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Defining moment in CAD management “Intentional” Incomplete revascularisation can be true bliss !

November 27, 2016 by dr s venkatesan

Critical multivessel CAD is commonly confronted by cardiologists .These patients either receive multivessel stenting, CABG, with or without optimal medical management(OMT) !

CABG is always done with intention of  complete revasularisation  for all significant lesions. Comprehensive  multivessel PCI though feasible is not practiced widely.Considering the diffuse nature of CAD no treatment is complete except probably intensive medical management.

As of now , addressing only one (or two ) critical lesions in a triple vessel disease by PCI though appear attractive and logical is considered unscientific.Guidelines are not clear in answering the issue.

multivessel-pci-ptca-courage-trial-syntax-cabg-freedom-bari-acc-aha-guidelines

In a triple vessel disease with a critical LAD lesion,  

Shall we do PCI for LAD and medical management for lesions in RCA or LCX  ?

How about this coronary wisdom  “While medical therapy can take care of less tighter lesions , only critical lesions need catheter based Intervention”

In fact, in STEMI setting we do apply this logic of  targeting one lesion (IRA) at a time. Why not in chronic coronary setting ? There are significant  pros and cons for this approach.While, most 0f us will go with the logical herd,an unique  paper by Mineok  asks us to think again(American Heart Journal, 2016-09-01, 157-165)

How do you define the completeness of revascularization? Is it not emprical ?

We know medical management has well documented advantages in chronic CAD. while multivessel stenting has its own hazards.Hence limiting the time spent within the coronary artery and reducing total stent length should be one of our important goals.

A mini quiz  . . .

How often you have left a fairly significant lesion (attending only the critical lesions )  in your practice ?

What do you think will happen to those non critical lesions  in the long run  ?

Do you believe earnestly drugs can take care of these lesions ?

Forget the science . Whats your experience and  gut feeling ? 

Do you agree , even surgeons do not always do a complete revascularisation either intentionally or for technical reasons ?

Finally ,why we are still  hesitant to call intensive medical therapy as a  “Revascularisation  equivalent”  inspite of valid proof for improved functional class, symptom relief , regression of atherosclerois , collateral preservation and improved microcirculaion.

Final message 

I would say , the science of coronary revascularisation in chronic CAD is stranded at a confused cross road even after three decades of aggressively grown interventional cardiology .At any given point of time medical  management can give a tough fight to catheter  based intervention in most stable IHD.

Hybrid therapy doesn’t always mean combination of PCI and CABG. Judicious mix of PCI and medical therapy is also  a hybrid modality that can bring CAD burden effectively in a meaningful fashion with less metal load.   If you can convert a critical triple vessel disease to non critical DVD or SVD with a single stent it should be welcomed without prejudice. 

With a section of cardiac scientists are in hot pursuit for a completely  bi0reabsorbable stents , let us adopt this “Minimalistic PCI approach” in multivessel CAD, till the time  we reach the “dream the end point” of modern coronary care , ie to  get rid of stent altogether by biological cure for atherosclerosis.

Reference

1.Mineok chang, Jung MinAhn, Nayoung  complete versus incomplete revascularization in patients with multivessel coronary artery disease treated with drug-eluting stents Kim,American Heart Journal, 2016-09-01, 157-165,

 2.Tamburino C, Angiolillo DJ, Capranzano P, et al: Complete versus incomplete revascularization in patients with multivessel disease undergoing percutaneous coronary intervention with drug-eluting stents. Catheter Cardiovasc Interv 2008; 72: pp. 448-456

3.Wu C, Dyer AM, King SB, et al: Impact of incomplete revascularization on long-term mortality after coronary stenting. Circ Cardiovasc Interv 2011; 4: pp. 413-421

4.Gao Z, Xu B, Yang YJ, et al: Long-term outcomes of complete versus incomplete revascularization after drug-eluting stent implantation in patients with multivessel coronary disease. Catheter Cardiovasc Interv 2013; 82: pp. 343-349

5.Ong ATL,Serruys PW. Complete revascularization: coronary artery bypass graft surgery versus percutaneous coronary intervention. Circulation. 2006; 114: 249–255

Posted in Cardiology -guidelines, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , , , | Leave a Comment »

What ails cardiology literature ? Watch out . . . Guidelines may easily misguide you !

November 21, 2016 by dr s venkatesan

If you think , the  various appropriate use guidelines for cardiology practice are collection of great scientiifc truths , beware . . .many  of them hide behind semantics.  (After all , English is an unique language one can play  with it !)

Is it not funny , to note a  recommendation  that goes with a caption “may be appropriate” conveys exactly the same meaning as “may not be appropriate” as well .

Here is a rare article which tries to expose the importance of  linguistic Interventions in cath lab that can Impact the patient outcome for good or bad.

http://www.invasivecardiology.com/articles/%E2%80%9Cmay-be-appropriate%E2%80%9D-pci-ambiguities-appropriate-use-classification?inter_email=alNyWXNEY3VFR3RzZEM2b3hHRjVseDIzWjlCdkN1Snp2MDlNbnR5RkVacz0%3D

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Teaching points in cardiology : Syncopes, Seizures & Silent Sudden deaths !

November 6, 2016 by dr s venkatesan

Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.

heart_and_mind

Cardiac seizure and Neural syncope : Require a balanced approach ! (Image courtesy http://3.bp.blogspot.com)

Real life experience now suggest, a bothering  number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

The issue is two fold. 

  • Cardiac patients mis-diagnosed as seizure
  • Primary seizure patients suffer a cardiac death (as seizure induced arrhymias or acute pulmonary edema )

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in  every seizure disorder.  As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)

Reference 

1.Zaidi A1, Clough P, Cooper P, Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol. 2000 Jul;36(1):181-4.

2.Leestma JE, Annegers JF, Brodie MJ, Brown S, Schraeder P, Siscovick D, et al. Sudden unexplained death in epilepsy: observations from a large clinical development program. Epilepsia. 1997 Jan. 38(1):47-55.

3.Kloster R, Engelskjøn T. Sudden unexpected death in epilepsy (SUDEP): a clinical perspective and a search for risk factors. J Neurol Neurosurg Psychiatry. 1999 Oct. 67(4):439-44

4.Leestma JE1, Walczak T, Hughes JR, K A prospective study on sudden unexpected death in epilepsy.Ann Neurol. 1989 Aug;26(2):195-203.

Posted in Cardiology - Clinical, Clinical cardiology, Syncope | Tagged | Leave a Comment »

Stroke secrets : If traffic is well regulated in circle of Willis . . . Chronic carotid occlusion simply doesn’t matter !

November 3, 2016 by dr s venkatesan

In early days of  medical school we were taught there is an important vascular grade separator in the base of  brain .God  would not have created this circle (of Willis ) without any purpose  , he must have designed it for a reason.

circle of willisHow good is the circle of  Willis to prevent a stroke ?

Unfortunately , we have not answered  this in detailed manner . Obviously  it can’t prevent all strokes however , it is strongly  believed it can  abort  many of  them .My guess would be but for its presence many of episodes of TIA, syncope ,near syncope would end up in stroke with various degree of deficit.

The other factor that tests the efficiency of circle  of Willis is the acuteness of the vascular insufficiency.Chronic carotid occlusion  as expected are well  tolerated . We failed to respect  this natural hemodynamic  sharing  and indulged in so many  unilateral carotid interventions with dubious results .

Here is a paper  with fresh  knowledge from Dr  Seemant Chaturvedi ,  Miamai , Florida .Hats off to the authors.

Are the Current Risks of Asymptomatic Carotid Stenosis Exaggerated?Further Evidence Supporting the CREST 2 Trial  Seemant Chaturvedi,  Ralph L. Sacco,JAMA Neurol. Published online September 21, 2015.

Internal carotid artery (ICA) occlusion when occurring in a chronic fashion  could be as benign as a small peripheral vessel occlusion .(Of course they can be symptomatic)

For all those patients with unilateral total carotid disease , let us thank the “circle of Hope” which if regulated by God whom should we fear ?

Secondary collaterals in stroke

There is one more collateral system that connects extra cranial branches of carotid to intra cranial  circulation though Opthalmic artery and leptomeningeal collaterals .This could help prevent or mitigate cerebral Ischemia . A rare review about this important concept worth reading for both cardiologist and neurologists( David S. Liebeskind Collateral Circulation  Stroke. 2003;34:2279–2284)

Further reading

carotid stenting crest 1 crest 2 ACAST ACSE CEA

cartoid stenosis current management stenting

http://www.amazon.com/Carotid-Artery-Stenosis-Treatments-Neurological/dp/0824754174

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A must read : A mini focused update on Dual Antiplatelet Therapy for Patients with CAD 

November 2, 2016 by dr s venkatesan

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

  1. Levine GN et al. 2016 ACC/AHA guideline focused update on duration of dual antiplatelet therapy in patients with coronary artery disease: A report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. J Am Coll Cardiol 2016 Sep 6;68:1082

Posted in acute coronary syndrome, anti platelet drug, cardaic pharmacology, Uncategorized | Tagged , , , , , , , | Leave a Comment »

Classic papers in cardiology : I think , this is probably one of the most Important publication and concept in STEMI ever published !

October 23, 2016 by dr s venkatesan

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  ?

knowledge-2

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.

Prognostic implications of TIMI flow grade in the infarct related artery compared with continuous 12-lead ST-segment resolution analysis. Reexamining the “gold standard” for myocardial reperfusion assessment. Shah A1, Wagner GS, Granger CB, J Am Coll Cardiol. 2000 Mar 1;35(3):666-72.

Posted in STEMI, STEMI -Managment, STEMI-Primary PCI, Wintage cardiology | Tagged , , , | Leave a Comment »

What ails modern medicine ? When “Nonsense” masquerade as scientific data . . . should “sense” has to leave quietly by back door ?!

October 16, 2016 by dr s venkatesan

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 ?

medical-data-ethics-futility

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 

1.Vinay Prasad, Adam Cifu,  John Ioannidis  Reversals of Established Medical PracticesEvidence to Abandon Ship   JAMA. 2012;307(1):37-38. 

2.Vinay Prasad Adam Cifu  Interventions that were tried in vain .  Cardiovasc Diagn Ther. 2013 Dec; 3(4): 228–235.

Posted in bio ethics, Cardiology quotes, Cardiology research topics, Cardiology Risk assesment, medical quotes, Two line sermons in cardiology | Tagged , , | Leave a Comment »

Mitral valve strands : Hey . . , What’s that moving object over AML ?

October 9, 2016 by dr s venkatesan

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 

  • Vegetations
  • Bland thrombus
  • Redundant leaflet /Chrodae (Marfan and variants)
  • Disrupted chordae (After MVR)
  • Flail leaflet
  • Fibroelastomas

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

1. Leitman M, Tyomkin V, Peleg  Clinical significance and prevalence of valvular strands during routine echo examinations. E  Eur Heart J Cardiovasc Imaging. 2014 Nov;15(11):1226-30

2.Aziz F1, Baciewicz FA Jr Lambl’s excrescences: review and recommendations.Tex Heart Inst J. 2007;34(3):366-8.

3.Cohen A1, Tzourio C, Chauvel C, Stroke.  Mitral valve strands and the risk of ischemic stroke in elderly patients. The French Study of Aortic Plaques in Stroke (FAPS) Investigators.1997 Aug;28(8):1574-8.
4. Roldan CA1, Schevchuck O, Tolstrup K Lambl’s Excrescences: Association with Cerebrovascular Disease and Pathogenesis., Cerebrovasc Dis. 2015;40(1-2):18-27.
5.Faisal Aziz, Frank A. Baciewicz, Jr.Lambl’s Excrescences .,Tex Heart Inst J. 2007; 34(3): 366–368
Links
Video clip of Lambl’s excrescence link to British society of Echocardiography 

Posted in cardiac anatomy, Echo library and gallery, echocardiography | Tagged , , | Leave a Comment »

Cardiology classics : Bernard Lown . . . The cardiologist who won Nobel “peace” prize !

October 2, 2016 by dr s venkatesan

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 )

 

drlown_history

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.

 

bernard-lown-dc-cardioversion-lown-institute

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.

lown-image

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 

Link to Wikipedia

nobel-prize-in-medicine-cardiology-drsvenkatesan-venkatesan-madras-medical-college

Posted in history of cardiology, Histroy of medicine | Tagged , , | 4 Comments »

How is management of polymorphic VT differ from monomorphic VT ?

September 22, 2016 by dr s venkatesan

Ventricular tachycardia is a regular wide qrs tachycardia.It can be monomorphic or polymorphic.

General diagnostic  rules In VT  (Gross though, with considerable overlap)

  • Polymorphic VT is more often Ischemic , drug induced, electrolytic, and includes many inherited VTs .Most primary  ischemic VT are polymorphic.
  • Monomorphic VT occurs  more common with structurally abnormal heart.(DCM, HOCM, ARVD etc .Please note late scar induced  VT are often monomorphic , which is also being referred to as Ischemic VT in literature )

*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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