Posts Tagged ‘A-fib’

It isn’t working

April 11, 2010

Durn it!

Dronedarone, the Atrial Fibrillation drug that has been highlighted here before, isn’t living up to the hype. It was already known that it is not as effective as Amiodarone, but it doesn’t have the side effects that drug has. The hope was that if you developed A-Fib at an early age, or have a milder form of A-Fib, you could be switched from Amiodarone to Dronedarone. Amiodarone is an effective suppressor of A-Fib but the side effects can be terrible.

In fact, the last time I wrote about Amiodarone, I was accused of using “scare tactics” to get my point across. I wouldn’t do that – Heart Defects areĀ  scary things; As any parent/CHDer knows. I’m not going to add to the hysteria. Behind every link on this blog is more information about a subject; click and read for yourself. HERE is the link I used the last time, it’s written by a Cardiologist. Obviously, he knows more about this drug than I do, and he isn’t a fan of Amiodarone, either.

Further testing has shown that Dronedarone is only half as effective in humans and doubles the rate of death! Dronedarone is recommended only as a second or third choice for people who can’t tolerate Amiodarone. Britain’s National Institute for Health and Clinical Excellence (NICE) gave the drug its approval after originally turning it down, based on its limited effectiveness and its price.

So while Dronedarone doesn’t look like it can be the answer everyone was looking for, perhaps it does have a place in the “medical toolbox”. For right now, the first drug of choice is still Amiodarone, and Cardiac Ablation is still an option.

And other researchers will continue to search for better answers.


New findings indicate source of A-Fib

December 29, 2009

Atrial Fibrillation, or A-fib, is one of the problems many CHDers will face. In a normal heart, an electrical signal is generated by the Sinoatrial node (also known as the SA node and is located near the top of the Right Atrium) and flows outward, causing the Atria to contract. When the electrical impulse reaches the Atrioventricular node, (AV node) it triggers its own electrical impulse which causes the Ventricles to contract, creating the “lub-dub” heartbeat we are all familiar with.

But when extra electrical impulses are moving through the heart’s electrical system, the Atria won’t contract, but rather fibrillate, or quiver. And if the electrical pulse isn’t strong enough the AV node won’t activate the Ventricles. A-fib is usually asymptomatic and painless, (though you can feel your heart beating out of rhythm) but there is a very real chance that the blood pooling in the not-quite-beating upper chambers can clot and cause a stroke.They can also lead to Congestive Heart Failure. (CHF)

One of the usual techniques used to stop A-fib is ablation. Before an ablation, the heart is examined closely and “mapped” to determine where the extra electrical impulses are coming from. Then a catheter is inserted through a vein in the leg or the neck and is guided to the heart. The sources of the extra electrical impulses are then “zapped” (or frozen) to knock them out, and the heart beat should be restored to normal. It doesn’t always work.

But researchers have recently determined that the cells that produce the heart’s electrical charge – and can cause Atrial Fibrillation – also express the protein DCT. DCT only originates from a couple of sources in the body, and only one inside the heart – the electrical current cells. So if scientists can learn a way to identify DCT cells in the heart, they’ll have a way to determine where electrical pulses can orgininate – and deaden the ones causing A-fib.

But this technology is a long way from being reality, if it works at all. Right now, studies are being conducted on mouse hearts. Mouse hearts are similar to human hearts, close enough to be used in research. But when it comes to transferring the results from a mouse to a man, there is a lot of difference!