Paul,
I am afraid also like you in start using the amiodarone. My doctors decided to use it in my first a-fib episode. Since I am tolerating well this a-fib, I've started the load phase (400mg/day) before the CV scheduled for June 20Th and if I return to sinus rhythm (I hope so) the dosage will be decrease to 200mg daily.
I'm only 30 and that's clear that long term using amiodarone is not good. My setpum is about 28mm and have no obstruction at rest and about 5mmHg at 120bpm. My mitral regurgitation in classified as "discrete". I'm often questioned about to have a very thick septum but with no obstruction. The reason for this is that the hypertrophy is mainly at septum's base (far from mitral valve). The posterior wall also have normal thickness (about 10mm). I have questioned my doctors also to evaluate if some invasive method (like myectomy) would be useful in my case to decrease either the diastolic dysfunction and the atrium diameter (mine is 47mm) as a consequence. They discarded this possibility because it's only used to obstructive patients.
The reason they have to decided put me on amiodarone is because it's more efficient to prevent a-fib recurrence. After my CV I will start to use experimentally an AT1 antagonist since researches in some countries (Brazil included) with non obstructive patients have shown about 10% decreasing in atrial diameter after 6 months with this med. If this happens also with me, they will also can take off this medicine with a higher probability that it will not return.
So I think there is some relationship between atrial diameter and a-fib but I don't know if it's the only one. The other interesting question to help answering the first is there is some researches showing if myocytes disarray and interstitial fibrosis in only present in the hypertrophic areas or in the whole heart of a HCM person.
Unfortunately there are more questions than answers...
William.
I am afraid also like you in start using the amiodarone. My doctors decided to use it in my first a-fib episode. Since I am tolerating well this a-fib, I've started the load phase (400mg/day) before the CV scheduled for June 20Th and if I return to sinus rhythm (I hope so) the dosage will be decrease to 200mg daily.
I'm only 30 and that's clear that long term using amiodarone is not good. My setpum is about 28mm and have no obstruction at rest and about 5mmHg at 120bpm. My mitral regurgitation in classified as "discrete". I'm often questioned about to have a very thick septum but with no obstruction. The reason for this is that the hypertrophy is mainly at septum's base (far from mitral valve). The posterior wall also have normal thickness (about 10mm). I have questioned my doctors also to evaluate if some invasive method (like myectomy) would be useful in my case to decrease either the diastolic dysfunction and the atrium diameter (mine is 47mm) as a consequence. They discarded this possibility because it's only used to obstructive patients.
The reason they have to decided put me on amiodarone is because it's more efficient to prevent a-fib recurrence. After my CV I will start to use experimentally an AT1 antagonist since researches in some countries (Brazil included) with non obstructive patients have shown about 10% decreasing in atrial diameter after 6 months with this med. If this happens also with me, they will also can take off this medicine with a higher probability that it will not return.
So I think there is some relationship between atrial diameter and a-fib but I don't know if it's the only one. The other interesting question to help answering the first is there is some researches showing if myocytes disarray and interstitial fibrosis in only present in the hypertrophic areas or in the whole heart of a HCM person.
Unfortunately there are more questions than answers...
William.
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