Aspirin (81 mg) and Atrial Fibrillation

[hugooc]

Hello everyone,

Cynaburst and I have exchanged a few messages about this topic (thank you Cynaburst!), but I thought I should also post this here in case others have more to add.

Here's my question:
What is the ideal way to treat paroxysmal events of atrial fibrillation on patients with HCM?

A brief background:
I was just diagnosed with atrial fibrillation after checking myself into the ER with a strange flutter sensation in my chest. I've had an ICD for two years and know well with how it feels to have ventricular tachycardia (quite common in my case). So, I knew it wasn't VT, but wasn't quite ready for a-fib at age 43. I am, apparently, quite sensitive to it. It bothers me to no end!

At the ER, the ICD was interrogated and it confirmed the onset of AFib last night at 6:37 PM. The report said "EPISODE STILL IN PROGRESS." The plan then became to use the ICD to attempt a cardioversion back into sinus rhythm.

Luckily, a few hours later, my heart converted on its own and I was sent home in sinus rhythm with instructions to take one baby aspirin/day (81 mg) and return if my HR would climb up to 100 BPM. I was also instructed to follow up with my EP in one month.

I obviously do not want to have a stroke. But I also want to avoid taking Coumadin and having my INR checked every two weeks. But my future seems crystal clear. My father lives with AFib and takes blood thinners. My mother also suffered with AFib for many years until her death this past January.

What should I do? Should I be satisfied with this course of action or should I be more aggressive and push for other treatment?

Thanks!
Hugo

[Pam Alexson]

Hi Hugo and I am sorry you have progressed or better yet stated.. your HCM has progressed to this point and onset of paroxysmal a-Fib has started.
I will quote Dr Martin Maron in repeating here what he said to me regarding the same for me. " I have a very low tolerance for a-Fib in an HCM heart."
That said I also have a low tolerance for all that it means and does to an HCM heart over time.
I was quite upset when after having a septal reduction myectomy and only having immediate post-op a-fib that was easily sent packing, that at year 3 post -op this little bugger started to present itself on several repeated occasions. After what I was informed were several self conversions back to normal sinus rhythm from small intervals of A-fib, it soon needed to be driven from me by my device being used or the external paddles..

I scrambled for information and to understand what was happening and what could happen with a-fib. So being clear and understanding Dr Maron's quotation, I called Dr Maron to let him know that I had been having these issues and that I wanted it stopped if at all possible. I did not feel that my EP was as aggressive as my HCM specialist would be and she was not. With my request for help Dr Maron made plans to have me admitted toTufts and I started Sotalol treatment under the direction of an EP whom he worked with closely.. The treatment has done its job and it has been 3 years, 4 in May that I have only had about 2-3 minor breakthroughs per year that were easily sent packing with my medication. Some of them I have known about and others I was unaware of apparently happening when I am asleep.

One thing I had to give into was the use of coumadin... as there was not a safe alternative to stroke risks from paroxysmal a-fib. Dr Maron felt the risk of stroke was a big concern and risk for an HCM heart.. so I have been taking that for over 3 years. The only issue was when I developed kidney stones ad no one seemed to know why I was bleeding and this kept recurring. Finally we saw at least one stone and I theorized that I also had gout and started on allourinol after my PCP listening to me did a test that confirmed it. The allopurinol seems to have kept the stone formation at bay and no more bleeding has taken place.

I did hate going for tests and sitting and waiting at hospitals and doctors offices falling out of therapeutic range over and over... waiting and waiting trying to be a patient and not go off emotionally and verbally due to frequent ineptitudes of so many hands in the pot... so I researched home testing. Lighting a fire under my PCP I got her to follow through with the paper work and I became her first home testing patient. It is convenient and efficient and this way I can test weekly which allows better and tighter controls on my INR and therefor any dietary influences can be corrected or bleeding times acknowledged and doses readily adjusted. I hated that when I ate something it took too long to adjust and I could fall out of therapeutic range for too long..Now I know first and right away and call in the results and the adjustments are expected and easy.

My EP is real strict as she should be and feels if INR is not between 2-3 for a one month duration if I should need cardioversion she will not do it without strict INR between 2-3 or without doing another TEE first to rule out a clot in the atria. My taking control of this has kept things in balance.
So from my story you can derive my opinion. It is your choice but I am pro- coumadin and proactive for finding the best method treatment / medication to keep a-fib away from the HCM heart as soon as possible. A-fib begets more a-fib and negative changes over time on the HCM heart.

Let us know what you do and and how you do... we all learn.

Best to you and sorry once again.
BTW I had taken aspirin for many years even before my diagnosis of obstructive HCM... I did this on my own because of my personal experiences and conclusions as a nurse seeing so many patients who had suffered strokes and had never taken prophylactic aspirin before their strokes or been instructed to do so regardless of their hypertension.
Pam

[Linda]

Hugo - I would call the EP today - why wait one month? He's your managing doctor. Make sure he knows what is going on. We are in the midst of holidays here, and that could slow down reports going to offices from ED's. Better to be cautious and secure than trust to fate.

Best wishes - Linda

[mbcube]

Hugo - Sorry too hear A-fib has visited you. I had a bit of it after my ICD implant & we watched it (and took asprin). When I had my myectomy, I again had a few bouts of it (one lasting 7 hrs) and thats when they decided to switch to coumadin. Now, I was not a fan of it, but having watched my mom become paralyzed, I opted for it. There was some arm-wrestling between my plumber & electrician as to the validity of Coumadin therapy in my case. I then asked my EP to coordinate with my Cardio and IF i was a good boy & had no instances of a-fib for 6 months, can I go off it. I did and know that at any time it could come back and I'll have to go back on it, but for now I'm happy with Asprin. Best of luck on this one & say 'ello to Paul.

[Largehearted]

Hugo.

I was 42 when paroxysmal a-fib hit. They started me on aspirin then. Over the years as more bouts hit, they put me on Coumadin and added an anti-arrhythmic, Sotolol, which has done an amazing job of holding me in proper rhythm. This is not a med without side effects, but a-fib for me was much worse. I am basically non-functioning when in a-fib.

The Coumadin is a pain, but really not all that bad. It sure beats a stroke! I hope you get the information you need to make the best decision for your situation.

Peace,

Leon

[Cynaburst]

Hugo - Glad you are getting a few different perspectives from those who have been there before you.

I am not sure what is the right approach for you to take...maybe aspirin is enough...but I really want you to discuss with your docs SOON (like don't wait a month!) and make an informed decision about the right course of action for you.

It is too late for me to go back in time and prevent my dad from having his strokes, but I can take the knowledge that I have gained from his illness and use it to your benefit.

I know that I have been a bit vocal in your case, but it is only because I care... :)

Take care of yourself friend.

Cynthia

P.S. I myself take 81 mg. aspirin daily and have ever since my myectomy 3+ years ago. I had some transient a fib episodes for a few weeks after surgery which lasted maybe 2 or 3 minutes each and always self terminated. I also have a strong family history of stroke, so I am like a hawk watching out for more. I am lucky that I feel every mistep my heart takes, so I am fairly sure that if I ever have a more substantial episode of a fib, I will feel it.

Another option that is coming into vogue for the prevention of stroke from a fib is the Watchman device which is a little filter that they place in the atrial appendage. It has been experimental, but you may see more of them used in the future as they eliminate the need for coumadin therapy.

[gfox42]

Hi Hugo,
My only experience with a-fib was post-myectomy. A few days after the surgery (while still in the hospital) I started into a-fib, and stayed in it for 4 or 5 days. They got ready to cardiovert me at one point, and then I spontaneously went back into sinus rhythm. And then back into a-fib. And this happened a lot; they decided there wasn't any point in cardioversion since I'd likely just slip back into a-fib. So they started amiodarone and coumadin. Kept me in the hospital a few extra days until my INR got into the right zone. The amiodarone did what it was supposed to, and I was in sinus rhythm by the time they discharged me. So far as I know, I've stayed there ever since.

So I was on coumadin for a few months. No, I didn't like it; both the checking of INR and the bruising were unpleasant. But they both seemed a minor annoyance compared with the alternative. After a few months, my cardiologist took me off both amiodarone and coumadin, since I'd had no signs at all of further a-fib.

I've been on baby aspirin ever since leaving the hospital too.

I can't say that coumadin is definitely the right thing for you, but I suspect that the others are right when they suggest that you talk to the EP as soon as possible rather than waiting a month.

Happy new year!

Gordon

[abilks]

Hugo, I am in a similar situation as you. I've had two bouts of atrial flutter this summer (btw, I'm 29). My defibrillator discharged 9 times the first episode and once the second episode. So, I was in a high rate flutter and for only a minute or so before i was cadioverted. I saw an HCM specialist after the first episode and was told i could do asprin or coumadin, it was up to me. I choose the baby asprin. After the second episode, I asked my local EP while I was in the ER and he said he doesn't push for coumadin unless the episode lasts over 48 hours. I haven't checked back with the HCM specialist, but after reading this, I know I should probably do that.

[Cynaburst]

I think that an episode that only last for a minute or two is of less concern than an episode like Hugo's that lasted for a day or so.

[Pam Alexson]

New Blood Thinner Could Replace Warfarin to Fight Venous Clots
Dec. 7 (HealthDay News) A new blood thinner called dabigatran etexilate may be just as effective in preventing dangerous venous clots as an old standby, warfarin, but much easier for doctors and patients to manage, a new study finds.

Dabigatran is marketed as Pradax in Canada and Pradaxa in Europe; it is not yet approved for use in the United States.

The new study, published early online Dec. 6 by the New England Journal of Medicine, follows on the heels of two other promising reports presented at the American Heart Association meeting in Orlando, Fla., last month. Those studies found that dabigatran appeared safe and effective in preventing blood clots when patients were treated for acute coronary syndrome, a cluster of symptoms that might indicate a heart attack; it was also found superior to warfarin in preventing strokes in patients with the irregular heartbeat known as atrial fibrillation.

In the new trial, warfarin and dabigatran seemed to perform equally well in helping patients with potentially dangerous clots in their veins avoid a subsequent clot or death over the next six months.

But it is in its ease of use that the newer drug appears to outshine warfarin, the authors of this latest study say.

Doctors have for years been looking for a safe alternative to warfarin, which is notoriously difficult to manage.

"For patients and health-care providers, dabigatran is a far more convenient drug than warfarin because it has no known interactions with foods and minimal interactions with other drugs and therefore does not require routine blood-coagulation testing," wrote the international team of researchers led by Dr. Sam Schulman of McMaster University and the Henderson Research Center in Hamilton, Ontario, Canada.

In the prospective trial, which was funded by dabigatran's maker, Boehringer Ingelheim, nearly 1,300 patients who had experienced a venous thromboembolism (VTE) received 150 milligrams of dabigatran in pill form twice a day. Another group of almost 1,300 patients was given warfarin, adjusted in dose to suit their particular needs.

Six months after the therapies began, 30 patients on dabigatran experienced another VTE compared to 27 patients on warfarin, for a 0.4 percent difference in risk, the authors report. Side effects such as major or minor bleeding were similar between the two groups, with slightly more bleeding events occurring in those on warfarin.

Based on the results, the authors conclude that, "a fixed dose of dabigatran is as effective as warfarin, has a safety profile that is similar to that of warfarin, and does not require laboratory monitoring."

Those optimistic findings echo those from the American Heart Association meeting in November. That study involved more than 1,800 patients in 24 countries with acute coronary syndrome -- a cluster of symptoms that might indicate a heart attack. Patients received one of four doses of dabigatran or a placebo on top of aspirin and the blood thinner Plavix.

The study found dabigatran safe in preventing blood clots in these heart patients. Researchers also saw reductions in mortality, nonfatal heart attack and stroke, although the trial was not specifically designed to look at efficacy.

"Dabigatran seems to be safe on top of dual antiplatelet therapy [meaning aspirin and Plavix]," study author Dr. Jonas Oldgren, chief physician in the department of cardiology at Uppsala University Hospital in Uppsala, Sweden, said at the time. "It has already been shown to have superior efficacy compared with warfarin."

And another trial, also presented at the AHA meeting, demonstrated that dabigatran outperformed warfarin in preventing strokes in patients with atrial fibrillation.

"Dabigatran appears to be superior to warfarin in terms of safety and more effective as well. This is the first alternative to warfarin that could signal a changing of the guard," Dr. Bernard Gersh, a professor of medicine at the Mayo Clinic College of Medicine in Rochester, Minn, said during the heart association conference. "I think there are still questions that need to be answered, but it's fair to say that warfarin has been around for many, many years and everybody hates warfarin. Patients hate warfarin. Doctors hate warfarin. It's not the most convenient drug, but it's effective and it is cheap."

"It's premature to say that a drug like dabigatran will take the place of warfarin," Gersh added. "There will be a lot of discussion about cost and convenience. It's a twice-daily dose and there are some questions about a possible higher rate of heart attack. I don't think this is truly resolved yet, but I think we can say that for the first time we have seen a drug that certainly has the potential to be an alternative to warfarin, and maybe even superior."


SOURCES: Dec. 6, 2009, New England Journal of Medicine, online; Bernard Gersh, M.D., professor, medicine, Mayo Clinic College of Medicine, Rochester, Minn.; Nov. 18, 2009, news conference with Jonas Oldgren, M.D., chief physician, cardiology, Uppsala University Hospital, Uppsala, Sweden; Nov. 18, 2009, presentations, American Heart Association annual meeting, Orlando, Fla.

[Pam Alexson]

Blood clot formation:

What causes blood clots?

When the blood becomes thick and the platelets, the clotting cells, tend to stick together, a blood clot forms.

So what causes “thick” blood? Three main things: 1) too much animal fat in the diet, 2) inadequate water drinking (dehydration), and 3) stress.

It’s no great secret that if one pours oil in water, the water becomes thicker. So, when you eat animal fat (meat, poultry, fish, eggs and dairy, such as milk, butter, yogurt, ice cream, cheese, etc.) your blood becomes thicker.

It’s also not surprising that blood becomes thicker when one is dehydrated.

Blood is composed of two general main components: 1) blood cells: mainly red blood cells (rbc’s), that carry oxygen around to the organs and cells, white blood cells (wbc’s) that fight disease, and platelets, that help your blood clot when you are bleeding, and 2) serum, formed primarily from water and some proteins.

If your body is dehydrated, you may not have enough water to make enough serum. But you will still have the same volume of blood cells, therefore, your blood will be thicker! (Same volume of solids - blood cells – but less fluid = thicker blood!)

But the total volume of blood in your body will be less because you have less serum than you should. The body has a splendid detection system for total blood volume. When the blood volume is low because of dehydration, your body produces a substance that constricts the blood vessels so the amount of space in the blood vessels in your body will perfectly fit your total blood volume.

If there were a discrepancy, you could have an “empty space” in your blood vessels, theoretically causing an air embolus, an air pocket that, when traveling through the heart, could cause death. So the body’s mechanism to eliminate that possibility is very efficient.

Thick blood is also one of the main causes of high blood pressure, in addition to the animal fat deposits that cause a narrowing of the blood vessels, termed arteriosclerosis. When the heart has to pump thicker blood through narrower (constricted) blood vessels, the heart must pump at a higher pressure to push the blood through, leading to HIGH BLOOD PRESSURE!


What causes dehydration?

The body loses ten glass of water every day just from the processes of daily living such as, digestion, making enzymes, etc. On hot days or when one is stressed, even more water is lost. If we don’t replace that water by drinking pure water, we will become dehydrated. The body is 75% water and the brain and nervous system are 85% water. Please note that the body is NOT 75% Coke, or 75% coffee, or 75% milk. It is 75% WATER!

WATER is needed to replace the WATER losses!

The main causes of dehydration are:

1) Caffeinated beverages such as coffee, tea, caffeinated soda, and chocolate. These take more water out of the body than comes in with the drink.

2) Drinking alcohol of any type causes dehydration.

3) A diet high in protein causes dehydration. Protein digestion requires a lot of water, that’s one reason why high protein diets cause weight loss. Americans eat about four times more protein than they need each day, which encourages diseases such as heart disease, high blood pressure and strokes (blood clots to the brain), all types cancer, osteoporosis and many other serious and/or life-threatening diseases.

4) Stress causes dehydration – and dehydration also causes stress to the body. When one is stressed, increased water drinking is mandatory. Extreme stress, however, may override the ability of increased water intake to compensate.