenase caused by acute perioperative myocardial infarction and by transatrial cardiac surgical procedures.
|
Richard
Re: CREATINE - I think you may all want to read this link November 23, 2003 04:27AM |
Joe,
That was a very interesting link from Cleveland Clinic. It makes sense to me that phosphorous could very well be a problem for both vagal and adrenergics. My episodes were mostly brought on by the extra output of energy, whether it be walking up a hill, playing golf, or digestion, however I have also gone out of rhythm by consuming free glutamate, which takes extra ATP's per Joe South's article posted a while back, to try to eliminate the excess. In a previous post to Mike, I mentioned that our heart is like a flickering light bulb that isn't quite getting enough power. I know that's a simplistic point of view, but phosphorous is luminescent, like a light bulb, and at least most of the processes in the body are phosphorylated.
Another thing in my posted link I found interesting was this:
Cr is derived from glycine and arginine by the formation of guanidinoacetate and ornithine in a reaction catalyzed by arginine:glycine amidino-transferase (AGAT) (Walker, 1979; Wyss and Kaddurah-Daouk, 2000).
I think the glycine in the Mg is helping people in the formation of creatine. In my case, I wasn't low intracelluarly in Mg, but I was low in glycine in serum. I think I will concentrate on glycine and creatine for a while, and see what I find.
I didn't use to be a big pop drinker, even before starting Paleo, and I don't think that's a good way for people to get their pho., because of the high content of sugar, however I find it strange that I converted on pop 3-4 times, and believe me when I say, it's hard to convert atrial flutter.
The article goes on to say:
Animal Studies. The effects of Cr on cardiac tissue have been investigated. A study by Sharov et al. (1987) showed a protective effect of PCr on cardiac tissue following ischemia. Using rabbit hearts, PCr was administered intravenously either before and during cardiac artery ligation or 30 min post-ligation. These investigators found a reduction in necrotic zone under both PCr treatments compared with controls (Fig. 4). Ruda et al. (1988) found that PCr administration reduced ventricular arrhythmia after acute myocardial infarctions, but the effects of Cr on cardiac tissue are still unclear. Other studies have also shown PCr to possess anti-arrhythmic activities (Rosenshtraukh et al., 1988). Feeding Cr to healthy rats or rats after a myocardial infarction failed to increase intramuscular Cr (Horn et al., 1998). The b-blocker bispropolol has been shown to increase total cardiac Cr up to 40% (Laser et al., 1996). The ability to increase Cr and related energetics in heart tissue may be one beneficial mechanism of the action of b-blocker therapy (Laser et al., 1996). Ingwall et al. (1985) have also shown that diseased myocardium has lower Cr content. Supplementation with Cr has also provided protection to cardiac tissue from metabolic stress (Constantin-Teodosiu et al., 1995)
This is where I get confused, because when taking beta blockers, I became extremely fatigued, and my heart was fighting constantly to stay in rhythm. I wasn't taking bispropolol, however, only toprol, so I wonder what the difference is. I'll do a search and see what I find.
Thank you for finding that link, Joe. By the way, my daughter's party was a success, and she had a wonderful time. My day didn't go so well, because I went out of rhythm. I was exerting a lot more energy helping get things ready. Hmmm??? I converted using extra flec, but it took a while. I'm now reassessing my supplementing regimen, esp. in light of these articles and Kjell provoking thoughts on my craziness. Thanks Kjell, if you're reading and I hope you are. I'm only going to concentrate on what I know I was low in, which was B12, folate, molybdenum, C because I know how important that is daily, E, a few other necessary nutrients, and phosphorous and/or glycine. I'm concentrating today, on my changes, more in depth. Had I stayed in rhythm, this wouldn't have been an issue.
Richard
That was a very interesting link from Cleveland Clinic. It makes sense to me that phosphorous could very well be a problem for both vagal and adrenergics. My episodes were mostly brought on by the extra output of energy, whether it be walking up a hill, playing golf, or digestion, however I have also gone out of rhythm by consuming free glutamate, which takes extra ATP's per Joe South's article posted a while back, to try to eliminate the excess. In a previous post to Mike, I mentioned that our heart is like a flickering light bulb that isn't quite getting enough power. I know that's a simplistic point of view, but phosphorous is luminescent, like a light bulb, and at least most of the processes in the body are phosphorylated.
Another thing in my posted link I found interesting was this:
Cr is derived from glycine and arginine by the formation of guanidinoacetate and ornithine in a reaction catalyzed by arginine:glycine amidino-transferase (AGAT) (Walker, 1979; Wyss and Kaddurah-Daouk, 2000).
I think the glycine in the Mg is helping people in the formation of creatine. In my case, I wasn't low intracelluarly in Mg, but I was low in glycine in serum. I think I will concentrate on glycine and creatine for a while, and see what I find.
I didn't use to be a big pop drinker, even before starting Paleo, and I don't think that's a good way for people to get their pho., because of the high content of sugar, however I find it strange that I converted on pop 3-4 times, and believe me when I say, it's hard to convert atrial flutter.
The article goes on to say:
Animal Studies. The effects of Cr on cardiac tissue have been investigated. A study by Sharov et al. (1987) showed a protective effect of PCr on cardiac tissue following ischemia. Using rabbit hearts, PCr was administered intravenously either before and during cardiac artery ligation or 30 min post-ligation. These investigators found a reduction in necrotic zone under both PCr treatments compared with controls (Fig. 4). Ruda et al. (1988) found that PCr administration reduced ventricular arrhythmia after acute myocardial infarctions, but the effects of Cr on cardiac tissue are still unclear. Other studies have also shown PCr to possess anti-arrhythmic activities (Rosenshtraukh et al., 1988). Feeding Cr to healthy rats or rats after a myocardial infarction failed to increase intramuscular Cr (Horn et al., 1998). The b-blocker bispropolol has been shown to increase total cardiac Cr up to 40% (Laser et al., 1996). The ability to increase Cr and related energetics in heart tissue may be one beneficial mechanism of the action of b-blocker therapy (Laser et al., 1996). Ingwall et al. (1985) have also shown that diseased myocardium has lower Cr content. Supplementation with Cr has also provided protection to cardiac tissue from metabolic stress (Constantin-Teodosiu et al., 1995)
This is where I get confused, because when taking beta blockers, I became extremely fatigued, and my heart was fighting constantly to stay in rhythm. I wasn't taking bispropolol, however, only toprol, so I wonder what the difference is. I'll do a search and see what I find.
Thank you for finding that link, Joe. By the way, my daughter's party was a success, and she had a wonderful time. My day didn't go so well, because I went out of rhythm. I was exerting a lot more energy helping get things ready. Hmmm??? I converted using extra flec, but it took a while. I'm now reassessing my supplementing regimen, esp. in light of these articles and Kjell provoking thoughts on my craziness. Thanks Kjell, if you're reading and I hope you are. I'm only going to concentrate on what I know I was low in, which was B12, folate, molybdenum, C because I know how important that is daily, E, a few other necessary nutrients, and phosphorous and/or glycine. I'm concentrating today, on my changes, more in depth. Had I stayed in rhythm, this wouldn't have been an issue.
Richard
|
Richard
Re: CREATINE - I think you may all want to read this link November 23, 2003 07:47AM |
Here's a bit more on creatine. I had forgotten that methionine, of which I was very low in, factors into the process.
Creatine. Creatine (N-[aminoiminomethyl]-N-methyl glycine) is a tri-peptide endogenously produced from glycine, methionine, and arginine in the liver, kidney, and pancreas (McArdle et al., 1999). Creatine can be found in the muscle, but also in brain tissue (Mujika and Padilla, 1997). Recent experimental findings have demonstrated that creatine provides significant neuroprotection against ischemic and oxidative insults (Holtzman et al., 1998; Balestrino et al., 1999). Sullivan et al. (2000) showed that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats after experimental traumatic brain injury. The protection seemed to be related to creatine-induced maintenance of mitochondrial bioenergetics. Mitochondrial membrane potential was significantly increased, intramitochondrial levels of ROS and calcium were significantly decreased, and ATP levels were maintained. This new agent should be intensively investigated before clinical studies for acute CNS injury are performed.
[pharmrev.aspetjournals.org]
Creatine is produced naturally in both humans and animals from the amino acids L-Arginine, Glycine and L-Methionine. Creatine is converted into Creatine Phosphate in muscle tissue where it, in turn, converts ADP to ATP to replace ATP consumed during exercise. Muscle fatigue occurs when the supply of Creatine Phosphate is exhausted and ADP can no longer be converted. The book "Creatine - Nature's Muscle Builder" contains additional information and case studies.
[jomarlabs.com]
Richard
Creatine. Creatine (N-[aminoiminomethyl]-N-methyl glycine) is a tri-peptide endogenously produced from glycine, methionine, and arginine in the liver, kidney, and pancreas (McArdle et al., 1999). Creatine can be found in the muscle, but also in brain tissue (Mujika and Padilla, 1997). Recent experimental findings have demonstrated that creatine provides significant neuroprotection against ischemic and oxidative insults (Holtzman et al., 1998; Balestrino et al., 1999). Sullivan et al. (2000) showed that chronic administration of creatine ameliorated the extent of cortical damage by as much as 36% in mice and 50% in rats after experimental traumatic brain injury. The protection seemed to be related to creatine-induced maintenance of mitochondrial bioenergetics. Mitochondrial membrane potential was significantly increased, intramitochondrial levels of ROS and calcium were significantly decreased, and ATP levels were maintained. This new agent should be intensively investigated before clinical studies for acute CNS injury are performed.
[pharmrev.aspetjournals.org]
Creatine is produced naturally in both humans and animals from the amino acids L-Arginine, Glycine and L-Methionine. Creatine is converted into Creatine Phosphate in muscle tissue where it, in turn, converts ADP to ATP to replace ATP consumed during exercise. Muscle fatigue occurs when the supply of Creatine Phosphate is exhausted and ADP can no longer be converted. The book "Creatine - Nature's Muscle Builder" contains additional information and case studies.
[jomarlabs.com]
Richard
|
Richard
Re: CREATINE - I think you may all want to read this link November 23, 2003 01:45PM |
Joe,
I thought I'd give you this link, as I have referred to it often. I gave it a while back and you may not have been here at the time. It's invaluable.
[web.indstate.edu]
Richard
I thought I'd give you this link, as I have referred to it often. I gave it a while back and you may not have been here at the time. It's invaluable.
[web.indstate.edu]
Richard
|
Richard
Re: CREATINE - I think you may all want to read this link November 23, 2003 04:53PM |
A bit more on energy in the heart:
Vanadate improves cardiac function and myocardial energy metabolism in diabetic rat hearts.
Noda C, Masuda T, Sato K, Ikeda K, Shimohama T, Matsuyama N, Izumi T.
Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa 228-8555, Japan.
Vanadium mimicking the metabolic effects of insulin is known to decrease serum glucose levels and to influence glucose metabolism in diabetes mellitus. However, it is unclear whether vanadium ameliorates the metabolic disorder in diabetic hearts causing myocardial dysfunction. The purpose of this study was to assess the effects of vanadium on cardiac performance and energy metabolism in diabetic rat hearts. Four groups of Wistar rats were studied: untreated control rats (group C, n = 8). vanadate-treated rats (group V, n = 10), untreated diabetic rats (group DM, n = 9) induced by streptozotocin. and vanadate-treated diabetic rats (group DMV, n = 8). Vanadate-treated rats drank a 1.5 mM sodium orthovanadate (Na3VO4) solution during a 4 week diabetic condition. Hearts were perfused with Krebs-Henseleit buffer after the diabetic duration. After the maximum left ventricular dP/dt and cardiac efficiency were calculated, the myocardial contents of ATP and creatine phosphate (P-Cr) and myocardial energy metabolism were assessed by cytosolic phosphorylation potential. Peak positive and negative dP/dt, and cardiac efficiency decreased significantly in group DM compared with group C, while there were no significant differences between groups C and DMV. The myocardial contents of ATP (micromol/g wet heart) and P-Cr (micromol/g wet heart), and cytosolic phosphorylation potential (M(-1)) increased from 2.72 +/- 0.46. 1.45 +/- 0.58. and 3,530 +/- 1,220 in group DM to 3.88 +/- 0.76, 3.81 +/- 1.36, and 11,200 +/- 2,400 in group DMV, respectively. It is concluded that vanadium restored the production of high energy phosphates in the myocardium and improved myocardial dysfunction by regulating metabolic processes in diabetic rat hearts.
[www.ncbi.nlm.nih.gov]
Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability.
Cha YM, Dzeja PP, Shen WK, Jahangir A, Hart CY, Terzic A, Redfield MM.
Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with (n = 6) and without (n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area (r = 0.73, P = 0.01) and inversely with atrial ATP concentration (r = -0.75, P = 0.005), CK activity (r = -0.57, P = 0.054), and AK activity (r = -0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.
[www.ncbi.nlm.nih.gov]
Richard
Vanadate improves cardiac function and myocardial energy metabolism in diabetic rat hearts.
Noda C, Masuda T, Sato K, Ikeda K, Shimohama T, Matsuyama N, Izumi T.
Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Kanagawa 228-8555, Japan.
Vanadium mimicking the metabolic effects of insulin is known to decrease serum glucose levels and to influence glucose metabolism in diabetes mellitus. However, it is unclear whether vanadium ameliorates the metabolic disorder in diabetic hearts causing myocardial dysfunction. The purpose of this study was to assess the effects of vanadium on cardiac performance and energy metabolism in diabetic rat hearts. Four groups of Wistar rats were studied: untreated control rats (group C, n = 8). vanadate-treated rats (group V, n = 10), untreated diabetic rats (group DM, n = 9) induced by streptozotocin. and vanadate-treated diabetic rats (group DMV, n = 8). Vanadate-treated rats drank a 1.5 mM sodium orthovanadate (Na3VO4) solution during a 4 week diabetic condition. Hearts were perfused with Krebs-Henseleit buffer after the diabetic duration. After the maximum left ventricular dP/dt and cardiac efficiency were calculated, the myocardial contents of ATP and creatine phosphate (P-Cr) and myocardial energy metabolism were assessed by cytosolic phosphorylation potential. Peak positive and negative dP/dt, and cardiac efficiency decreased significantly in group DM compared with group C, while there were no significant differences between groups C and DMV. The myocardial contents of ATP (micromol/g wet heart) and P-Cr (micromol/g wet heart), and cytosolic phosphorylation potential (M(-1)) increased from 2.72 +/- 0.46. 1.45 +/- 0.58. and 3,530 +/- 1,220 in group DM to 3.88 +/- 0.76, 3.81 +/- 1.36, and 11,200 +/- 2,400 in group DMV, respectively. It is concluded that vanadium restored the production of high energy phosphates in the myocardium and improved myocardial dysfunction by regulating metabolic processes in diabetic rat hearts.
[www.ncbi.nlm.nih.gov]
Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability.
Cha YM, Dzeja PP, Shen WK, Jahangir A, Hart CY, Terzic A, Redfield MM.
Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA.
The failing ventricular myocardium is characterized by reduction of high-energy phosphates and reduced activity of the phosphotransfer enzymes creatine kinase (CK) and adenylate kinase (AK), which are responsible for transfer of high-energy phosphoryls from sites of production to sites of utilization, thereby compromising excitation-contraction coupling. In humans with chronic atrial fibrillation (AF) unassociated with congestive heart failure (CHF), impairment of atrial myofibrillar energetics linked to oxidative modification of myofibrillar CK has been observed. However, the bioenergetic status of the failing atrial myocardium and its potential contribution to atrial electrical instability in CHF have not been determined. Dogs with (n = 6) and without (n = 6) rapid pacing-induced CHF underwent echocardiography (conscious) and electrophysiological (under anesthesia) studies. CHF dogs had more pronounced mitral regurgitation, higher atrial pressure, larger atrial area, and increased atrial fibrosis. An enhanced propensity to sustain AF was observed in CHF, despite significant increases in atrial effective refractory period and wavelength. Profound deficits in atrial bioenergetics were present with reduced activities of the phosphotransfer enzymes CK and AK, depletion of high-energy phosphates (ATP and creatine phosphate), and reduction of cellular energetic potential (ATP-to-ADP and creatine phosphate-to-Cr ratios). AF duration correlated with left atrial area (r = 0.73, P = 0.01) and inversely with atrial ATP concentration (r = -0.75, P = 0.005), CK activity (r = -0.57, P = 0.054), and AK activity (r = -0.64, P = 0.02). Atrial levels of malondialdehyde, a marker of oxidative stress, were significantly increased in CHF. Myocardial bioenergetic deficits are a conserved feature of dysfunctional atrial and ventricular myocardium in CHF and may constitute a component of the substrate for AF in CHF.
[www.ncbi.nlm.nih.gov]
Richard
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