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We know,  classical Atrial flutter (Also referred to as typical /Common AF) records  saw toothed F waves  due to continuous atrial electrical activity across a macro- reentrant circuit within right atrium.

Though this  saw tooth pattern is easily recognised , it’s often difficult to say  whether the saw is facing upwards or downwards ?

ie  Is the flutter waves are inverted or upright ?

The general rule is the shallow stroke (one with a lesser slope) is to be termed  as antegrade  / initial deflection that will determine the direction of flutter waves.

mechanism-of-inverted-flutter-waves-in-atrial-flutter-saw-tooth

This is because , the forward limb traverses the slow path  of the circuit namely the cavo-tricuspid Isthmus, it then ascends up in the inter atrial septum (There by inscribing inverted F  waves  in leads  2,3,aVF .The return circuit  is relatively fast,  crossing the antero -lateral   free wall  right atrium and hence the later half saw tooth has a  sharp deflection )

In Reverse typical flutter  the flutter waves are upright (with a shallow slope ) in inferior leads but still uses the cavo- tricuspid Isthmus

* Note: In lead the polarity of F waves in V1 it will be opposite of that of inferior leads.

mechanism-of-flutter-wave-upright-or-inverted

Why should we bother about direction of flutter waves  ?

It may not be important for those hifi EP guys who can ablate complex arrhythmia with intra cardiac GPS catheters and accurate electro anatomic mapping system. Still , the  surface ECG always help us understand the basic circuits of flutter.

Reference

atrail-flutter-review-best

Reverse typical flutter should not be confused with atypical flutter where typical saw tooth waves are uncommon.The later group is termed as atypical atrial flutter that arises from various other focus including left atrium.

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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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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

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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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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

1.Is Brugada VT monomorphic , polymorphic or both ?

2.Is Amiodarone Indicated in Brugada syndrome ?

.

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Cardiac failure is defined as a clinical syndrome where the cardiac output is inadequate and fails to fulfill the metabolic demands of body  or its able to do so, only  at a raised filling pressure, causing the classical symptoms of exertional dyspnea.

Consider this simple equation,

A 70 kg normal human requires an EF of 60 %  to supply blood  to his total body mass. If his EF falls to 30 % , certainly he is going to  struggle with reduced cardiac  output by 50 %. Now , theoretically if he loses his weight by 50 % (70 to 35 kg ) in-proportion to the loss in EF, . . . isn’t likely , he goes back to the original ” comfort zone” again as his metabolic demands are  declined by 50 %  and hence easily managed with the severely compromised  EF of 30 % .

Is this a scientific or quixotic logic ?

By all means , it appears the later is right ! but wait . .  nothing is Idiotic in a true scientific democracy ! Human beings can live a near normal life with one kidney, one lung, half the liver function and brain function ! Nothing wrong in wondering  why not , one can live comfortably  with “half heart” function?(ie EF of 30 %)

Having said that ,cardiac failure is not a simple mathematics of EF % .It’s extremely important to understand cardiac failure is systemic disease (often an inflammatory reaction  as well) which progress to a  net catabolic sate  .Numerous named and unnamed counter hormone response(ACE,NEP, BNP etc)  retains salt and water.At some stage the body either adopts or  mal-adopts to it.Countering or mimicking these hormones has been a major therapeutic strategy.(ACEI, ARBs )

The final end point of cardiac cachexia is nothing but extreme response of the body to reduce its weight  (with Tumor necrosis factor /IL6) .Survival occurs with whatever available cardiac output that matches metabolic supply to tissue.

Now ,coming to the title discussion,  If weight-loss is the ultimate compensatory mechanism in chronic HF , what about conditioned and monitored weight reduction  regimen ?

The management of cardiac failure after addressing all specific problems like structural ,functional abnormalities plus or minus  revascularization should include a mandatory  exercise training program that help optimize the weight.Reducing total body mass is directly going to improve the cardiac function, or  at-least make it static and might dramatically  relive symptoms and increase survival.However , the beneficial effect of exercise is  mainly attributed to improving muscle mitochondrial function and augmenting exercise capacity.

Where is the evidence coming  from ?

 

excercise training in heart failure

wieght reduction in cardaca failure

A point of controversy !

There are few reports  that suggest good-weight is essential as a body reserve during the catabolic state of HF.In fact, low fat and cholesterol was unwelcome in some statin and  HF  studies. Some provocative papers even  suggested a paradox  where weight loss could be counterproductive in HF (I strongly dispute this as do many others.)

(T.B Horwich,The relationship between obesity and mortality in patients with heart failure J Am Coll Cardiol, 38 (2001), pp. 789–795)

Final message

Unfortunately , truths without  evidence is worse than plain falsehood !

When heart as a pump is failing , we go for  sophisticated drugs, ICDs CRT devices, variety of surgeries etc . Shall I say , none of them has conquered the inevitable. We know ,HF’s mortality and morbidity is next only to burden of cancer.Applying  all our wisdom , intentional and monitored weight reduction  may be  best bet to unload the heart in many of the HF patients .Mind you, this comes  free of cost ! and that is not the only reason it  should be tested in every such patients .My own experience and interpretation of available data would suggest its going to work in all  and the benefits are going to be  overwhelminng in overweight patients .

Dear heart failure patients . . .Wishing you all a  controlled weight loss  and a happy life !

 

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Less than a century ago an easy chair  was enough to manage this most important medical emergency of mankind. Of course, at that time mortality of STEMI was estimated to be around 30%.We have since pushed the in-hospital death rate down to less than 10 %  and its around 5-8% currently.(*The lifeless chairs were able to save 70 lives is a different story!)

Heparin , thrombolytic agents, critical coronary care has helped us to achieve this , of course It must be admitted primary PCI also played a small role (at best 1 % ) in our fight against this number one killer.

Now, why not combine  both lysis and PCI ?

The concept of PIA (Pharmaco Invasive approach) came into vogue  primarily for two reasons.

1.If thrombolysis and  pPCI are powerful strategies by individual merits why not combine both and achieve double the benefit ?

2. Since pPCI is going to be a logistical nightmare in most points of care and we can’t afford to lose time . So, let us lyse first and consider PCI later !

Unfortunately medical science is not math .One plus one in medicine is rarely two !

Though , it looks attractive , Pharmaco invasive approach  has its own troubles.Fortunately , most of them are man-made, few are beyond our knowledge though.

Following general rules  may help us

  • STEMI  should ideally managed by early thrombolysis (or PCI) in all deserving patients.
  • Don’t wait for PCI if you think , there will be delay or reduced expertise and poor track record of the center in this modality.
  • Pharmaco invasive  therapy is not a default in all STEMI .Do good quality , monitored  lysis , (Not necessarily new generation thrombolytic .(I prefer one hour sustained thrombolytic regimen , not the hit or miss bolus) .As a learned cardiologist we need to assess individual patients according to the type and risk of MI.Its not wise to blindly follow the guidelines ,because these guidelines , though based on evidence never answers a query in a single patient perspective !

The key “branch points”  in decision making  after lysis

  • Invasive strategy  should begin within one hour if the patient has failed  thrombolysis and has developed any mechanical issues.( Mind you, LVF requires good medical stabilization .Rushing  such patients to cath lab without application of mind can be disastrous )
  • If the Initial  lysis is excellent and the patient is asymptomatic  one need not proceed with invasive limb at all.(A significant chunk of apparently failed lysis by ECG are asymptomatic and comfortable , these are patients require delicate assessment regarding further intervention. )
  • If the MI is large and the clinical  stability is “not confirmed” one may  proceed urgently within 24 h.
  • In any case there is no role for invasive approach after 24 hours* Unless fresh ischemia  suspected to come from IRA or  non IRA.
  • Having  said that, there are many centers that do a diagnostic  angiogram alone just prior to discharge  (48-72h) for risk stratification and then take a genuine call for a possible PCI or  CABG. In my opinion it appears a sensible strategy , though a non invasive stress  test pre/post discharge can even avoid that  coronary angiogram !

One issue with Rescue PIA

Though by current definition  PIA is to be done  3-24 hours , don’t wait for the 4th hour if you have recognized a failed thrombolysis earlier than three hours.( Ofcourse , as the gap between P and I gets too narrowed it may  carry some adverse  effects witnessed in routine facilitated PCI -Refer FINESSE study ) Similarly,there need not be a blanket ban on PCI beyond 24 hours if residual ischemia is active.

Final message

PIA is a dynamic  coronary  re -perfusion strategy . Nothing is fixed in science. . The optimal gap between Pharmaco and invasive strategy  can be anywhere between  1 hour to “Infinitely deferred” depending upon individual risk perception and wisdom of the treating cardiologist.

 

 

 

I

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