Left to My Own Devices

September 6, 2013

Welcome to my blog.  Let me introduce myself.

I am Edward J. Schloss MD, but I’ve been called Jay all my life.  Online, I’m @EJSMD, and I work as a clinical cardiac electrophysiologist at The Christ Hospital in Cincinnati, Ohio.  Although my primary professional focus is direct patient care, I also do a lot of clinical research with The Lindner Research Center here at the hospital.  I take care of a variety of patients with electrical disorders of the heart, but in recent years I’ve focused most of my practice on the care of patients with pacemakers and ICDs (implantable cardioverter defibrillators).  I implant and extract devices as well as provide the follow up care of these patients.  We don’t have fellows or residents in our lab, so I am the operator for all of my procedure.  I am fortunate to be surrounded by a remarkable team of physicians, nurse practitioners, nurses, technicians, medical assistants, industry personnel and administrators that keep everything running smoothly.  I am madly in love with my best friend Kendahl, and we’ve been married for over 24 years.  We have three amazing children ages 15, 20 and 21.  I have a bio up on our practice website.

Although this blog is just starting (see my prior two posts), I’ve been actively writing about cardiology and healthcare in online and social arenas for a few years.  I’ve considered starting a blog for a while and jump in now with some degree of trepidation.  Left to My Own Devices will serve as a platform for me to communicate issues primarily affecting my professional world.  As the name implies, expect to hear a lot about pacemakers and ICDs and other issues in cardiology.  I do hope, however, to extend my reach into broader arenas of healthcare in which I have passion, such as healthcare policy and electronic medical records.  I’ve already written a lot on twitter about these issues and done a bunch of long form journalistic pieces on Cardiobrief.org or Forbes.com.  For the blog, I’m hoping to find the sweet spot between 140 characters and 1000 words.

I’d like to recognize a few important people who’ve helped me along the way:

–       J. Rod Gimbel MD single handedly started the Cleveland Clinic Heart Center website from the fellows room back in 1994, just before I started training there with him.  Naturally, all but a few thought he was crazy.  Rod showed everyone that the web is a viable platform to “narrowcast” cardiology content to a specialized audience.  He is still breaking down barriers with his research on MRI of pacemakers and I am proud to be one of his coauthors.

–       Wes Fisher MD is a practicing EP in Evanston, IL and truly is the blogfather of cardiology.  He’s still cranking out regular amazing content at DrWes and on twitter.  Wes hosted my first ever blog comment back in 2008 and has continued to mentor and promote me unfailingly since that time.  He is a bold, entertaining writer who knows just how to skate the line between smartass and wise guide.  He’s the guy shining lights into the blind alleys of health care policy.

–       Larry Husten at Cardiobrief, Forbes.com,  Cardioexchange, and twitter is an first-rate real medical journalist who gave me my first break by posting my summary of the St. Jude Riata Lead Summit back in January 2012.  With that offer, I suddenly felt like a legitimate writer.  With his broad platform and wise editorial guidance, I’ve been able to dramatically expand my reach.  He sets a high bar for excellence, and when I send him content, it still kind of feels like Senior English class back in high school.

–       John Mandrola MD is an electrophysiologist in Louisville, KY who blogs at Dr. John M.  John and I started out as “twitter buddies” and now we’re good friends in real life too.  His humanity permeates all he writes, and if you were sick, this is the kind of guy you’d want as your doctor.  It’s flattering to be supported and promoted by such as great guy and insightful writer.

I finally started the blog this week because I really needed to find a home for the the two posts I just published.  For years I’ve had other ideas bubbling up,  and this forum will allow me to decompress.  Since I don’t really have a roadmap built, it still remains to see exactly where Left to My Own Devices takes me.  I can assure you, though, that what you read will be honest and filled with passion.

EJS

September 6, 2013

Echo CRT Trial – Going Narrow Doesn’t Broaden CRT Population

September 3. 2013

A once promising indication for cardiac resynchronization therapy (CRT) in selected heart failure patients with narrow QRS intervals has suffered a major blow with the premature termination of the Biotronik sponsored multicenter EchoCRT trial reported today at the European Society of Cardiology in Amsterdam.

Cardiac resynchronization therapy was developed in the late 1990s as a treatment in patients with systolic heart failure.  A series of seminal trials including MUSTIC, MIRACLE and COMPANION firmly established biventricular pacing as an effective treatment for advanced systolic congestive heart failure by the early 2000s.  The patients in all of these early trials had LVEF <= 35% and wide electrocardiographic QRS complexes (>120msec or more) as a marker intraventricular dyssynchrony that could be improved with CRT.

Later trials including MADIT CRT and REVERSE showed benefit of CRT in patients with milder symptomatic classes of heart failure, but the study populations still required wide QRS complexes and severe LV dysfunction.

Analysis of these and other studies has suggested that the treatment benefit of CRT may be confined to the left bundle branch block population and the most recent US society guidelines for CRT now reflect this, assigning less weight to the non-LBBB wide QRS population.

For years, investigators have suggested that there may be an unmet need for CRT in patients with systolic heart failure who do not have wide QRS complexes, but appear to have treatable dyssynchrony by echo.  Small studies, commonly single center, have shown CRT benefit in this population when pre-procedure screening echocardiography has shown evidence of dyssynchrony.  A larger randomized study RETHINQ, reported in 2007, however, failed to show any benefit in a heart failure population with echocardiographic dyssynchrony and narrow QRS.  Some criticized the study for its design, with particular attention to the type of echo parameters used to define dyssynchrony.  This past February, however, another randomized trial of CRT in patients with narrow QRS, LESSER-EARTH was terminated prematurely without benefit.  This trial, however, did not have any echocardiographic enrollment requirements and was also limited by very slow enrollment (85 patients over 8 years).

One isolated recent bit of supporting evidence for narrow QRS CRT came from the NARROW-CRT trial that was reported this past April. This trial showed benefit of CRT in a small, randomized sample of heart failure patients with narrow QRS and echo criteria for dyssnchrony.  They were randomized to CRT-D vs. D-ICD with minimal pacing.  The biventricular paced group had a significantly higher proportion of patients that improved their heart failure clinical composite score. (41% vs. 16%) and exhibited a trend toward improvement in survival and heart failure hospitalization.

The best, and possibly last remaining hope for the CRT in the narrow QRS population has rested on the EchoCRT trial, which was reported today at the European Society of Cardiology meeting in Amsterdam and simultaneously published in New England Journal of Medicine.  Biotronik sponsored this investigator-initiated randomized, multicenter trial, which began enrollment in August 2008 with projected enrollment of 2330 patients.  Study patients had Class III or IV heart failure with LVEF <= 35%, diastolic LV dimension greater than 5.5cm and QRS duration < 130 msec.  Prior to enrollment, all patients had echocardiography with modern, advanced dyssynchrony measurements including tissue doppler and speckle tracking imaging.   A single core lab at the University of Pittsburgh reviewed all echoes, and patients were enrolled in the trial only if they met predetermined indices for dyssynchrony.  Once determined eligible, all patients underwent placement of a biventricular ICD with blinded randomization to active CRT=ON versus CRT=OFF.  The primary endpoint was a composite of time to first hospitalization for heart failure or all-cause mortality over a minimum of one year.  Duration of the trial was event driven and had been expected to have been completed in December 2012.

On March 13, 2013, the EchoCRT data safety and monitoring committee notified the trial sites that the trial would be terminated prematurely due to futility.  There had not been a public disclosure of this news until April of this year when this was discussed in an  ACC summary of the NARROW-CRT trial publication  and later reported by Cardiobrief.  No details of the trial results were available until this week’s report.

The Echo CRT trial enrolled 809 patients over mean 19.4 months.  The composite outcome of death or heart failure admission was reached in 28.7% patients getting CRT vs. 25.2% of the blinded controls.  There were 45 deaths in the CRT group and 26 in the control group.  Although neither of these values reached statistical significance, it is worth noting that the trial was terminated for futility before comparative power could be reached, and the death data appears to show ongoing curve divergence upon termination of the trial.  When analyzed specifically for cardiovascular death, the CRT group did have statistically significant excess death (37 vs. 17, P=0.004).  None of the nine pre-specified subgroups showed benefit from CRT, and more procedural harm was demonstrated in the CRT group.

After this extremely discouraging, but well run trial, it seems unlikely that there will be a future for CRT in the narrow QRS heart failure population.  Given the current strict regulatory environment, off label implants are likely to be heavily scrutinized and discouraged.  It also seems unlikely that another large-scale trial in this population will be carried out.

 

Although the results of EchoCRT likely eliminates the promise of CRT as a primary treatment for narrow QRS systolic heart failure, the overall field of biventricular pacing continues to advance.  The positive findings of the BLOCK HF trial published earlier this year may lead to an indication for CRT as a preferred pacing therapy in patients with heart block and LV dysfunction.  BIOPACE has a similar design as BLOCK HF and is reported to be in follow up.  In addition, the recently initiated MIRACLE EF trial will look at CRT as a primary treatment in heart failure patients with LBBB and mild LV dysfunction.  The ongoing PROMPT trial is evaluating LV or biventricular pacing as a treatment to prevent adverse myocardial remodeling early after myocardial infarction.

CRT Super-Response and the Power of Twitter

CRT Super-Response and the Power of Twitter

An unusual example of super-response to biventricular pacing and a commentary about real time academic collaboration via social media.
August 30, 2013

  1. What follows is a two day exchange on twitter earlier this week.  What was intended as a quick unknown case for the heart failure device community turned into something a lot more interesting.  Below I’ve organized the twitter posts and responses in the order in which they occurred and then follow with a discussion.  The topic is very specific to the pacemaker/ICD community, but the implications are much more broad.  Stay with me.

    First up is a ECG and electrogram recording from a biventricular ICD case that demonstrated some unusual findings.  I posed the question “What is interesting about this tracing?”
  2. Does anybody with interest in biventricular pacing wanna guess why I think this tracing is unique? twitter.com/EJSMD/status/37…
  3. Shortly after my post, a few folks took the bait and @ replied with their thoughts.
  4. @EJSMD RBBB with RV-EGM coming first… could explain why pt responded? but I don’t know why “super”
  5. @EJSMD despite underlying RBBB, LV activation is late in QRS duration. hindawi.com/journals/crp/2…
  6. Jeff is one of my industry support folks.  He and I have talked about this topic a lot.  He’s really smart and got it right away.
  7. @jvober Jeff, you’re like the smart kid in the front row going “Ooh Ooh, call on me!!” Hang back, let the other kids have a chance. 🙂
  8. @EJSMD why do u Measure the RV – LV interval from onset of RV to peak of LV? Interval seems pretty long
  9. @PAC_Aware The interval measured is called the qLV: Onset of surface QRS to LV lead activation. The LV mark may be a little late.
  10. I offered a study citation for those interested.
  11. Those interested in my CRT tracing may wish to review this study on qLV measurements @PAC_Aware: eurheartj.oxfordjournals.org/content/early/…
  12. @PAC_Aware So do you see what is interesting about this particular tracing?
  13. Below comments reply to those from @tobymarkowitz.  As his account is locked, I am not able to add these to the Storify narrative.
  14. @tobymarkowitz Interesting. We have not systematically evaluated CRT withdrawal in super-responders, but our anecdotal exp. has been poor
  15. The next morning I posted an annotated form of the tracing with an explanation of what was going on that I found interesting.
  16. F/U to CRT case: Here’s a RBBB CHF pt with normalized EF after CRT. Note evidence of LB delay by QLV & old ECG: twitter.com/EJSMD/status/37…
  17. Answer to yesterday’s CRT case up on last tweet: @tobymarkowitz @PAC_Aware @jvober @glibaudio @amcj1 Thanks for you contributions!
  18. Follower @amcj1 found this intriguing and we then passed around a few ideas about these findings and their broader application.  This exchange got me really excited about the power of twitter as a tool for real time academic collaboration.
  19. @EJSMD thank you, it’s very interesting. I wonder if it’s the case to measure Q-LV in every RBBB with low EF to decide BiV implantation
    • @amcj1 BINGO! Sounds like a hypothesis we could test.
  20. @EJSMD I was thinking about that… which catheter though? EP-CS and you measure Q-LV on the lateral/posteroL dipoles? or use a LV catheter?
  21. @amcj1 Currently we use the LV lead. Years ago there was .014 guide wire with bare end that could record EGMs. Very thin EP cath maybe.
  22. @EJSMD using the LV lead is expensive (in Italy, at least) and not so easy to do (long & short sheaths, guidewire, possibly contrast…)
  23. @amcj1 Agree, LV lead should only be used if you are committed to using it anyway. Not good tool for deciding CRT vs. no CRT.
  24. @EJSMD do you think/know if LV on the CS catheter (body) is approximate/correlates with the one on the LV lead (branch)
  25. @amcj1 Not sure, but suspect you’d have to get into lateral branch to know if LV is late. I’ll take a look in future cases.
  26. @EJSMD I’ll check as well we use an EP catheter to engage CS, I’ll record it and compare to the final LV; theoretically, it’s base vs. mid..
  27. @EJSMD .. if you stay at the same level (I mean, posterior vs PL vs lateral).
  28. @EJSMD ok, I better stop to bother you – you intrigued me, though! 🙂
  29. @EJSMD I’ll keep you updated, if you like!
  30. @amcj1 Definitely. Look at QLV times in the main body of CS and validate w lat veins. May be easy way to predict CRT resp in RBBB/IVCD.
  31. Real time twitter collaboration w @amcj1 could lead to a new tool to predict CRT response in non-LBBB. How cool is that? I’ll post storify.
  32. Discussion:

    The case presented is an example of CRT super-response in a patient with right bundle branch block (RBBB).  Let’s talk about the specifics of this interesting case, and how Twitter might be harnessed as a tool for real-time academic collaboration.

    Much of what I present here is true EP weenie stuff and I doubt I’ll be able to make it interesting to all but hardcore device/CHF folks.  Hang with me, though, because there’s a important lesson in here.

     

    CRT super-response has been defined in the literature as a >20% improvement in EF (http://www.ncbi.nlm.nih.gov/pubmed/20382271) or residence in the top quartile of EFs seen in a study population getting CRT (http://content.onlinejacc.org/article.aspx?articleid=1208648).  For my purposes, I like to keep it simple and describe CRT super-response as normalization or near-normalization of LV function after placement of a biventricular pacemaker or ICD.
    Seeing a CRT super-responder is one of the great pleasures in my practice, and I suspect most EPs and CHF doctors who work in this arena would agree with me.  Having been involved in management of heart failure patients for years before CRT was developed, I still find it amazing that you can take someone so sick and make them so much better with comparatively little effort.
    Factors that favor CRT super-response in the previously cited studies include female sex, nonischemic cardiomyopathy, LBBB and wide (>150 msec) QRS interval.  In practice, that is what I’ve seen.  I bet I could host a big picnic with all the happy LBBB non-ischemics we’ve helped by getting their EF over 50%.  On the other hand, the RBBB population doesn’t do nearly as well.  This is reflected in the latest CRT guidelines (http://circ.ahajournals.org/content/126/14/1784.full.pdf html) which assign non-LBBB with QRS <150 to a class IIB indication.
    Intuitively it makes sense that RBBB patients would not do so well.  We believe the main mechanism of CRT to be relief of intraventricular dyssynchrony by pre-exciting a late activating LV wall.  RBBB patients need not have any left sided delay, so it makes sense that many won’t response to LV lateral wall pacing.  We know that some RBBB patients also have co-exiting left bundle delay, and perhaps these will be the patients that respond the best to CRT.
    In the lab at The Christ Hospital, we’ve been using QLV (onset of QRS on surface to LV activation) measurements to define late electrical activation during LV lead placement for years.  We hook up our leads to the EP recording system and display them under the ECG recording.  This allows to easily see what is late when we are picking pacing sites in the coronary veins.  We try to favor long QLV measurements when settling on the pacing site.  It turns out the maximizing QLV with LV lead placement correlates well with favorable long term response to CRT.  I first saw an abstract  on this response from Jag Singh at Mass General.  In the tweets above I cited similar work from Michael Gold and others in the SMART-AV trial (including my old Cleveland Clinic mentor Pat Tchou).
    I’ve been paying close attention to QLV measurements at all of our cases, so when the patient presented above came though the lab for a pulse generator replacement, I was really surprised by what we saw.  Here was a male ischemic RBBB patient who super-responded (EF went from 20% pre-implant to 50% on his most recent echo).  That alone is pretty unusual.  Moreover, when we measure QLV in RBBB patients, we rarely see the LV lateral wall activate very late.  This patient had really late activation of the LV with a QLV, measuring 106 msec or 62% of the total QRS.  This really looked more like a true LBBB patient to me.  When I pulled up the old ECG (shown in the answer slide), it made sense.  This patient presented first as a LBBB patient, but over the years has developed additional RB delay.  In effect the LBBB is hidden by the RBBB.  Certainly the left axis is a clue, that this would be going on, but when I look at QLV in RBBB/LAFB patients, they are still typically very short.
    I put this up on twitter as a fun challenge and to get some input from some of the smart EP folks who follow me.  I’ve enjoyed participating in the unknown cases in the blogosphere (particularly those from Dr. Wes (drwes.blogspot.com).  For such an obscure topic, I was thrilled that a few people took the time to respond.
    After the answer was posted @amcj1 and I traded a few tweets that I thought were really cool.  Bear in mind I have never met or spoken to @amcj1.  Frankly all I know is the he or she goes by CJ and works in Italy.  He or she thought it would be interesting to use this as a tool to predict CRT response in non-LBBB patients.  That was exactly my thought as I prepared the case presentation.  Would the presence of a long QLV be a good way to decide whether or not to place an LV lead in these borderline patients?  We both think that this would be worth exploring.  Over a few tweets CJ and I worked out what might be a practical way to explore this hypothesis.  Maybe getting a QLV from the main body of coronary sinus with an EP recording catheter would give us the information we need to decide whether to go on to commit to an LV lead.  We could get that data quickly and relatively cheaply.  Clearly much more work needs to be done, but I can see the germ of a valuable research study here.
    I’m certain social media has an untapped role in the advancement in science.   In the world of healthcare, we are really only scratching the surface of what is possible.  Imagine Twitter exchanges like we covered above on other difficult topics in medicine.  Through real time collaboration, we could harness the collective intelligence of the many to reach conclusions and create ideas that none of us could accomplish on our own.  No topic is too obscure if the reach of the media is broad.  Social media is democratic in the best sense of the word.  The best ideas will percolate to the top, independent of the usual barriers such as academic status or job title.
    Edward J. Schloss MD FACC FHRS
    Medical Director, Cardiac Electrophysiology
    The Christ Hospital
    Cincinnati, OH
    @EJSMD

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