Aa
PVC's/ PAC's
I'm 33 years old when I was 27 I had a short episode of A-fib my Cardiologist though it was holiday heart. After that short episode I was never troubled by any arrhythmias until three months ago I started having palpatations. My Cardiologist put me on a 24 hour monitor which reveled 20,800 superventricular beats and 1,800 pvc's. All my lab results where normal,nuclear stress test normal,echo normal.My Cardiologist recommeded a wait and see approach since I had no other symptoms. My only other medical problem is HTN for which I take 150mg Avapro.I'm not over weight, don't smoke and don't drink anymore. My question is.
1. Should I consider medication to suppress the arrhythmias?
2. Does this predispose me to going into other A-fib episode?
3. Would sugery be an option should this continue?
Thank you!
1. Should I consider medication to suppress the arrhythmias?
2. Does this predispose me to going into other A-fib episode?
3. Would sugery be an option should this continue?
Thank you!
Pluto,
You always seem to ask very interesting questions! You ask above why PACs often lead to afib. Here's my understanding. To have afib, two conditions must be fulfilled: (1) you need an electrical trigger like the etopic pulse causing a PAC; and (2) you need an arrhythmic substrate (i.e., an atrium that is overly sensitive/susceptible either because of abnormal electrochemistry or size).
(1) Studies have shown (see e.g., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15078396&dopt=Abstract ) that PACs almost always precede the start of afib (I read in another article where 93% of afib cases are associated with PAC initiation).
(2) The electrochemical susceptibilty/sensitivity of the substrate is related to factors such as stress, ingestion of alcohol, imbalance between critical ions (Na, Ca, Mg, K), etc. So a person with PACs would tend to be more susceptible to experiencing "holiday heart" even though their heart might otherwise be "structurally sound".
The other factor that makes the atrium highly susceptible is its size. The normal size range of the left atrium is 3-4 cm. Generally, atria enlarge as time passes (i.e., strong correlation with age, blood pressure, valve problems, etc.). So, if for no other reason, as a person ages their LA increases. AFIB is essentially an oscillation phenomena dependent on the surface area of the atria. Unfortunately relatively small changes in atrial size lead to faily large area differences. A person with an LA of say 4.5 cm has an atrial area that's 65% larger than someone with a LA of 3.5 cm (when the LA exceeds 5, the area more than doubles). So, even if that person's atrial electrochemistry is "normal", they are predisposed to support afib (i.e., the setup of multiple reeentrant electrical wavelets) if they have PACs. In such cases, to prevent afib, the sensitivity of the heart has to be turned way down using antiarrhythmic drugs or if ablation is opted, substrate modification is needed.
Now why doesn't this happen with PVCs? Here I'm not so sure. I would guess it has something to do with the physical characteristics of the atria vs the ventricles. An overworked atria expands while an overworked ventrical thickens so that even when it's outer diameter increases, it's inner diameter may be shrinking. Also, the ventricles are "wired" differently than the atria. The ventricles have three bundle branches while the atrial wiring is far simpler. I suspect that the branching fibers sub-divide the ventricles in a way that makes it more difficult to sustain wavelets. Just a guess.
Tony
You always seem to ask very interesting questions! You ask above why PACs often lead to afib. Here's my understanding. To have afib, two conditions must be fulfilled: (1) you need an electrical trigger like the etopic pulse causing a PAC; and (2) you need an arrhythmic substrate (i.e., an atrium that is overly sensitive/susceptible either because of abnormal electrochemistry or size).
(1) Studies have shown (see e.g., http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15078396&dopt=Abstract ) that PACs almost always precede the start of afib (I read in another article where 93% of afib cases are associated with PAC initiation).
(2) The electrochemical susceptibilty/sensitivity of the substrate is related to factors such as stress, ingestion of alcohol, imbalance between critical ions (Na, Ca, Mg, K), etc. So a person with PACs would tend to be more susceptible to experiencing "holiday heart" even though their heart might otherwise be "structurally sound".
The other factor that makes the atrium highly susceptible is its size. The normal size range of the left atrium is 3-4 cm. Generally, atria enlarge as time passes (i.e., strong correlation with age, blood pressure, valve problems, etc.). So, if for no other reason, as a person ages their LA increases. AFIB is essentially an oscillation phenomena dependent on the surface area of the atria. Unfortunately relatively small changes in atrial size lead to faily large area differences. A person with an LA of say 4.5 cm has an atrial area that's 65% larger than someone with a LA of 3.5 cm (when the LA exceeds 5, the area more than doubles). So, even if that person's atrial electrochemistry is "normal", they are predisposed to support afib (i.e., the setup of multiple reeentrant electrical wavelets) if they have PACs. In such cases, to prevent afib, the sensitivity of the heart has to be turned way down using antiarrhythmic drugs or if ablation is opted, substrate modification is needed.
Now why doesn't this happen with PVCs? Here I'm not so sure. I would guess it has something to do with the physical characteristics of the atria vs the ventricles. An overworked atria expands while an overworked ventrical thickens so that even when it's outer diameter increases, it's inner diameter may be shrinking. Also, the ventricles are "wired" differently than the atria. The ventricles have three bundle branches while the atrial wiring is far simpler. I suspect that the branching fibers sub-divide the ventricles in a way that makes it more difficult to sustain wavelets. Just a guess.
Tony
I have tried to post, but system always says filled quota for the day so here we go.I hope its okay to seek help here.
I am a 43 year old female with a history of sinus tach related to panic attacks. This started 9 years ago and I do take meds for the anxiety. Starting in October I started having bouts of rare PAC's went to the doc, had holter monitor, echo, blood work. Everything looks good.I have had a lot more heart palps this month, they drive me crazy. I do take atenonol 25mg. per day and my doctor increased it to 37.5.
In nutshell I feel this hard beat and then am a bit tachy for a few minutes, this can repeat itself over the next hour. My doc seems to think the palps come then the anxiety comes in.For months I was waking up off and on during the night with a fast heart rate until I began taking my beta blocker in the morning and evening.Now I seem to sleep better but these ugly things (palps) bother me in the day especially if my day is busy and I haven't been eating every couple of hours not eating seems to aggravate all this.
My dad has afib and had a heart attack in October caused by afib/aflutter.My doctor assures me that I am okay. But I get scared everytime I feel that jump in my throat. It is helpful to read that others feel as I do. This has been a stress filled month....could I be hyper sensitive to feeling these right now or does being tired bring more pac's on?? My doctor said we could do the holter again, which I will probably give a try. I also have seen a Natuopath who has put me on magnesuim malate with potassuim. I would eat dirt to stop these. Any hints would be appreciated !!! My heart goes out to all of you.!!!!
I am a 43 year old female with a history of sinus tach related to panic attacks. This started 9 years ago and I do take meds for the anxiety. Starting in October I started having bouts of rare PAC's went to the doc, had holter monitor, echo, blood work. Everything looks good.I have had a lot more heart palps this month, they drive me crazy. I do take atenonol 25mg. per day and my doctor increased it to 37.5.
In nutshell I feel this hard beat and then am a bit tachy for a few minutes, this can repeat itself over the next hour. My doc seems to think the palps come then the anxiety comes in.For months I was waking up off and on during the night with a fast heart rate until I began taking my beta blocker in the morning and evening.Now I seem to sleep better but these ugly things (palps) bother me in the day especially if my day is busy and I haven't been eating every couple of hours not eating seems to aggravate all this.
My dad has afib and had a heart attack in October caused by afib/aflutter.My doctor assures me that I am okay. But I get scared everytime I feel that jump in my throat. It is helpful to read that others feel as I do. This has been a stress filled month....could I be hyper sensitive to feeling these right now or does being tired bring more pac's on?? My doctor said we could do the holter again, which I will probably give a try. I also have seen a Natuopath who has put me on magnesuim malate with potassuim. I would eat dirt to stop these. Any hints would be appreciated !!! My heart goes out to all of you.!!!!
engine1,
Thanks for the post.
Q:"1. Should I consider medication to suppress the arrhythmias?"
In general terms, we consider suppressive therapy for arrhythmias when the total percentage of beats reaches 8-12%. 20,800 beats in a 24 hour period is roughly 20-25% of the expected total number of beats. However, other patient factors need consideration, like symptom status before decisions are made.
Q:"2. Does this predispose me to going into other A-fib episode?"
The answer is that depends on what were the supraventricular beats. If the majority of the beats were from a sustained SVT, then perhaps no. If the majority of the beats were PACs, then perhaps yes. A review of the holter should allow answer of this question.
Q:"3. Would sugery be an option should this continue?"
An ablation procedure is an option for cure of afib in certain selected patients. Ablation procedures use catheters introduced via needle sticks as opposed to direct cutting. Very, very few ablation procedures require general anesthesia, certainly less than 1%.
Thanks for the post.
Q:"1. Should I consider medication to suppress the arrhythmias?"
In general terms, we consider suppressive therapy for arrhythmias when the total percentage of beats reaches 8-12%. 20,800 beats in a 24 hour period is roughly 20-25% of the expected total number of beats. However, other patient factors need consideration, like symptom status before decisions are made.
Q:"2. Does this predispose me to going into other A-fib episode?"
The answer is that depends on what were the supraventricular beats. If the majority of the beats were from a sustained SVT, then perhaps no. If the majority of the beats were PACs, then perhaps yes. A review of the holter should allow answer of this question.
Q:"3. Would sugery be an option should this continue?"
An ablation procedure is an option for cure of afib in certain selected patients. Ablation procedures use catheters introduced via needle sticks as opposed to direct cutting. Very, very few ablation procedures require general anesthesia, certainly less than 1%.
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