Archive for the ‘Electro physiology’ Category

A 5-minute session: Answers are my own. Please cross-check.

1. Is Brugada syndrome clinical or ECG diagnosis?

Always clinical. Never get confused on this.

2. Spontaneous type 1 vs Induced Type 1 (from type 2) which carries more risk?

Both are risky since they are close cousins. But, spontaneous type 1 is the dreaded devil. 

3. Is Brugada primarily a defect of myocardial depolarization or repolarisation?

Not clear. Often in both. In fact a mismatch between them. (Don’t ask how Na+ Channel defect affects repolarisation !)

4. Is Brugada VT is monomorphic, polymorphic?

Both. What determines morphology is not clear though. (All de-nova monomorphic VT will degenerate to polymorphic en route to cardiac arrest)

5. Should  Fever induced Brugada pattern be investigated further?

Better, it is not to be reported in ECG. May not be important in the majority if there is no adverse family history. (If the patient is well educated and afflicted  by Dr.Google and cardiologists can’t escape from ordering sophisticated tests)     

6. What is the overlap between ERS and Brugada?

It is all about the Idiosyncrasy of the K+ channel phenotypes ( Transmural dispersion heterogeneity )  

7. Is a benign Brugada better than a malignant ERS?

Yes, it would seem so. (Inferior or Infero -lateral ERS prone for primary VF in case they develop ischemic / ? also non-ischemic stress)

8. How important is the link between Brugada and Long QT 3 syndrome?

A rare entity, but It is double jeopardy for VT risk. The entire action potential width is vulnerable right from phase 0 to 3 or 4 A case report Sandhu A Clin Case Rep. 2017;5(8):1315-1319.

9. Is Amiodarone really contraindicated in VT?

Not really. Though Amiodarone unmasks Brugada, it can still be used during episodes of VT in patients with manifest or unmanifest Brugada. Maybe in Long QT 3 overlap, it may perpetuate the VT.

10. How important is the structural myocardial defect in Brugada?

Not important in the majority. Though localized RVOT abnormalities are noted in some..RV abaltion can be succesful in odd case.

11. What happens to the ST segment in Brugada during exercise stress?

ST-segment may normalize in some. A stress test can help to risk stratify.  Subramanian M, J Cardiovasc Electrophysiol. 2017 Jun;28(6):677-683.0

12. Which drug is probably best for Brugada as of now?

Quininde , A fairly specific blocker of Ito current. However, it needs to be used diligently. Management of Brugada Syndrome: Belhassen B, Rahkovich M, Michowitz Y, Glick A, Viskin S Circ Arrhythm Electrophysiol. 2015 Dec; 8(6):1393-402.

13. Is ICD definitive therapy?

Obviously not. But, definitely life-saving in high-risk survivors. I guess definitive therapy is possible for future generations through the science of genetic reprogramming of Na+ channels. (Of course, our planet shouldn’t succumb to man-made climatic arrhythmia, by then ) 

14. Does widespread genetic testing & screening of families help in the management and reduce anxiety?

Cracking the genomic code of cardiac ion channels is the ultimate sophistication (Blueprint of fate ?) However, there is no guarantee this information is going to ease out the family members who harbor a genocopy with or without a phenocopy. 

15. Is Brugada getting undue attention in cardiology literature compared to many other common arrhythmias?

      You can answer this …………………………………….


Further reading

Li KHC, Lee S, Yin C, et al. Brugada syndrome: A comprehensive review of pathophysiological mechanisms and risk stratification strategies [published correction appears in Int J Cardiol Heart Vasc. 2020 Dec 19;32:100699]. Int J Cardiol Heart Vasc. 2020;26:100468. Published 2020 Jan 21. doi:10.1016/j.ijcha.2020.100468


Read Full Post »

Junctional tachycardia(JT) is often a misunderstood arrhythmia. Technically,  any tachycardia arising from the AV junction could be termed as JT.Even AVNRT was considered as a form of Junctional tachycardia till recently.The crux of the issue is , true anatomical extent and borders of  so called AV junction is  yet to be clearly demarcated .The common perception that  AV node is a discrete  structure is  an anatomical illusion  , rather its collection of  condensed fibers with proximal  nodal approach and distal fanning .

Now , we have a  proper definition by the apex scientific bodies  ACC/AHA/HRS 2015)

definition of junctional tachycardia

Source :2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: Executive summary A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society April 2016Volume 13, Issue 4, Pages e92–e135

Please note :The key point is , JT by definition  should  be a focal  /automatic tachycardia either due to triggered activity or after depolarisation and the boundaries of  junctional tissue is liberally extended up to  His bundle.

Read  related post  :What does the term junctional tachycardia mean in current era?




Read Full Post »

These are the common ECG terminologies with which clinical cardiology is being practiced over the years .In this era of instant interventions the exact meaning for these terms  may not matter much for many of us.Still , Ischemia could denote a more benign connotation , while injury suggests an emergency (like an accident) .Of course , this is a dangerous way of defining them. Still, there may not be an entity called  “chronic injury”. while chronic ischemia is all too common.

Logistically , both could  mean the same (except the perception) and related to the intensity of the index reduction in blood supply to the varying thickness of myocardium.While injury is diagnosed by ST segment elevation , ischemia is diagnosed by ST depression  or T inversion.

No, its wrong , come again please ,

Shall we say . . . most injures are ST elevating  while most ischemia are ST depressing , but  still injuries can be ST depressing  as well.  We know Ischemia can be sub-endocardial , transmural or  rarely sub-epicardial ,while injury can either be sub-endocardial or subepicardial (Rarely transmural ?)

Can you refine it ?

Only  subepicardial ischemia(Injury)  elevates  ST  segment while sub endocardial ischemia depress it.The leads facing the affected subendocardial and epicardial surface will determine whether its going to be ST elevation or depression .

Go further,

Does the opposing sub-endocardial and sub-epicardial forces negate or  cancel out  ? If so what is the status  of reciprocal ST depression in STEMI if remote ischemia occurs in sub-endocardial  or  sub-epicardial zones ?  Can there be reciprocal ST elevation for primary ST depressive forces ?

If ischemia and Injury are to be defined only with reference to ST segment , which area of myocardium is linked to  critical T wave ischemia (Both Tall T and dynamic Wellens type T )

Still more , If Injury is  represented by ST elevation,  then what represents  infarct ?

ST elevation in acute MI-STEMI is actually due to  transmural* injury while infarct is represented by Q waves in strict sense.In that case not all acute STEMIs are not true Infarcts.Thats why many STEMI can get totally aborted with zero LV dysfunction and negligible enzyme release.  (Should we call these as Non Infarct STEMIs ?)

*Though STEMI results in  transmural ischemia , it is the sub-epicardial zone of injury that elevates the ST segment. This  implies any degree of subepicardial injury is suffice to elevate ST segment (eg pericarditis) and transmurality of ischemia is not mandatory.

What is reversible vs irreversible Injury ?

If irreversible injury is equivalent to infarct , reversible injury is same as ischemia ? (Whats the histopathological  correlates , Cell swelling, mitochondrial / nuclear death .(We know , enzyme release are  linked to cell death even in  chronic stable angina )

Where is the epicardium  for the IVS ?

Most ACS involve interventricular septum .In this case does septum has  any defined sub-epicardium or endocardium? How does septal STEMI forces behave with reference to partial or full thickness septal  infarct ?

Final message

Acute Ischemia and injury can mean “one and the same thing” or  “totally different” entities  depending upon  the totality of obstruction within the coronaries and  sparing of  sub epicardial zones of  myocardium. In my view , any acute ischemia can be labeled as injury.Bifurcating ACS into STEMI and NSTEMI has largely removed the embarrassment of these entities .

Be grounded

Forget the basic science , electro-physiological concepts can wait.Lets live in a realistic world. Get to know the underlying lesion . What can be done for it ? Go ahead , wheel your patient to cath lab . Alert the staff .Be pragmatic ,make sure your patient has sufficient insurance coverage to open up  all his blocks ! That’s it !


The intention is not to confuse the readers.Only to make us realise ,the gap in  basic science is “huge and wide” which I hope is  filled up by the generation next !

Read Full Post »

Inserting an ICD  for  DCM  may a be great therapeutic success  for the physician  as well as the patient . But there is one big truth hidden behind the statistical screen.

Following  study  provides dramatic data from Maanhiem in Germany in about 561 patients who had ICD .The long term patient outcome after appropriate shocks were much worse  than those without    shocks .This was more pronounced in Ischemic DCM .

appropriate and inappropriate shocks ICD

Source : Streitner et al ,University Medical Centre Mannheim, Mannheim, Germany PLoS One. 2013 May 10;8(5):e6391

The fact that these patients continue to throw VT , some thing is wrong in the cellular  milieu or a fresh scar / fibrosis / ischemia is progressing .Further , the VTs and the  subsequent  shocks  set in temporary  hemodynamic instability .We have evidence , EF can be depressed for days  worsening the long-term out come.

While it is easy  to blame it on natural course of DCM , there are  solid reasons to believe  , shock induced myocardial damage is definitely contributing to this  excess mortality.

One important  clinical tip is to screen  all  these so called Idiopathic DCM  patients  who  had appropriate shocks.  They should be monitored for fresh signs of any systemic illness  , like a  connective tissue disorder , chronic granulomatous lesions  like sarcoid etc .To our surprise  some specific  myocardial disease may unmask themselves in the natural history. Identifying them may offer a dramatic cure .

Final message

Some where along our EP mind-set  we are conditioned to think  , as along as there is an ICD in situ and it appropriately  shocks, every thing is bliss ! Blame it  on semantics . The  word “appropriate”  inappropriately  soothes  our nerves.

The fact of the mater is , every appropriate shock is a  grim reminder  that the heart  in question  is restless electrically and VT continue to emanate  from diseased  myocardium  . It could  mean either the LV   is destabilising  , or the original  disease  is   progressing  or a new disease  is evolving .

Mean while, paradoxically , inappropriate shocks give us a quixotic comfort , since the  heart is not really  throwing any dangerous arrhythmia, after all it is  the device related  false alarm   that  could be easily  reprogrammed!


ICD appropriate and inappropriate shocks

Read Full Post »