DAPT -Dual anti-platelet therapy has become a standard in many clinical situations of CAD.There has been significant confusion about ,Indications, best combination, duration of DAPT, withholding of DAPT, conversion to MAPT (mono) etc.The JACC september 2016 issue brings much needed clarity on this issue.
Link to key summary from NEJM journal watch.
http://www.jwatch.org/na42407/2016/09/28/update-dual-antiplatelet-therapy-patients-with-coronary?
Full text guideline
Posted in acute coronary syndrome, anti platelet drug, cardaic pharmacology, Uncategorized | Tagged aspirin vs clopidogrel in post pci dapt vs mapt, current guidelines for dapt after pci, dapt, dapt what is it ?, focused guideline for dapt after pci des bms, jacc 2016 dapt, Levine GN et al. 2016 ACC/AHA guideline dapt, nejm dapt guidelines | Leave a Comment »
How do you evaluate the success of thrombolysis or primary PCI ?
If you say its coronary angiogram and the final snapshot of TIMI flow , you need to read further. If you thought its actually the quantum of ECG ST regression . . . great , you can exit this page with credits.
CAG may not be the gold standard in defining PCI success , it just tells you whether IRA is patent or not .Instead , the good old ECG tells you about whether the myocardium is successfully reperfused or not . TIMI flows are simply not good enough to identify adequacy of myocardial reperfusion .
By the way , who is telling this ?
It appears there is only a narrow gap between Ignorance and Knowledge !
That’s what the simple message I got from this landmark study published in year the 2000 in JACC by Shah.A in the thrombolytic era.The Importance of this paper has far reaching consequences (If and only if we are willing to accept and understand the concept and apply as a whole in PCI era )
While success of thrombolysis is faith fully subjected to the acid tests of myocardial perfusion , primary PCI is rarely ever assessed in terms of ST segment regression.
What is the next logical step this study should lead us to ?
I think I am not provocating , . . How to get rid of the prevailing practice of jacking up the success rate of primary PCI ? ( Conveniently, Ignoring the echo detected significant LV dysfunction on follow up ) Mind you, this has resulted in creating a new crop of patient sub group called “Angiographic success and myocardial failure”
Reference.
Dear colleagues , please go thorough this article . Its from the thought leaders , Duke University ,North Carolina. I would argue the cardiology fellows to discuss this paper in detail in their journal club as “classic paper” till they completely understand the conclusion .Though its done with GUSTO 1 data in primarily lytic population, its conclusions are very much valid as an assessment tool in reperfusion by any means.I am afraid, even 16 years after this paper got published ,the truth has not penetrated to the targeted population within the cardiology community.
Posted in STEMI, STEMI -Managment, STEMI-Primary PCI, Wintage cardiology | Tagged assessment of reperfusion stemi, ecg gold standard, ira patency vs ecg st regression, thrombolysis vs primary pci | Leave a Comment »
Bedside wisdom
We have been using unfractioned Heparin for long , and its is better than any other anticoagulants in ACS . . .
Our observation shows that Streptokinase has distinct advanatge over Tenektepelase as it works longer duration . . .
My experience says Diuretic and beta blockers are still good as first line therapy for Hypertension . . .
Mind you , there are infinite number of such wisdom in every sub specialty of medical field.
However , the typical response from any modern scientific intellect would be . . .
Stop it . . . Its old stuff folk , What does the current data say ?
Common uttering in scientific forums,
Is there data backing up your treatment modality ?
Is there sufficient data ?
Come’on , grow up , don’t talk about experience in a scientific forum . . . come out with data man !
No one seem to care the quality of the data . Every one bothers about the quality of the Author and Journal instead . if its X Y Z its ok If its A B C no its not acceptable data.
Probably , Data is most misused word in medical science.
In scientific world, “unpublished sense” goes straightway to dustbin ,while we have so many avenues for the published nonsense to be celebrated (Still, bulk of guidelines in cardiology is backed up by Level C evidence which means experience of experts !)
By the way what do we mean by data ?
Its organised collection of genuine scientific information , that’s post processed , follow it up with sound inference and faithful questioning and debate that should ultimately end up as “clinical application” in patient domain for consumption.(No prizes for guessing , whats happening in real world !)
OMG, give us back that elusive Common sense . . . which I think we lost some time at the turn of this millennium !
Wrong or useless data : Who will recall ?
Once applied to patient , these data is to be scrutinized and monitored . If we find a study conclusion and reality does not match , we need to stall the data from adversely exploding .Every stake holder should have the power to do it. There have been instances a treatment modality got banished in one country is legally permitted in other country knowing fully well the futility.
Final message
Modern scientific Data* is not God sent. Its created , synthesised and disseminated in various mind factories. All you require is , backing up with some pioneering journal publication with huge impact factor.It’s not really blasphemy to question things which doesn’t make sense .Unfortunately , wrong data can be tackled only with further data .(There is no other means I guess !)
When does “good common sense” become hard data and evidence ?
Its the act of publication , so please guys whenever you find some contamination in so-called scientific data please post here. To begin with I am registering a new Journal “Commonsense journal in cardiology”
*Please note, data is not a bad word as this write-up seem to suggest.Naturally occurring , epidemiological and observational data about diseases are the foundations for medical science .The issue become murky when few motivated humans play brutal games at the sensitive interface between science and truth.
It should be acknowledged , there is a distinct risk of this fight against falsehood end up in blocking true progress of science . Still , Homo sapiens are (believed to be !) intelligent enough to differentiate good from bad , that’s the reason God gave us the sixth sense !
Link to Lown Institute (Started by Cardiologist and Nobel peace prize Laurate Dr Lown who strives hard to pursue this goal)
Further reading : Scientific Reversals in cardiology
Posted in bio ethics, Cardiology quotes, Cardiology research topics, Cardiology Risk assesment, medical quotes, Two line sermons in cardiology | Tagged Lown Institute, medical ethics, what is scientific data | Leave a Comment »
Hey , What’s that moving object over AML ? It looks odd, it doesn’t look like a thrombus or a vegetation.
Yes, I agree , its moving independently but I think , Its benign threads of fibrin attached to the valve .They are called as valvular strands.
Is it ?, I haven’t heard about it ! Can you please tell me something about it.
Strands are highly mobile, fine, filiform threadlike excrescences that is seen arising from valvular structures. Synonym : Its same as Lambl’s excresceneces , the Czech physician who described it over Aortic valve in 1860.
The following TEE clip shows strands attached to Aortic valve
Incidence
Reported Incidence of valvular strands varies .Some reports suggested it may be up to 5-10 % .( SPARC study Mayo clinic 1999 its staggering 46 % !)The reason for such high incidence is, many of us are still not clear what we refer to as strand.The imaging modality also has a say. With improving resolution of TTE and liberal TEE use more strands are detected .A recent large study from Israel , suggest a good news , in large population based study (21,000) true strands are observed in just around 1 %.(Marina Leitman 2014 )
Is it Physiological or Pathological ?
The valve closure lines are physiologically stressed , some amount of denudation of endothelium is expected .This leads to a thrombus formation along with the exposed mucopolysacchride layers of the valve form a filiform ,filamentous structure. .To call it physiological or pathological is left to our wisdom and perception. The size however matters. It could be the reason behind many unexplained strokes.
What is the natural history of these strands ?
Its difficult to believe It may persist for lifetime.If its truely fibrinous strands it may have a life cycle and disappear.
Size
Should be less than 1 mm.
Length varies between 3 mm to 5 mm
Location
Can be seen in any valve or even in aortic root.
Attachment : Atrial side of mitral valve and ventricular side of Aortic valve.
Strands over prosthetic valve is also reported.
Clinical significance
It has three common issues.
One: Getting confused with other more pathological entities.
Two : Risk of stroke.
Three: Nidus for normal native valve endocarditis ?
Strands may closely mimic
Risk of dislodgement and stroke
These strands are minute. It seems plausible dislodgement need not necessarily result in stroke or other organ ischemia.We don’t know whether it gets dissolved on transit.However the risk of stroke is increased in most reports except few studies(Roldan).
Management
First question to ask is , Should we inform our patients about these ubiquitous accessory valve tissues if detected incidentally ?
Largely benign and can be ignored in most.A follow up echo may be adviced once in a year or 2. (I have one anxious patient after I reported such strands in Marfan syndrome )
In patients who has h/o stroke presence of these strands gains importance and is an indication for anticoagulation.
Surgical excision of large strand is a dramatic option and is rarely performed.
Queries with no answers
Is it accessory valvular (mesenchymal) tissue ?
Does Atheromatous plaque contribute to these strands in Aortic valve ?
Strands , if disappears by natural means , do they regrow from the same spot of raw surface ?
Final message
Fibrous strands detected over the valves by routine echo are uncommon .However , It may give considerable anxiety if documented and reported to our patients and physicians .Though these have negligible clinical significance , the risk of stroke is increased in those with large strands.
Reference
2.Aziz F1, Baciewicz FA Jr Lambl’s excrescences: review and recommendations.Tex Heart Inst J. 2007;34(3):366-8.
Posted in cardiac anatomy, Echo library and gallery, echocardiography | Tagged infective endocarditis vegetation, mitral valve strand, thrombus or vegetation or strands | Leave a Comment »
Great men dream , but they just do not sit idle. They do what they are passionate about .History just follows them or they create it.Here is a brief story of an ordinary man born in a small European country Lithuania in 1921 ,lived much of his life in the east coast of USA ,transformed into a brilliant cardiologist based in Brigham Hospital , Boston.
He is Dr Bernard Lown , best known as a founder of what is used in every coronary care unit and cardiac surgical theaters around the world . Yes, the DC cardioversion was invented by Lown in the year 1961.(Of course, it was an Improvement upon the pioneering work of Zoll’s AC power line for defibrillating the heart which was impractical and caused much injury )
Dr.Bernard Lown (Born 1921) ,With his Invention of DC Cardioversion machine Currently working in Harvard University
He was also the brain behind the conversion of local anesthetic agent Lignocaine to cardiac anesthetic which revolutionized the treatment of ventricular arrhythmia.(What a simple but a path breaking idea to use membrane stabilising action of local anesthesia to sedate the heart when it behaves erratically !)
We can also credit him for rediscovering Digoxin and found the secret that potassium supplementation can largely overcome toxicity of this drug which was otherwise lifesaving in dilated , failing hearts running amok with delirium tremors (Surname for Atrial fibillation in those days !)
While the Invention of DC cardioversion had a dramatic impact all over world , he simultaneously popularized the concept of coronary care units along with Julian in London and Dr Day in Kansas city.
Its said great men’s mind are perennially restless.Accordingly ,he was worried about the impending nuclear war with USSR and other global powers then. He collaborated with Russian cardiologist Dr. Eugene Chazov. It became a hugely popular peace organisation International Physicians for the Prevention of Nuclear War (IPPN) for which he got ultimately the Noble prize for in 1985.
During one of his Noble lectures (Linked to video)
It turned out to be “lovely Irony” for a man who probably should have got a Nobel prize for medicine for inventing DC cardioversion , ended up with Nobel peace prize for his fight against a man made disease called “Nuclear proliferation”.
Its heartening to note he has visited my country(India) and was awarded with Mahatma Gandhi peace prize as well.He is now 95, active in Harvard currently turned his vision towards eradicating Inappropriate medical treatment from the noble profession .I wonder , for a man who fought against a nuclear war, what does this new Initiative mean ? Does he equate the medical profession in its current form and the direction in which travels to something that’s grossly unacceptable ?
Whatever it is , I humbly endorse his views and has since dragged me to his Institute.
I just joined the institute and signed a declaration . I wish every physician who take oath on Hippocrates should strengthen Dr Lown’s Doctrine .
Reference
Posted in history of cardiology, Histroy of medicine | Tagged bernard lown, dc cardioversion, history of cardiology | 4 Comments »
Ventricular tachycardia is a regular wide qrs tachycardia.It can be monomorphic or polymorphic.
General diagnostic rules In VT (Gross though, with considerable overlap)
*Its important to realise any VT will transform to polymorphic just prior to degenerating into VF.
Management Issues.
The management of VT in acute setting is same irrespective of morphology of QRS complex.Either you DC shock or administer Amiodarone, Lignocaine , and other reserve drugs.
The issue comes only in stable VTs.In stable VT or if VT recurrence it’s advisable to bother about the ethology and choose a drug.Its believed , Amiodarone is contraindicated in true polymorphic VT that was precipitated by prolonged QT interval or Brugada syndrome.
In Ischemic VT , lignocaine may be preferable over Amiodarone as the later may prolong the QT interval and VT could recur if the index VT was triggered by ischemia induced prolonged QT and subsequently gets worsened by the drug Amiodarone.(please note, Lignocaine has neutral or even shorten the QT)
Let me conclude with a controversial observation, many of VT storms we are witnessing only in the era of Amiodarone.Most episodes of VT Storm are polymorphic and often precipitated after blouses of Amiodarone punctuated with DC shock. With an explicit pro arrhythmic potential of this drug, I strongly believe some of the episodes of VT Storm is iatrogenic and it tends to disappear as the drug effect of Amiodarone weans off.
Final message
In monomorphic VTs, drug choice and selection may not be that important , polymorphic it could make a big difference !
Always ask a query whether the VT you are tackling (in any setting )is likely to have precipitated by prolonged Action potential duration (Read as QT Interval ) ? Of course ,one can’t get a clear answer to this in bed side .But, if you have strong reasons to suspect , better to avoid drugs that prolong action potential duration ( Amiodarone comes top in this list, though it can terminate VT of any ethology with any morphology because it has all 4 group action of Waghaun williams !)
Comments welcome from EP experts , still to understand things in perspective.
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Brugada syndrome is probably the most fascinating discovery in Inherited cardiac Ion channel dysfunction that linked the basic sciences to bedside . Its due to genetic defect in SCN gene that results in sodium channel blockade of phase of action potential to cause troublesome ventricular tachycardia (Phase 2 reentry ) . Now we realise, there are some phenotypic expressions to this gene defect . RV epicardial anatomical substrates are found to responsible for these Arrhythmias.
So ,does Brugada turn out to be a structural heart disease (At least histological ) ? Where is the evidence coming from ?
Now, we realise RF ablation of epicardial aspect of RVOT / Adjacent anterior RV wall can eliminate Brugada pattern confirming anatomical defect at cellular level. Our changing perception of Brugada from pure functional to anatomical cause is exciting and intriguing as well ! ICDs were the specific therapy so far.This discovery make it RF ablation an option.
The recent data from Brugada himself was presented in World congress of electrophysiology / European Heart Rhythm Association (EHRA) EUROPACE-CARDIOSTIM 2016 confirming the therapeutic benefit of targeting the epicardial structural phenotypic substrares (Ref 3 )
Final message
We have been taught Brugada syndrome is a primary electrical disease .It was never considered as structural heart disease. Knowledge evolves slowly, so we shouldn’t conclude prematurely .Shall we conclude , Brugada syndrome is truly a structural heart disease at least in some ?*. This makes RF ablation a new cure for Brugada , making it a useful alternate modality to ICD , Of course there can be an overlap between ARVD and Brugada syndrome. Mind you RF ablation scores over ICD on any given day as its potential cure , while ICD is just a back up device and it simply wait & watch for the VT to occur.We also know ICDs are still learning human EP data, and are not intelligent enough to differentiate true VT from false ones with acceptable error** margin.
* Let the experts decide
**Acceptable ? What do you mean by that ?
Reference
Questions queued
2.Is Amiodarone Indicated in Brugada syndrome ?
.
Posted in Uncategorized | Tagged brugada syndrome, structural abnormalities in brugada | 1 Comment »
Posted in Cardiology - Pioneers, Clinical cardiology | Tagged cardaic apical impulse, lv apical torsion rotation counterclock wise, radiological clinical anatomical apex, what is true anatomical lv apex | Leave a Comment »
Its a funny world out there in medical science, more so in the field of cardiology ! A new treatment comes as a revolutionary breakthrough , lives merrily for a while . . . only to blink , few years down the lane . . . and make a sheepish exit !
Here comes some important knowledge from Rome , European society of cardiology conference 2016 .Its the much expected NORSTENT study from Norway,with a largest number (9013 patients comparing one to one BMS vs DES ) with up to 6 year follow up data ,exposing the limitations and the possible false superiority of DES over bare metal stents .It almost concludes there is no meaningful preference for DES over BMS in obstructive CAD in terms of survival .(ACS included)
For over a decade billions of dollars were drained with a hyped scientific concept of coating the stent with drugs to prevent restenosis . DES , was able to effectively pull the BMS down and out by statistics. This, in spite of the strong concern of DES, interfering with normal healthy endothelisation of the stented segment which resulted in unexpected sudden DES related thrombosis. The power of commerce is huge , it can finish of a useful modality,if available cheap.This happens even in a lesser developed country like India.
I guess,the obituary for BMS is already written in most part of the world. (I can vouch for it my city Chennai !) Now that NORSTENT has come out, though belatedly, I wonder any company wants to manufacture BMS in a big way ! Can it infuse a fresh life into BMS which I believe is surprisingly sitting alive in it’s graveyard .
Baremetal stents where are you ? My patients need you !
Counter thought and a rebuttal !
Many will say my interpretation of the NORSTENT study is wrong and its a indecent attack on a proven scientific concept of DES which is the only way to reduce restenosis rate.
But , what is the big deal in preventing restenosis,if DES doesn’t save significant lives ?
The argument that DES reduces repeat revascularisation is largely irrelevant as it amount to only angiographic gratification and reduced threshold for intervention and ultimately imply inappropriate re-intervention in the BMS group.(Only Clinical restenosis ie symptomatic, flow limiting stenosis require attention .We need that specific data from NORSTENT . )
Don’t believe blindly in whatever is written here .Read for yourself and decide ! The NORSTENT from Norway published in NEJM August 2016 http://www.nejm.org/doi/full/10.1056/NEJMoa1607991
Posted in acute coronary syndrome | Tagged are DES really superior, BMS prevails over des, BMS VS DES debate, NORSTENT STUDY 2016 NEJM, what is the current role for bare metal stents | Leave a Comment »
Interventional Cardiologist’s favourite play time is to get rid of of obstructions across any blood vessel , valve or a conduit . This has been well practiced for over 2 decades in both coronary and valvular obstruction.Now they wanted more and have since started implanting valves percutaneously. (Aortic valve -TAVR in particular )
Why do balloons work in Mitral stenosis but not in Aortic stenosis ?
It remains a mystery at-least to me ,how PTMC (Percutaneous mitral commissurotomy ) became a default strategy for relieving mitral valve stenosis, while BAV (Balloon Aortic valvotomy) was never considered good enough for opening Aortic stenosis.
The reason is, mitral stenosis(Rheumatic) primarily involve the commissures, while degenerative aortic stenosis involve leaflets more and calcification is much extensive and hence balloons are less effective .Since the initial reports of BAV had more complication like stroke , AR, the interest has waned (except in children with BCAV ).
The arrival of TAVR in big way has made things difficult for BAV to prove its real worth and at best it was considered a bridge therapy.Curiously , BAV is often used as an integral part of TAVR as pre-dilatation with various wires across the valve.Hence , every procedure of TAVR,whether you like it or not carries the huge risk of BAV (please note,these are the same risk which made it unpopular earlier !)
Now , with accumulating data(Funny we got trained in BAV during TAVR we have double confirmed BAV is not that risky after all, even in calcific aortic valve. We also learnt BAV does open up the valve significantly (exact gain contributed by BAV during the TAVR is not quantified as yet).Hence many believe BAV is grossly underutilized modality .
Final message (As usual , without evidence )
BAV, considered just a bridge therapy to TAVR/SVR , (mind you,it may not be flimsy bridge , but a near permanent steel bridge that can outsmart the much hyped TAVR!) Let us recall again the mitral valve logic where you just require dilatation for stenosis .Some degree of AR during BAV is acceptable as do we accept MR in PTMC.As I said earlier the perceived complications of BAV has rapidly declined. For those who are interested in health economics , a single patient’s cost of TAVR can be shared and could confer a fresh bout of life to 20 patients with severe aortic stenosis who can be tackled well with BAV.
I agree , BAV can not reach the glory of PTMC, but definitely its going to come back and expected to give a tough fight to TAVR in atleast high risk patients.BAV has a potential to become a therapy of choice in patients with critical aortic stenosis with severe LV dysfunction as even a small gain in orifice with a balloon can provide a big booster effect on LV function.
A thought and a counter
BAV is retro technique with low efficiency and with high complication rate .
However, isn’t ironical , complications with TAVR ,which includes 25 % of permanent pacemaker assistance is accepted .(with a pride ?) while that of BAV is magnified and made to look unacceptable.Of course , many have mastered BAV and complications has come down recently .I have heard few anecdotal examples where TAVR was abandonded for some reason after pre-dilating the aortic valve and patient doing fine with BAV in the long term.Its being predicted BAV is going to reemerge (already is !) as a useful strategy in critical calcific Aortic stenosis
The emprical utterrings in this discussion are dangerous and unethical and not evidence based !
It would appear “not doing” a large randomised trial comparing one to one (BAV vs TAVR) in a real “high risk” setting of AS amounts to ” unethical” act as complication with BAV has grossly reduced in recent times ! Its our duty to provide best or near best to our patients.Let us ensure reasonable inferiority/Non inferiority is accepted that can prevail over a perceived superior modality , if it comes at low cost !
Further reading
1.
Posted in baloon aortic valvotomy, bav vs tavr | Tagged bav vs tavr, current status of baloon aortic valvotomy | Leave a Comment »
Dr.S.Venkatesan MD 