Aa
Atrial fibrillation
I have periods of persistent atrial fibrillation. The first was in 2010 and was successfully cardioversed precisely after six months. The second period was in spring 2012 and was cardioversed after six weeks' warfarin treatment. The present period is going on now (from 6. January) and will be cardioversed after 7 weeks from the beginning.
An electric cardioversion immediately after the onset of AF is possible only when one is 100% sure that it has not lasted more than 48 h. Otherwise one must be on Warfarin (Marevan) so that INR is on the therapeutic level at least for three weeks. At all times of my AF, I have had INR on the therapeutic level (2-3) soon and mainteined it there for all the AF time (and a few extra months). At the meantime I have used "children's aspirin).
Is it good to keep people with AF for too long times?
Why do doctors not study causes of AF? I myself have suggested eg. dehydration, infections and hyperparathyroidism for causes of AF.
I have not had thorough heart studies and discussions in a hospital. I have organized them at sevearal private doctors' offices. When people go to electric cardioversion to the hospital, it is performed in a steady stream with only short discussion with the doctor.
ECG has been done several times. I have a small leakage of mitral valve. During the second period of AF the leakage was possibly slightly larger than during the first AF. With AF, my pulmonary pressure rises and left atrium enlarges. ProBNP rises at least to over 2400. Doctors did not begin to measure it, I ordered the measurement myself. But the rise does not matter. I have respiratory difficulties. After the six-month AF in 2010 the left atrium, however, shrank to normal (in 2011). Enlargement of the left atrium is thus not a cause of my AF but a consequence. Is it good to keep me with AF?
My blood pressure and pulse have always been very variable. I am now 65 years. In the nineteen eighties I often had paroxysmal tachycardia. Atenolol was begun and I am still using it. Possibly I got CFS (ME) in the eighties.
At the change of 2009-2010 I had some infections, and before the AF period in 2010 I ordered a test for autonomic nervous system. In 1/3-maximal grip (maximal was 30.4) test my blood pressure was 259/140 (at rest before the test 153/80). The increase was: systolic 106 mmHg and diastolic 57. In Valsalva test pulse reaction was weak. In deep breathing test respiratory arhythmia was weaker than normal. In orthostatic test blood pressure reactions were strong: at 30 sec systolic +47 and at 3 min systolic +87. Atenolol 50 mg and Thyroid 2,5 G were in use. As a conclusion of the autonomous nersvous systen test it was said that, the result did not clearly deviate from normal. The weak pulse reaction can result from already high pulse at the beginning. Maybe sympaticotonia causes the greater blood pressure increase and the higher pulse.
My blood pressure and pulse are very variable during the AF, and also without AF. During AF my diastolic pressure is sometimes increased. Sometimes, when sitting, my blood pressure varies between 98/71 and 141/109. In an ambulatory (24 h) blood pressure test (without atenolol) in 2006, my systolic pressure varied between 98 and 228 (mean 141). Diastolic pressure varied varied between 44-113 (mean 84). The pulse varied between 64 and 137 (mean 91). I was ashtonished, because my pulse pressure minimum and maximum were 14 and 134!! Why?
I have chronic sinusitis. At the change of 2012-2013 I have had dyspnea and respiratory infection and norovirus. I have some inconsistency in my iron status. I have not iron deficiency but have small and pale red cells. Maybe I have slight secondary anemia due to infections. I have too low IgG3 and complement lectin pathway. I have nodules in my lungs. They have not increased in size during two years. I am on thyroid medication (Thyroid Erfa). Partial diabetes insipidus could not be excluded in a water deprivation test. I have Sjoegren's syndrome and cervical dystonia. The latest diagnosis is too thick endometrium. I am using 25 mcg estrogen and every second month progesterone (Terolut).
When I on January 6 2013 was in the Emergency unit, my red cell count was 5.52, hemoglobin 153 and hematocrit 0.45. Na+ was 146 (137-144 normal!), fP-gluc 6,6 (!, no diabetes).
I think that I was dehydrated. My dehydration may be due to partial diabetes insipidus, hyperparathyroidism, or vitamin D. Vitamin D intake was increased early in autumn 2012 from 25 mcg to 50 mcg. Then I had, according to a doctor, to increase D-vitamin intake to 100. At the end of 2012 I had increased it to 75 mcg, and then I was one day at 100 mcg. I did not feel good and dropped it back to 75 mcg on the next day. Then early in the morning of the next day (Jan 6) I found atrial fibrillation. I dropped the vitamin to 50 mcg. Then I once tried to take 75 again and got polyuria and thirst, and dropped it back to 50 mc. It can be suggested that the vit D increase was a cause for the onset of AF. ???
An electric cardioversion immediately after the onset of AF is possible only when one is 100% sure that it has not lasted more than 48 h. Otherwise one must be on Warfarin (Marevan) so that INR is on the therapeutic level at least for three weeks. At all times of my AF, I have had INR on the therapeutic level (2-3) soon and mainteined it there for all the AF time (and a few extra months). At the meantime I have used "children's aspirin).
Is it good to keep people with AF for too long times?
Why do doctors not study causes of AF? I myself have suggested eg. dehydration, infections and hyperparathyroidism for causes of AF.
I have not had thorough heart studies and discussions in a hospital. I have organized them at sevearal private doctors' offices. When people go to electric cardioversion to the hospital, it is performed in a steady stream with only short discussion with the doctor.
ECG has been done several times. I have a small leakage of mitral valve. During the second period of AF the leakage was possibly slightly larger than during the first AF. With AF, my pulmonary pressure rises and left atrium enlarges. ProBNP rises at least to over 2400. Doctors did not begin to measure it, I ordered the measurement myself. But the rise does not matter. I have respiratory difficulties. After the six-month AF in 2010 the left atrium, however, shrank to normal (in 2011). Enlargement of the left atrium is thus not a cause of my AF but a consequence. Is it good to keep me with AF?
My blood pressure and pulse have always been very variable. I am now 65 years. In the nineteen eighties I often had paroxysmal tachycardia. Atenolol was begun and I am still using it. Possibly I got CFS (ME) in the eighties.
At the change of 2009-2010 I had some infections, and before the AF period in 2010 I ordered a test for autonomic nervous system. In 1/3-maximal grip (maximal was 30.4) test my blood pressure was 259/140 (at rest before the test 153/80). The increase was: systolic 106 mmHg and diastolic 57. In Valsalva test pulse reaction was weak. In deep breathing test respiratory arhythmia was weaker than normal. In orthostatic test blood pressure reactions were strong: at 30 sec systolic +47 and at 3 min systolic +87. Atenolol 50 mg and Thyroid 2,5 G were in use. As a conclusion of the autonomous nersvous systen test it was said that, the result did not clearly deviate from normal. The weak pulse reaction can result from already high pulse at the beginning. Maybe sympaticotonia causes the greater blood pressure increase and the higher pulse.
My blood pressure and pulse are very variable during the AF, and also without AF. During AF my diastolic pressure is sometimes increased. Sometimes, when sitting, my blood pressure varies between 98/71 and 141/109. In an ambulatory (24 h) blood pressure test (without atenolol) in 2006, my systolic pressure varied between 98 and 228 (mean 141). Diastolic pressure varied varied between 44-113 (mean 84). The pulse varied between 64 and 137 (mean 91). I was ashtonished, because my pulse pressure minimum and maximum were 14 and 134!! Why?
I have chronic sinusitis. At the change of 2012-2013 I have had dyspnea and respiratory infection and norovirus. I have some inconsistency in my iron status. I have not iron deficiency but have small and pale red cells. Maybe I have slight secondary anemia due to infections. I have too low IgG3 and complement lectin pathway. I have nodules in my lungs. They have not increased in size during two years. I am on thyroid medication (Thyroid Erfa). Partial diabetes insipidus could not be excluded in a water deprivation test. I have Sjoegren's syndrome and cervical dystonia. The latest diagnosis is too thick endometrium. I am using 25 mcg estrogen and every second month progesterone (Terolut).
When I on January 6 2013 was in the Emergency unit, my red cell count was 5.52, hemoglobin 153 and hematocrit 0.45. Na+ was 146 (137-144 normal!), fP-gluc 6,6 (!, no diabetes).
I think that I was dehydrated. My dehydration may be due to partial diabetes insipidus, hyperparathyroidism, or vitamin D. Vitamin D intake was increased early in autumn 2012 from 25 mcg to 50 mcg. Then I had, according to a doctor, to increase D-vitamin intake to 100. At the end of 2012 I had increased it to 75 mcg, and then I was one day at 100 mcg. I did not feel good and dropped it back to 75 mcg on the next day. Then early in the morning of the next day (Jan 6) I found atrial fibrillation. I dropped the vitamin to 50 mcg. Then I once tried to take 75 again and got polyuria and thirst, and dropped it back to 50 mc. It can be suggested that the vit D increase was a cause for the onset of AF. ???
I am still in the sinus rhythm. My respiratory problems continue. I began to use Ventoline four time per day. I asked for the measurement of blood gases but did not get it. On next monday I 'll have spirometria. In April I'll get a Ct scan of my lungs because of an older nodule.
Glad you were successfully converted, sorry it took 3 shocks. I have been exhausted after cardioversion and another time not so much. Maybe it depends on the voltage. Good luck with the pulmonologist. Keep us posted on how you're doing.
I have been on the therapeutic level of warfarin from January 8. My cardioversion today succeeded but not very easily. At last time (last summer) it succeeded easily. Now they used first 150 J and then 200 and again 200.
I am very tired and don't dare to do much. I mentioned my respiratory problem without any comment from doctors. Because the problem is continuing, I fear that it may cause AF again. I have slight pain in my epigastrium.
I am very tired and don't dare to do much. I mentioned my respiratory problem without any comment from doctors. Because the problem is continuing, I fear that it may cause AF again. I have slight pain in my epigastrium.
I didn't read over all the posts again, so not sure if this was covered, but in the first 48 hours of afib, my EP said I could be converted without worry because the risk from clots doesn't start until then. The problem is, you might have afib and not know it. Actually, the first cardioversion I needed, the hospital put me on Lovenox and they still would not convert me without a TEE to rule out clots.
COMMUNITY LEADER
I have been on warfarin for at least 15 years, I tolerate it well, mostly no side effects and while I am at risk of bleeding it has never been a problem. I live my life much the same, run, hike, ride a bike, work with power tools...
My doctors would not "allow" me to go off of warfarin even when I was in normal rhythm - they said I could slip into AFib at any time, even in/out while I was sleeping, so I had to guard against clots in any case.
When I had heart surgery and a mini-maze I believe if I had stayed in normal rhythm for several months I would have been taken off of all medications, but alas I went back into AFib after about 30 days.
My doctors would not "allow" me to go off of warfarin even when I was in normal rhythm - they said I could slip into AFib at any time, even in/out while I was sleeping, so I had to guard against clots in any case.
When I had heart surgery and a mini-maze I believe if I had stayed in normal rhythm for several months I would have been taken off of all medications, but alas I went back into AFib after about 30 days.
Tomorrow I'll go to see a cardiologist professor. I'll ask what are the causes for my AF and possibilities to eliminate them. Possibly some heart studies can be done.
My path to get treatment for the first Af was incomprehensibly long and tortuous. It was a six-month path. No information from the hospital for many months, although I enquired. I'll ask tomorrow whether cardioversions here could in the future be done earlier than after several weeks on warfarin. Three weeks would be enough to prevents blood clots. I'll have a cardioversion on the next week, it makes then over seven weeks on warfarin. Cardioversions (except emergency ones) are done in a nearby town only on one day per week. It would be awful if my cardioversion does not succeed at the next time or later. I do not want to take warfarin for the rest of my life. No, no, no!
I am very angry. Long lasting AFs may worsen the leakage of my mitral valve. Enlargement of my left atrium can become permanent. CHF is knocking on my door. My father, however, lived to 96 years age. At the end he had a very large heart and very congested coronary arteries. I hope that I am as lucky as he in living long.
I have sometimes shortage of breath. It has begun as early as in 2007. It was bad in 2010 during the AF. I have proceeded on the solving path: my liver and pencreas enzymes (ALAT and amylase) were normal. Hyperventilation has also been excluded. It was not, however, excluded during excercise, only when sitting and standing. It is possible that when my heart rate increases during excercise, I may hyperventilate. I have a pulse oximeter. When I go out to walking, my spO2% rises to 99-100%. Some time after the walk it drops to 95. My normal O2% is 98 when I am sitting.
There are still two possible causes for dyspnea. One is possible contractibility of smaller coronary arteries. The other could be problems of the stomach or esophagus. In 2010 my stomach was healthy, but there were small red spots. I don't know what they were, possibly they were caused by warfarin? I have had some problems in my smller bronchioles in 2009, but my respiratory function had then improved (although I have some unknown nodules in my lungs). My recent respiratory infection has gone. It lasted for several weeks.
Best wishes!
My path to get treatment for the first Af was incomprehensibly long and tortuous. It was a six-month path. No information from the hospital for many months, although I enquired. I'll ask tomorrow whether cardioversions here could in the future be done earlier than after several weeks on warfarin. Three weeks would be enough to prevents blood clots. I'll have a cardioversion on the next week, it makes then over seven weeks on warfarin. Cardioversions (except emergency ones) are done in a nearby town only on one day per week. It would be awful if my cardioversion does not succeed at the next time or later. I do not want to take warfarin for the rest of my life. No, no, no!
I am very angry. Long lasting AFs may worsen the leakage of my mitral valve. Enlargement of my left atrium can become permanent. CHF is knocking on my door. My father, however, lived to 96 years age. At the end he had a very large heart and very congested coronary arteries. I hope that I am as lucky as he in living long.
I have sometimes shortage of breath. It has begun as early as in 2007. It was bad in 2010 during the AF. I have proceeded on the solving path: my liver and pencreas enzymes (ALAT and amylase) were normal. Hyperventilation has also been excluded. It was not, however, excluded during excercise, only when sitting and standing. It is possible that when my heart rate increases during excercise, I may hyperventilate. I have a pulse oximeter. When I go out to walking, my spO2% rises to 99-100%. Some time after the walk it drops to 95. My normal O2% is 98 when I am sitting.
There are still two possible causes for dyspnea. One is possible contractibility of smaller coronary arteries. The other could be problems of the stomach or esophagus. In 2010 my stomach was healthy, but there were small red spots. I don't know what they were, possibly they were caused by warfarin? I have had some problems in my smller bronchioles in 2009, but my respiratory function had then improved (although I have some unknown nodules in my lungs). My recent respiratory infection has gone. It lasted for several weeks.
Best wishes!
COMMUNITY LEADER
Happy to see you are getting good help in your study for a path forward.
I have no idea how long I was in AFib myself, but I can recall deciding to "get healthy" at about the age of 45, stopped smoking and stated exercising, including running and was then very conscious of my HR as I tried to exercise for 30 minute runs at my maximum. I didn't use a continuous monitor, just felt my pulse and watched the clock. I didn't notice any irregularity. But at some point, maybe age 55+ I noticed some irregularity, so much for the cardiovascular benefits of running, and was referred to a cardiologist. He didn't need even an EKG as I was in permanent (continuous) AFib. After meds failed to convert, he tried only Toprol XL (a BB), he did an electrocardioversion. It held for about 4 months. A second cardiologist put me on propafenone (rhythmol) and did another cardioversion which lasted for about 18 months, I continued the propafenone during that period. This may be enough history to make the point that in my experience:
1) I could be in AFib for extended periods - months and still be converted with shock.
2) cardioversion was never permanent.
The second point may have been due to a leaky mitral valve which was causing an ongoing enlargement of my left atrium. The valve was repaired and the surgeon said there may be some reduction in the size of the left atrium now that the "back pressure" was gone. I was in NSR following surgery and a mini-maze for about 30 days and the AFib returned. Follow up echocariograms, one only a week ago, have not shown any reduction in the size of my left atirum.
I am now on "rate control" and "clot management" (warfarin). I am now also undergoing a "closer look" at this programs dose levels as I have complained about fatigue.
I was happy to read in the last post that stroke risk due to a clots breaking loose is lower when in constant AFib, my condition. I do maintain an IR between 2 and 3, which may prevent the formation of clots, that's the plan in any case.
I try not to think about it, but my many visits to this web Community belies that statement, still it is only times like now that I wonder what's going to get me CHF or Stroke. I think stroke is the biggest worry as my heat appears to be structurally reasonable but somewhat enlarged.
I have no idea how long I was in AFib myself, but I can recall deciding to "get healthy" at about the age of 45, stopped smoking and stated exercising, including running and was then very conscious of my HR as I tried to exercise for 30 minute runs at my maximum. I didn't use a continuous monitor, just felt my pulse and watched the clock. I didn't notice any irregularity. But at some point, maybe age 55+ I noticed some irregularity, so much for the cardiovascular benefits of running, and was referred to a cardiologist. He didn't need even an EKG as I was in permanent (continuous) AFib. After meds failed to convert, he tried only Toprol XL (a BB), he did an electrocardioversion. It held for about 4 months. A second cardiologist put me on propafenone (rhythmol) and did another cardioversion which lasted for about 18 months, I continued the propafenone during that period. This may be enough history to make the point that in my experience:
1) I could be in AFib for extended periods - months and still be converted with shock.
2) cardioversion was never permanent.
The second point may have been due to a leaky mitral valve which was causing an ongoing enlargement of my left atrium. The valve was repaired and the surgeon said there may be some reduction in the size of the left atrium now that the "back pressure" was gone. I was in NSR following surgery and a mini-maze for about 30 days and the AFib returned. Follow up echocariograms, one only a week ago, have not shown any reduction in the size of my left atirum.
I am now on "rate control" and "clot management" (warfarin). I am now also undergoing a "closer look" at this programs dose levels as I have complained about fatigue.
I was happy to read in the last post that stroke risk due to a clots breaking loose is lower when in constant AFib, my condition. I do maintain an IR between 2 and 3, which may prevent the formation of clots, that's the plan in any case.
I try not to think about it, but my many visits to this web Community belies that statement, still it is only times like now that I wonder what's going to get me CHF or Stroke. I think stroke is the biggest worry as my heat appears to be structurally reasonable but somewhat enlarged.
Thanks to all of you for your posts. Is_something_wrong, here a doctor said to me that my situation is challenging but he will try to solve.
I have been diagnosed with primary hyperparathyrpoidism in 2011. I have slight hyperplasia in my right lower parathyroid ( shown by Sestamibi Technetium). A doctor said that there may be some hyperplasia in all my parathyroids if there is in one.
Later, an Endocrinologist thought that I may have vitamin D deficiency. And I could have secondary hyperparathyroidism. He wanted to lower my PTH and calcium. Early in autumn 2012 I had to increase my vitamin D intake from 25 to 50 mcg. And at the end of 2012 I had to increase it to 100. After being at 100 for one day I did not feel well and dropped it back to 75. Early in the next morning I got atrial fibrillation. I don't know surely that the vitamin D increasing was the cause, but it can be suggested. Now I am taking vit. D 50 mcg. My ionized Ca is at the upper limit, varying over and under.
My left atrium has been only slightly dilated during AF. It is good that it can shrink back to normal when I do not have AF. I think it will no longer shrink if I have many longer periods of AF. I have never had short AF episodes. But as early as I was younger I had often tachycardia and high blood pressure. Nowadays my systolic blood pressure sometimes goes down to below 100mmHg. The diastolic pressure is sometimes elevated. These may be caused by disorders of autonomic nervous system. How could these be cured?
ANP has not been measured for me. Does it give more information than proBNP?
I have been diagnosed with primary hyperparathyrpoidism in 2011. I have slight hyperplasia in my right lower parathyroid ( shown by Sestamibi Technetium). A doctor said that there may be some hyperplasia in all my parathyroids if there is in one.
Later, an Endocrinologist thought that I may have vitamin D deficiency. And I could have secondary hyperparathyroidism. He wanted to lower my PTH and calcium. Early in autumn 2012 I had to increase my vitamin D intake from 25 to 50 mcg. And at the end of 2012 I had to increase it to 100. After being at 100 for one day I did not feel well and dropped it back to 75. Early in the next morning I got atrial fibrillation. I don't know surely that the vitamin D increasing was the cause, but it can be suggested. Now I am taking vit. D 50 mcg. My ionized Ca is at the upper limit, varying over and under.
My left atrium has been only slightly dilated during AF. It is good that it can shrink back to normal when I do not have AF. I think it will no longer shrink if I have many longer periods of AF. I have never had short AF episodes. But as early as I was younger I had often tachycardia and high blood pressure. Nowadays my systolic blood pressure sometimes goes down to below 100mmHg. The diastolic pressure is sometimes elevated. These may be caused by disorders of autonomic nervous system. How could these be cured?
ANP has not been measured for me. Does it give more information than proBNP?
Hello.
I was asked to provide some feedback on your question. I must start with saying I'm not a doctor, and your question is complex and difficult to answer, but I will try to share some information. Also, you seem very knowledgeable about medicine in general and cardiology especially.
First, you are right that before cardioversion, one must be certain that no clots have formed in the atria. Actually, the risk of stroke is not highest while being in atrial fibrillation, but when converting to sinus rhythm (naturally or by cardioversion). When the left atrium is not beating (during a-fib), the clots usually just stay where they are, but when the atria are beating again, clots may break off the walls and follow the blood stream. Risk of clots increase after 48 hours of untreated a-fib, which is why you need 3 (4 in Norway) weeks on anticoagulants before cardioversion. Often a TEE (esophagal echocardiography) is performed to check if clots have formed in the atria before cardioversion.
Atrial fibrillation is not a life threatening condition, given that 1) clots are not forming (anticoagulation) and 2) the heart rate stays within reasonable limits, in other words, an average heart rate of 70-90. A faster heart rate (over time, months or years) can make the left ventricle dilate (tachycardiomyopathy) and a slower heart rate can cause tiredness, dizziness, fainting, etc. Of course, many of us can tolerate a slower heart rate, it depends on our physical condition and overall health.
It is not clear to me if you suffer from hyperparathyroidism or not. It sounds a bit weird, if you are, why are you ordered to take vitamin D supplements (which increase serum calcium)? Of course, do NOT make changes without asking your doctor, but your serum calcium must be carefully monitored. Too high (or too low) calcium may cause a variety of arrhythmias, including atrial fibrillation.
Atrial fibrillation may have a lot of causes. Most of them are related to structural changes in the left atrium (dilatation or hypertrophy) which tends to worsen BY having atrial fibrillation, which is why atrial fibrillation starts with brief episodes and ends up as a permanent condition. Hypertension seems to be a major risk factor. There are also a lot of non-cardiac causes, such as electrolyte imbalances (calcium especially), excess catecholamines, hyper/hypothyroidism, stimulants, drugs, alcohol. You are right about sympathetic/parasympathetic a-fib, the condition may occur with both. Atrial fibrillation often origin from the pulmonary veins (PACs that origin here can set off atrial fibrillation). If your heart rate is very slow, those "pacemakers" can take over, which is why atrial fibrillation is commonly seen in the setting of sinus node dysfunction (tachy/brady syndrome).
If some of your doctors have suggested a pacemaker combined with increased dose of beta blockers, you may suffer from this condition. The cause can both be within your sinus node, or your ANS. From your blood pressure fluctuations and heart rate fluctuations, it doesn't seem unlikely that you suffer some sort of autonomic dysfunction which affects the sinus node. If so, treatment with a pacemaker can help relieve lots of your symptoms. Of course, I can't say if this is the right treatment for you or not. Your doctors (and you) must decide.
Pulmonary vein ablation means to isolate the electrical activity from your pulmonary veins (so they can act as wild as they would like to, the activity will still not reach your heart) which can cure atrial fibrillation in 70-80% of patients. However, it depends a lot on how your left atrial function is, if your left atrium is severely dilated (you mention elevated NT-proBNP, though not ANP) See:
http://en.wikipedia.org/wiki/Atrial_natriuretic_peptide
If you want to know more about pulmonary vein ablation, please see:
www.hjertecentervarde.dk or www.hjertecentervarde.no (the latter focus more on PVA as 50.000 Norwegians are suffering atrial fibrillation without getting proper treatment). The webpage is Danish and the hospital is located in Denmark.
Sorry I'm not able to provide a better answer, but your question is fairly complicated. Good luck, and please write back if you have further questions!
I was asked to provide some feedback on your question. I must start with saying I'm not a doctor, and your question is complex and difficult to answer, but I will try to share some information. Also, you seem very knowledgeable about medicine in general and cardiology especially.
First, you are right that before cardioversion, one must be certain that no clots have formed in the atria. Actually, the risk of stroke is not highest while being in atrial fibrillation, but when converting to sinus rhythm (naturally or by cardioversion). When the left atrium is not beating (during a-fib), the clots usually just stay where they are, but when the atria are beating again, clots may break off the walls and follow the blood stream. Risk of clots increase after 48 hours of untreated a-fib, which is why you need 3 (4 in Norway) weeks on anticoagulants before cardioversion. Often a TEE (esophagal echocardiography) is performed to check if clots have formed in the atria before cardioversion.
Atrial fibrillation is not a life threatening condition, given that 1) clots are not forming (anticoagulation) and 2) the heart rate stays within reasonable limits, in other words, an average heart rate of 70-90. A faster heart rate (over time, months or years) can make the left ventricle dilate (tachycardiomyopathy) and a slower heart rate can cause tiredness, dizziness, fainting, etc. Of course, many of us can tolerate a slower heart rate, it depends on our physical condition and overall health.
It is not clear to me if you suffer from hyperparathyroidism or not. It sounds a bit weird, if you are, why are you ordered to take vitamin D supplements (which increase serum calcium)? Of course, do NOT make changes without asking your doctor, but your serum calcium must be carefully monitored. Too high (or too low) calcium may cause a variety of arrhythmias, including atrial fibrillation.
Atrial fibrillation may have a lot of causes. Most of them are related to structural changes in the left atrium (dilatation or hypertrophy) which tends to worsen BY having atrial fibrillation, which is why atrial fibrillation starts with brief episodes and ends up as a permanent condition. Hypertension seems to be a major risk factor. There are also a lot of non-cardiac causes, such as electrolyte imbalances (calcium especially), excess catecholamines, hyper/hypothyroidism, stimulants, drugs, alcohol. You are right about sympathetic/parasympathetic a-fib, the condition may occur with both. Atrial fibrillation often origin from the pulmonary veins (PACs that origin here can set off atrial fibrillation). If your heart rate is very slow, those "pacemakers" can take over, which is why atrial fibrillation is commonly seen in the setting of sinus node dysfunction (tachy/brady syndrome).
If some of your doctors have suggested a pacemaker combined with increased dose of beta blockers, you may suffer from this condition. The cause can both be within your sinus node, or your ANS. From your blood pressure fluctuations and heart rate fluctuations, it doesn't seem unlikely that you suffer some sort of autonomic dysfunction which affects the sinus node. If so, treatment with a pacemaker can help relieve lots of your symptoms. Of course, I can't say if this is the right treatment for you or not. Your doctors (and you) must decide.
Pulmonary vein ablation means to isolate the electrical activity from your pulmonary veins (so they can act as wild as they would like to, the activity will still not reach your heart) which can cure atrial fibrillation in 70-80% of patients. However, it depends a lot on how your left atrial function is, if your left atrium is severely dilated (you mention elevated NT-proBNP, though not ANP) See:
http://en.wikipedia.org/wiki/Atrial_natriuretic_peptide
If you want to know more about pulmonary vein ablation, please see:
www.hjertecentervarde.dk or www.hjertecentervarde.no (the latter focus more on PVA as 50.000 Norwegians are suffering atrial fibrillation without getting proper treatment). The webpage is Danish and the hospital is located in Denmark.
Sorry I'm not able to provide a better answer, but your question is fairly complicated. Good luck, and please write back if you have further questions!
I am very angry because they kept me in serious atrial fibrillation for six months. I have pointed out the mistake to the hospital, wihtout any answer. I also pointed out the second long AF period, and I am thinking to do a third reproof. AF does not cause symptoms to some people, but my physical performance impared and I had respiratory difficulties.
Sleep apnea was excluded in 2011.
One doctor said that an ablation may be difficult, there may be many focuses of origin of electric currents around the pulmonary veins. Another said that the ablation could be done even at my age. I know that the procedure has many risks. My other diseases also contribute to the risks.
A couple of doctors have suggested an artificial pacemaker with use of a more effective beta blocker or other medicine. I cannot use calcium channel blockers, digoxin or many betablockers. A problem could be that, when effectively blocked, my heart heart beating cannot increase enough during excercise, eg. going uphill or upstairs. The pacemaker could prevent too low pulse. As to betablockers, I think that my heart, or autonomic nervous system tries to work very hard to counter the blocking effect. There is a quarrel, and often my sympaticotonia wins. The cosequence is then tachycardia or varying heart rate.
In 2010 I used Multaq at the end of the AF period. The sinus rhythm could be returned with multaq and electric cardioversion together. Maybe it could have succeeded even without Multaq. I was waiting for cholecystectomia. My liver enzyme (ALAT) increased for some time, but it could not surely be attributed to Multaq. It could also be due to cholelithiasis. After the cardioversion I used Multaq for a couple of months. I had weird symptoms, eg. neck muscle weakness and pain, shaking etc. The Multaq dose was first decreased to half, and a few months later ended totally, because one doctor suspected it as a cause of my cervical dystonia. I don't know whether it really was a cause.
In 2010 one doctor suggeted trying Cordarone. I did not dare to use so dangerous a medicine. I already had pulmonary and thyroid problems, which Cordarone could be able to worsen.
My first AF period began after hard working on a hot spring day. I was thirsty and did not go to drink early enough. When I went to drink, the AF began. The second began when I was in my bed in the morning. I was very relaxed and turned onto my stomack aiming to continue sleeping. The third AF began during sleeping. But I had weird heart beat rhythm possibly for about two weeks before the AF. The two latest AF periods may have begun due to too low heart beating in a relaxed (parasympathetic) state.
Sleep apnea was excluded in 2011.
One doctor said that an ablation may be difficult, there may be many focuses of origin of electric currents around the pulmonary veins. Another said that the ablation could be done even at my age. I know that the procedure has many risks. My other diseases also contribute to the risks.
A couple of doctors have suggested an artificial pacemaker with use of a more effective beta blocker or other medicine. I cannot use calcium channel blockers, digoxin or many betablockers. A problem could be that, when effectively blocked, my heart heart beating cannot increase enough during excercise, eg. going uphill or upstairs. The pacemaker could prevent too low pulse. As to betablockers, I think that my heart, or autonomic nervous system tries to work very hard to counter the blocking effect. There is a quarrel, and often my sympaticotonia wins. The cosequence is then tachycardia or varying heart rate.
In 2010 I used Multaq at the end of the AF period. The sinus rhythm could be returned with multaq and electric cardioversion together. Maybe it could have succeeded even without Multaq. I was waiting for cholecystectomia. My liver enzyme (ALAT) increased for some time, but it could not surely be attributed to Multaq. It could also be due to cholelithiasis. After the cardioversion I used Multaq for a couple of months. I had weird symptoms, eg. neck muscle weakness and pain, shaking etc. The Multaq dose was first decreased to half, and a few months later ended totally, because one doctor suspected it as a cause of my cervical dystonia. I don't know whether it really was a cause.
In 2010 one doctor suggeted trying Cordarone. I did not dare to use so dangerous a medicine. I already had pulmonary and thyroid problems, which Cordarone could be able to worsen.
My first AF period began after hard working on a hot spring day. I was thirsty and did not go to drink early enough. When I went to drink, the AF began. The second began when I was in my bed in the morning. I was very relaxed and turned onto my stomack aiming to continue sleeping. The third AF began during sleeping. But I had weird heart beat rhythm possibly for about two weeks before the AF. The two latest AF periods may have begun due to too low heart beating in a relaxed (parasympathetic) state.
I agree, sooner is better for cardioversion. The longer you are in afib, the harder it is to reverse. I will be following your post and answers as you raise a many pertinent questions. I, too, have wondered why afib does not seem to be taken seriously by the medical community -- it is considered a "stable" condition (compared to what? a heart attack, I guess). My cardiologist says my afib was caused by my sleep apnea that was undiagnosed, therefore untreated, for several years. Good luck to you.
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A neighbor or yours in Norway may be the best to discuss, I expect he will respond shortly.
You raise a number of important/interesting facts, and it does seem little about the cause of AFib is known. In my case it seems likely that an enlarged left atrium - assumed caused by a leaky mitral valve (repaired in 2007) is at least part of the cause. I is a big part of the fact my doctors no longer try to get me back in normal sinus rhythm... I am on "rate control" only. My symptoms are not considered sufficiently grave for a try at repair using ablation - my mini-maze done during heart surgery failed.
It is my understanding that the longer one is in AFib the harder it is to convert. I believe long term AFib - may take years, causes irreversible fibrous of the atrium.
So, sooner the better for conversion. Has ablation been discussed with you - sorry if I overlooked in reading your post..
You raise a number of important/interesting facts, and it does seem little about the cause of AFib is known. In my case it seems likely that an enlarged left atrium - assumed caused by a leaky mitral valve (repaired in 2007) is at least part of the cause. I is a big part of the fact my doctors no longer try to get me back in normal sinus rhythm... I am on "rate control" only. My symptoms are not considered sufficiently grave for a try at repair using ablation - my mini-maze done during heart surgery failed.
It is my understanding that the longer one is in AFib the harder it is to convert. I believe long term AFib - may take years, causes irreversible fibrous of the atrium.
So, sooner the better for conversion. Has ablation been discussed with you - sorry if I overlooked in reading your post..
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