Melissa you seem to be overly defensive and that is what I take out of this blog.  You treated an adult who had the opportunity to behave like an adult.  You educated him with regards to his treatment and the importance of compliance.  He had a rare side effect of cardioversion and now you seem to think that the burden of proof of compliance is your own.  It may be - and if this comes to litigation that may be what decides a decision of 12 unqualified individuals.  Thank you for sharing this because there will be no cardioversions that I perform on Pradaxa unless a separate disclaimer is signed by the patient to say that embolic events are not predictable on this medicine given the lack of proveable anticoagulant activity.  Thank you again.

Sara,

I appreciate your comments. I really didn't mean to convey a defensive posture. This patient and I enjoy an excellent relationship despite his non compliance and occasionally short fuse.  Even if the patient was not compliant, it may be that he did the very best that his capabilities allow him to do. Not everyone is blessed with the same ability to manage such issues. I believe your suggestion to obtain a separate disclaimer is actually covered by any standard cardioversion which states clearly that stroke is a possibility but you can never have too many disclaimers or too much documentation I suppose! 

Melissa

Just out of curiousity, why the cardioversion in the first place?  It didn't sound like he was having disabling symptoms from his atrial flutter.  Why the anti-arrhythmics?  We now know that rhythm vs rate control has no role even in patients with depressed LVEF (I believe it was Denis Roy's trial that showed us that - http://www.nejm.org/doi/full/10.1056/NEJMoa0708789).  Was the cardioversion and anti-arrhythmic therapy done for symptoms, prognosis, reduction of medications in a non-compliant patient - to keep him in sinus rhythm, and for what purpose?

As you know, I am not a cardiologist, but always willing to learn.

 

Dan 

Great question Dan,

Though the mortality data demonstrates no difference in sinus vs. atrial fib, the quality of life indicators are often better in those with sinus rhythm. I believe his last admission was for chest tightness and shortness of breath which precipitated an ER visit. (yep, quitting smoking might just help better than 50 Joules! and last longer too!!)

Thanks for posting,

Melissa

Hi Melissa

 

Writing from the other side of the pond(UK) it seems to be a different world over there(well it is , it is not socialized medicine as we know it in the UK). Free from the constraints of financial pressure, therefore I am not sure i would have been brave enough to cardiovert this patient on pradaxa. I have seen strokes on well coagulated patients on warfarin and even occ in TOE patients to attempot it without the good old warfain for 6 weeks wiht good INR control. The statement about TOE is also disquietening for us over here- A TOE is not without its risks  and one cannot be blase about this. I would rather 6 weeks of OAC rather than TOE if I had a choice. Anyway pardon the moral lecturing - im sure a retroscope is a wonderful thing.

 

Kumar

1.  Pradaxa in RE-LY showed fewer post-cardioversion CVAs compared to coumadin.  Event rates were small but this data is good enough for me.  The data for coumadin vs TEE is largely based on PRO-TEE (which wasn't that much or a larger cohort). 

 2.  Melissa-I see no issues with anything you did.  Would you consider yourself at blame if a patient stopped Plavix after he said he would be compliant and you implanted a DES?  Just b/c you hit a button, not sure much changes.  You reviewed risks and asked pt direcly about compliance.  Adults need to take some responsibility.  If you TEEd pt and had complication, that would have been a bigger (and avoidable) complication in my mind. 

 

3.  Dan-AF-CHF and AFFIRM are great trials but some pts fail rate control (too symptomatic, tough to rate control, soft tachy-brady who might do better with rhythm control then an immediate PPM, etc).  All AF-CHF, etc tells us is an initial strategy or rate control is just as good (maybe even better based on hospitilizations).  Not sure about this patient but from someone who rarely employ rhythm control, you have to admit a small percentage or patients greatly benefit.

Rob,

I appreciate your post. I always regret any poor outcome in any patient under any circumstance, as any physician and just try to replay every conversation, every visit, etc. to examine whether I could have said anything differently to motivate or inform this patient more effectively.  For some, it's nearly an impossible task but every case is worth a re examination. 

Thanks

Melissa

Rob, patients who fail rate control or are extremely symptomatic warrant referral to an EP specialist. I would leave management in their hands - pharmacological or electrical therapy, or whatever they prescribe. But such patients are the rare minority. Most people deserve a trial of rate control and anticoagulation first - many anti-arrhythmics are toxic, something that cannot be said for our modern beta blockers and calcium channel blockers (ie rate controllers).

Dan,

In our area, patients who fail rate control or are symptomatic are just referred to a general cardiologist. We will then load the patient with meds and then cardiovert, or change their meds for rate control.  We only tend to utilize an EP if we need an ablation procedure or further recommendation for medication changes.  I rarely refer early to an EP unless the patient expresses a desire to avoid certain meds or if we have failed multiple meds. Very rarely, I've requested an AV nodal ablation ( around three times that I can recall) but I utilize afib ablator(s) fairly frequently with good success.

Thanks for your post

Melissa

AF is not an EP disease.  With respect to all of my EP partners, I only need them if AF ablation is in the discussion.  We all train in antiarrhymics management.  It isn't an EP only disease, much as CAD is not an interventionalist only disease.  My average patient with LVH, CAD and LVSD is going to have limited optoins to even choose from with regards to antiarrhytmics.  It's much more straightforward than many things.

 To say that nobody benefits from rhythm control based on AF-CHF is akin to saying nobody benefits symptomatically from revascularization based on COURAGE.  I've read the data and heard the arguments.  I'm sure 95%+ of my patients are managed with rate control, probably more.   That being said, I'm sure if you wake up one day with highly symptomatic palpitions and pAF with RVR (with rates then in 50s when you're in sinus), you'll welcome that flecanide, Tikosyn, sotalol and even amiodarone are options, despite their "toxicity".  

The majority of AF patients are well-managed with anticoagulation + rate control.  I agree thatsymptomatic pAF patients (not the case that was posted here) certainly benefit from a rhythm control approach in terms of QoL, but probably not for mortality or stroke prevention or EF preservation (or any of the many reasons that have been put forth to support the superiority of rhythm control).  Medicine should also be personalized to the patient and trials not blindly extrapolated from.  By the way, I'm not sure why you (?sarcastically) put toxicity in quotes.  AFFIRM and other trials do suggest a higher incidence of hospitalizations and probably mortality too (if you look at the trends) from the anti-arrhythmics being applied in these trials (similar, no doubt, to the anti-arrhythmics being applied in practice).

I agree with the colleagues - about the real indication of cardioversion... I did not see the patient, but if he was stable with rate control, had no severe congestive heart insufficiency... As mentioned, mild cardiomyopathy, age 68 years, not younger... The guidelines are documents do "guide", we need to individualize each situation, and in this case just oral anticoagulation and rate control - I believe the two points would be resonabvle. Indeed, I do not trust in any 6-8 weeks of oral anticoagulation, even with warfarin, to say 100% of safe cardioversion... Medicine is not as Maths, an exact science. So, complications may occur... I love your post! Rgds Mara

Melissa,  Thanks for posting this interesting case.  I too agree with those who came to your defense and pointed outplace that you should not be responsible for having to confirm that what the patient tells you is factual.  I do, however, have two additional points to raise:

(1) Is the patient on anticoagulation now and, if so, what agent?

(2) Wouldn't it be nice if we could solve the VKA management problem?  The drug itself is very safe and effective if we could just find a quick and easy way to keep the INR in range....right?

Based on 4 small studies that we and 3 other groups have done (see Bussey, HI. J Thromb Thrombolysis 2011; 31:265–274), INR self-testing (as covered by CMS) with online management requires 10 min/wk for the patient and < 3 min/wk for the clinician to achieve a level of INR control of approximately 80% time in range while virtually eliminating INRs at the extremes (< 1.5 or > 5).  And, it can be performed from anywhere in the world with internet access.  A frequent challenge to this approach is "the lack of internet access" but, in fact, 75% to 82% of U.S. households have internet access (see http://www.webpronews.com/topnews/2008/05/14/18-of-us-households-have-no-internet-access. http://www.marketingcharts.com/interactive/home-internet-accessin-us-still-room-for-growth-8280/nielsen-internet-access-household-income-February-2009jpg/. and http://www.internetworldstats.) - and access can be gained from most hotels, internet cafes, and cruise ships.   Further, in our experience, those patients who do not have internet access at home often have a neighbor, friend, or relative (often the same person who drives them to the anticoag clinic) who is more than happy to assist the patient with the online "virtual visit".   In our own study, the Duke Anticoagulation Satisfaction Survey data indicated a strong patient preference for this type of management (vs usual or clinic care).  Perhaps the most telling question was that only 62% of patients at the start of the study indicated that they would recommend anticoagulation to a friend with their same condition.  But after 3 to 6 months on self-testing with online interactive management, 100% indicated that they would recommend such therapy to a friend with their same condition.

In concern of the Re-Ly cardioversio sub-analyze, I have doubts about 6 cardiovasculars deaths that occurred on the 30 days after cardioversion. I didn’t find any information about wich therapeutic group, these patients were allocated. If we suppose that all these deaths might be due to a tromboembolic event, depends on wich therapeutic group they occurred, the safety of Dabigatran for cardioversion may change dramatically.

2 points:

1. The 2006 AHA recommendation for anticoagulation prior to cardioversion is 3 weeks (as per the ACUTE trial in the NEJM 2000), then 4 weeks after.  I don't know that 6 weeks prior is any better.  It's certainly more difficult and makes non-compliance more likely.

 

2. If he just had flutter, an ablation would be a reasonable, and more definitive approach than a cardioversion.  Also it would obviate the need for long term anticoagulation.

Melissa,

 Your blog is always informative and often provocative. Today is no exception. Thanks for sharing. I'd appreciate if you or one of those posting above could share any information or references on Pradaxa and PTT. My daughter has been on Coumadin for 20+ years with 2 peripheral embolic episodes and episodic lapses into atrial fib with cardioversion. She has hypertrophic cardiomyopathy and usually good rhythm control on Multaq. Her cardiologist has been reluctant to switch her to Pradaxa because of the lack of measurement tools. Though I never practiced cardiology, I've nonetheless been actively involved with my daughter and her cardiologists in discussions and clinical decision making and remain a bit at sea re Pradaxa. Thanks for any information.

Another excellent blog post, as usual.  I'm wondering if you or any others are utilizing thrombin time for Pradaxa "monitoring"?

Pradaxa,like Coumadin is an anti coagulant.As such,it has the property of potential:"consumption coagulopathy/ITP".The issue is not the potential stroke,but prevention of arrythmias that leads to this cascade of events.It is my opinion is that maintaining an optimal Lipoproteins statusis the"Name of the game".I would start with H.D.L. control through lifestyle modification and Niacin IR(Immediate release).I am aware that I opened a big"Padora Box".People are wellcome to discuss.

D,thanks for your post.

though I can't advise you with regard to a decision, I can speak in general regarding the topic. Pradaxa is a Godsend for those who have ridden a veritable Yo-Yo with regard to their INR control efforts. There are intelligent compliant folks who work hard and whose schedules simply won't accomodate an INR in the physician's office. I have a couple of folks doing their own INR"s at home and are doing well.  One patient, however,  could never figure how to make the machine work so they sent it back to the company.  If one could do their own INR, I think that's the best monitoring effort the warfarin world has to offer. The THINR's trial did not really reflect a comparison with real world experience with INR monitoring and therefore home monitoring was deemded non inferior.

We are still in the learning curve with Pradaxa, though it's getting better. The most significant hurdle is the lack of monitoring, to which you alluded.  Though a  PTT is probably better than nothing, I think that should have been exquisitely ironed out before this drug came to market, or the FDA should have burdened the company to develop a monitoring tool that would be mass marketed at the same time it came onto the market.(Hey America, yet another opportunity to squeeze cash out of our ailing population, what gives? What's taking you so long?) We have no guarantee that FFP will work to reverse its effects, but it's still given for those who don't have time to "skip a couple of doses of Pradaxa".  We also must respect the GFR of any patient considering surgery and skip three to four days, but as I've asked many times, is it three or is it four days we skip? Who knows.  

I think if I were given the choice, from a purely personal perspective, I have a normal GFR and very busy person, I'd probably take one of these drugs to avoid INR debacles.  I think where we are going to see more and more problems are in the elderly.  I'm seeing gut bleeds and bruising even in patients whose GFR's are  projected as normal and even at low doses.  It seems that what we can conclude from those patients is that many of them have never had their INR to remain in the therapeutic range for any length of time, therefore, their coagulation system and bleeding tendencies have never truly been challenged.  If you swallow a Pradaxa tablet, you are anticoagulated and you will stay anticoagulated for the duration until you miss it.  

 Most of my patients totally love it and are doing well.  

I appreciate all of your posts and believe this interesting discussion is very beneficial for practitioners as well as patients who might be considering a switch. 

Melissa

Hello form the Middle East.

Thank you for these discussions, I personally learn from them alot in particular comparing different factors in clinical decision making that vary across continents (and sometimes within the same).

 2 points:

1- For us were getting the patients to present to the Coumadin Clinic is a challenge, I am sure Pradaxa is a Gift from Above.

2- On the other hand, I totally support the idea that we need to put in some safety guage before cardioversion on Pradaxa like PTT. This can serve:

a- an audit for compliance

b- and more importantly, I would hate to live a plavix-resistance like recurring story secondary to genetic variations on Pradaxa (speaking of hindsight).

thanks

Great post Melissa , you really have done good job pouring your heart writing this post almost in 3 or more dimentions.I wish I saw which specific med combination he was on.This coment is of course in retrospect and some of us have been old fashioned so pardon me if I do not use sophiscated words. I feel this soul has been at high risk for cva for multiple reasons.He just timed the stroke so well  and tasted your kind hearted helping hand.I do not know if he continued to drink recently.If he was, there were 2 reasons coming in the way of elective cardioversion.Underlying severe lung disease itself could be important cause of the dysrrythmia and disqualify him for conversion.If one uses antiarrythmic in a pt. not varifiably anticoagulated------high risk situation esp. at cardioversion and for that alone-----tee is a must even if one has gotton away with it so far.Here he was not stable for tee so why convert him.Because of underlying major lung problem esp. if he is drinking-----high risk of reoccurence of atr. flutter/fib. ----so not a candidate for cardioversion.I do not think he was suitable for ablation either.Just my thoughts.Never hurry up to cardiovert unless hemodynamically compromise evident or symptoms suggestive of that.You can always think about it when dust settles.Thanks for your time.I keep on learning.

Melissa, thanks so much for sharing your tips on prescribing Pradax (as it is known here).  The main problem with prescribing it locally is that no one can seem to afford it.  The government has not yet approved it in our low income and senior populations.  The only people who therefore can get it are those who will pay out of pocket or have private insurance plans, and those are few and far between in the type of people who need it (people who have had a stroke from AF and are off work; seniors with AF; etc).  It is however a major advance over warfarin with fewer systemic bleeds, fewer ICH, no monitoring, immediate anticoagulation, few drug interactions (other than P-glycoprotein-excreted drugs), little diet interaction, and lower rates of embolic stroke.  Other than the price, what's not to love? (yes I know, lack of monitoring can also be a burden as well as a boon)

Gentlemen,

Your thoughts and comments are appreciated. Dan, I'm suprised you don't have government approval yet. I would think the cost of bleeds/INR monitoring and strokes would have made it a bargain, but we are still in the infancy of prescribing this compound, so it may be a while before it proves its muscle. 

Hussain, what are the affordability factors in the middle east?  

Hans, you make some great points. Hind sight....wish I could purchase some of that before hand?  : )

Melissa

Melissa,

Very interesting piece bringing up issues not generally considered until "it happens to you."  The use of a PTT before cardioversion is a nice way of determining compliace (at least recent) much the same as many of us use the PT/INR prior to cardioversion.  I agree with you that Pradaxa is a convenient, interesting drug, but also has many of its' own issues we are just beginning to be confronted with.

 In the short time the drug has been available, I have seen two large GI bleeds in patients who were on coumadin for years without problems.  Ditto for GU bleeds.  The dyspepsia issure, even with food, is not inconsequential either.

A helpful, very user friendly drug, but certainly not without much though which you have illuminated in your vignette.

 Thanks, very well written and appreciated,

 Mark

Thanks so much Mark. I think it's an important discussion and glad you have participated!

Melissa