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Arrhythmia Management 

Atrial fibrillation is associated with double the mortality rate per year, a three-fold increase in cardiovascular mortality and there is an increased mortality even in lone atrial fibrillation which is atrial fibrillation that we define as being present in the absence of other underlying disease or pathology. So these are people with normal hearts. They are not hyperthyroid or arrhythmia, atrial fibrillation, atrial fibrilation, atral fibrillation.

We talked about stroke risk. Paroxysmal strokes, a one to two-fold increase over the general population. So paroxysmal atrial fibrillation, short duration, has a slight change in risk. Nonrheumatic heart disease, a five-fold increase in risk. So if you have heart disease, the risk is substantially

What are the etiologies? When we look at this, I think it is important to keep these things in mind. The number one cause associated with atrial fibrillation, and I think itís probably causative, is hypertension. Hypertension causes the left ventricle to hypertrophy and thicken, makes it stiffer, makes the pressures in the left ventricle go up. The left atrium is integrally attached to the left ventricle. Increased pressure in the left ventricle leads to increased pressured in the left atrium. That causes it to stretch and dilate and it causes it to lay down additional fibrotic materials. That leads to atrial fibrillation.

Ischemic heart disease. Itís not the way that we sometimes get our students to think about it which is

Clearly, COPD is a cause, especially when you get to cor pulmonale. Rheumatic heart disease, AV valve insufficiency. Anything that causes the atria to stretch and dilate is associated with atrial fibrillation. Thatís an easy way to think about. "Gee, pulmonary hypertension leads to RV enlargement

Clearly, pericarditis should be considered in new onset of atrial fibrillation. Congenital heart disease can be associated with it. Alcohol is something you ought to question about when you see a patient with new onset atrial fibrillation. This is called the "holiday heart" syndrome. Alcohol, in certain people, is a direct toxin. It was discovered actually by some navy physicians. It seems that after youíre out on a ship for about six months and you

Thyrotoxicosis is listed as a cause of atrial fibrillation and even I look at this. Now, you have three choices in a hierarchy. You have euthyroid, hypothyroid and hyperthyroid. The number one presentation in someone with atrial fibrillation when you check a thyroid is what? Euthyroid. Whatís

Again, if you have fulminant hyperthyroidism, you have that velvety skin, warm perspiration, hyperreflexia, heat intolerance, etc, yes. That can stimulate the heart to high output in atria fibrillation. Then one of the more common causes that we look is lone atrial fibrillation. Lone atrial fibrillation

When we look at what produces symptoms with atrial fibrillation, three things can cause it. Loss of atrial function, rapid ventricular response and irregularly irregular rhythm. All of these reduce cardiac output. Before I develop a treatment strategy, this is really the crux of what Iím trying to figure out. Is it loss of atrial function? If so, I need to restore atrial function. Who is going to be susceptible or require atrial function? Patients with stiff

Rapid ventricular response. If their problems are related to a fast heart rhythm, then by controlling their heart rhythm, their symptoms will dramatically improve.

What about irregularly irregular rhythm? This actually has been documented to decrease ejection fraction and cardiac output just by having the variability. So we have to look towards regularization. Now, if you think about this, sinus rhythm gets rid of all three of these problems. Chronic atrial fibrillation can lead to AV valve leak and ventricular dilatation which leads to further aortic valve leak which leads to

It is not good, however, to look at the left atrial appendage for clots and it is good for looking at with Doppler but not of the left atrial appendage. So if you have someone with embolic disease, the right answer is to look for transesophageal echocardiography not transthoracic. Transesophageal is

What about stroke prevention? We said atrial fibrillation is bad and it is bad for two reasons. It increases your risk of stroke and it may be associated with increased mortality from dilatation of the heart. That is still being worked out. There has been at least six studies now looking at anticoagulation versus placebo.

When I went through medical school, and even during my cardiology fellowship, my approach to atrial fibrillation was based on science. That science was if I had a patient who came in with atrial fibrillation who had a stroke, I then anticoagulated everybody that followed until I had a significant

Now we know that there is a different approach to this. We need to go with stroke prevention and the way to do that is with Coumadin. This is actually one of the trials that looked at a range of 1.5 to 2.7. Right now, in 1998, we know that we should keep our INRs between 2 and 3. Knowing that and accomplishing that are two different things. Anybody who prescribes rat poisoning Ė and itís always good to tell patients that. In

So weíre going to measure a protime to keep the INR. Even in the best of scenarios, youíre only likely to keep them in range 50% of the time. Thereís a whole science and Iíve been really trying to work out how we could do this more precisely but itís very difficult because there is lots of variability in this.

If you go below 2, there is increased risk of stroke that is related to how much below 2 you are. So 1.5, as an average, is significantly more likely to have a stroke. Above 3 the risk of intracerebral bleeding goes up dramatically. So we try to keep that in that range so you have to kind of balance back and forth the relative risks and benefits.

Aspirin. There are some trials that suggest that aspirin is effective. Weíll go through some of my recommendations as we get a few more slides in and placebo but this is what the Copenhagen trial did was these numbers. In that trial, they had 1,007 patients randomized, 335 patients to Coumadin, 336 to aspirin, 336 to placebo. The number of embolic events were 5, 20, and 21. Guess what? That was statistically significant. The SPAF trial out

One of the things with these trials is you donít need a million patients to figure out that this is a difference. We also know that stroke, for most of our elderly patients, is the thing they desire least. There are basically three things that can happen and when I talk to patients, especially with life threatening arrhythmias, they donít mind dying so much as they fear being disabled and being a burden. By preventing strokes, weíre really

What about control rate in anticoagulate versus maintenance of sinus rhythm? There are several trials going on right now. The largest in the United States is called the AFFIRM trial. That trial will be out probably in the year 2005. That is to look at these two issues. Now, I will tell you as

There was just a recent trial out in, I believe, the New England Journal of Medicine in the last two to three weeks that looked at low risk patients. Those were actually, they said, patients who were 65 without significant hypertension who had no previous strokes and who were women who were

So you have to balance between the two of those. The risk of having an intracerebral bleed is about 1.5% per year and as you get older, into your 80s, that risk goes up. In your 60s, that risk is lower. You need to put that into your equation when deciding about anticoagulation. So if someone has atrial fibrillation with significant LV dysfunction and congestive heart failure, has long standing hypertension, Iím going to tend to anticoagulate those people because they are at increased risk. If someone has had an embolic event, Iím going to treat those people.

Typically, when I try to restore sinus rhythm, I keep them on anticoagulation for four weeks before and four weeks after therapy. The reason for 

This, again, just kind of came to me when I had a physicianís wife in who had had atrial fibrillation and I said, "Gee, weíve got to get this taken care of. You need to come into the hospital and weíre going to start anticoagulation." Then once I got her in, I said, "Well, why donít we use low molecular weight heparin" because she complained about having a lot of friability and having difficulty drawing blood. I said, "Well, gee, if we use enoxaparin, we donít have to follow your PTT." Then I said, "And if weíre not following your PTT and you donít have an IV, you probably donít even need to be in the hospital." That really has been a 

Digoxin is not effective in converting atrial fibrillation to sinus or controlling rate with exercise. We talked about that before. Rate control versus maintenance of sinus rhythm is an issue that is up in the air. It is not wrong to control rate in atrial fibrillation although, again, my preference is

One other point before I get off of this that I think is important because it came up yesterday as a question, antiarrhythmic agents for the treatment of atrial fibrillation have been associated with an increased mortality on retrospective meta-analysis. Quinidine and most of those typical agents have been found to increase sudden death mortality. When the SPAF investigators looked at this retrospectively what they found is that people with left ventricular dysfunction were the ones at highest risk. Again, if you have someone less than 40% EF and they have a history of heart failure, those are the people I will use amiodarone as my first drug of therapy for the atrial fibrillation control.

If I am treating everybody else, I will typically use drugs which are safe, well tolerated and effective. For me, that generally is propafenone or quinidine first, sotalol as a second line drug and then other drugs. You can use procainamide and I will use procainamide for elderly people who have

Other drugs such as flecainide is a very potent drug to get them out of atrial fibrillation. In truly normal hearts, i.e. those without left ventricular hypertrophy, itís a pretty good drug. So in a young healthy person I will use flecainide Tambocor as a treatment.