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This is an ECG of a 25-year-old, recorded in master health check-up. 

It was reported as ERS pattern of concern. When he went for an expert opinion, he was suggested to understand, there is a small risk of SCD. That’s it, the panic has set in already, which got amplified in the following conversation..

How small is the risk,?  he wanted to know.

Yours’ is possibly an intermediate risk.

Intermediate means what?  Do I have any genetic or EP studies to predict the risk accurately?

Sorry, we have some gene mapping but all primitive. We aren’t sure. But keep calm, nothing will happen.

Do I need to screen my parents ?

No, but if you are anxious you may take an ECG for them 

If they also show the same pattern, it becomes more significant, is it not doctor?

Hmm yes, maybe.

This is a brief story of this young man, whose life was made miserable by the apparently widening knowledge base of cardiologists

ERS: A brief opinionated review

The term early repolarisation in ECG is used for more than half a century. It’s about the behavior of the Ito channel, at the left shoulder of the action potential, when phase 0 hands over the baton to 1, at the onset of repolarisation. The problem is the rapidity with which K+ exit from the cell, which is heavily influenced by genetic control. Not only that, the ratio of epi vs endocardial density of these Ito channels determines, the timing, magnitude, and shape, of the J point.

 It would be mind-boggling to know the prevalence of such ERS patterns in the general population. One estimate suggests it could be anywhere between 3 to 13  % depending upon the criteria used. Let us assume the mean as 5 %. Then, it would be 30 crores of human beings in our habitat show this ECG pattern. If applied, in my city Chennai alone 5 lakh people could carry this tag.

While it is true, some forms of ERS and J wave syndrome can be markers of serious ventricular arrhythmias, either spontaneous or at times of Ischemia. Currently, It has become a fad, in cardiology academic circles*, to propagate the idea that ERS is no longer a benign condition. This is not acceptable at any degree of cognition. This happened mainly after few studies in powerful journals created some alarmist views. (*Maybe there is a bit of truth there. I still have doubts about whether we interpreted the Michel Haïssaguerre  study properly)

Final message

ERS is a widely prevalent normal ECG variation with a minuscule risk. High-risk subsets need to be screened only if the J waves encroach and spill dangerously into the ST segment as well. Of course, this pattern is of serious concern if there is a family history of young SCDs has occurred.

The purpose of scientific knowledge in medicine is to reduce suffering. I wish, at no point in time, it can increase anxiety. We need to introspect, whether to report such ECG entities at all. In the name of patient empowerment,  let us not create Iatrogenic, knowledge-induced panic. Labeling a person with a fearful entity and then keep reassuring and asking him to forget, is not a fun exercise. Meanwhile, indiscriminate reporting of such mass ECG phenomena can potentially turn out to be a commercial game.

For advanced readers: Important queries for fellows

  1. Why Inferior lead ERS is more risk prone than lateral?
  2. What happens to ERS pattern during exercise?
  3. What is the genetic and structural overlap between ERS and Brugada? 
  4. If ERS develops unstable angina will the ST elevate or normalize or depress?
  5. How will be the RVOT and RV wall motion in ERS?


Here is a good review of this topic by

1.Dr. KK Sethi et al.Indian Heart Journal. 2014

2. Hanboly NH. Haissaguerre syndrome: The gray area still exists. Nig J Cardiol 2017;14:59-64.


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The main reason for all those jitters, we cardiologists, get every time we puncture the IAS is not due to a lack of expertise and experience perse. There are two more reasons. First and foremost, it is still largely a blind* procedure. (Even in this era, where drones with HD vision shoot one-meter targets from a 1000 KM range )  *TEE and ICE are there, but they rarely give enough confidence. 

The second reason is more important and is rectifiable. It is the perception error in our anatomical cognition, that is fed to us from first-year medical school. We are made to believe (at least to people like me ) The right atrium is aligned like a perfect box on the right side, sharing a wall called IAS, and the left atrium is obediently placed left of the right atrium. Please realize the heart is such a complex twisted single tubular organ, the venous end, in a stunning backward loop brings the LA  most superior and posterior to the right atrium overriding the left-right relationship.) 

The right atrial terrain and IAS with multiple bumps and holes. Note the true IAS constitutes only 20% . This is where our punctures need to be.

Development of IAS 

IAS development and the number of layers it sandwiches, the tortuous tracts of PFOs, the fossas, and its variable limbus is a big topic. Further, It is worth recalling, the true IAS hardly forms 20 % of the area of the interatrial contact surface.

(the differential regression of sinus venous,  along with infolding of the roof and along with curious septum spurium , the ubiquitous septum secundum make the texture, area & shape of IAS, a fascinating creation, though troublesome for the cardiologists ! ) Whoever named that part of vanishing  IAS  as spurious, (I think it is Henrry Grey ) has much fore-vision.


Forget about all this. Tell me how to cross this difficult terrain 

Coming to the real world of interventions,  we need to do targeted punctures in different spots of IAS in various interventions.(Mitra clips, LAA device, PTMC, PV abaltions, Mitral paravalvular leaks , TMVR etc) This has made this task even more tricky. Experts are always there to help us out. Like swimming, it can never be learned in books.

This 19-minute clip from. Seoul, South Korea is an excellent resource. Thanks to  Dr. Sang Weon Park 


Along with sound anatomical knowledge, improved hardware, and imaging like deflectable sheaths, TEEs, and ICE (intracardiac echo ), let us hope, it will soon become an easier task for everyone.

Final message

 Understanding “attitudinal cardiac anatomy” with fluoroscopic overlay is the key. Again, it needs to be stressed, “Right is not right, and left is not left” when it comes to true atrial geo position. LA is equally posterior, superior, and of course to the left of RA. Some of my colleagues are blessed with a special 3-dimensional skillset  (Inherited ?) I failed miserably to understand this, till very late. I am sure, Dr. Park’s video will help all our youngsters to cross the difficult gateway to the left side of the heart. 


One more good read

B. O’Brien et al. / International Journal of Cardiology 233 (2017) 12–22


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Fibrillation is a continuous, chaotic muscular activity. In AF, atrial muscle is expected to lose all coordinated contractions with fibrillatory waves replacing P waves. Have you ever spotted a suspicious  P wave in a strip of otherwise explicit AF?  If not, this write-up is not for you.

An evolving rare theme in Atrial fibrillation 

Have a look at this ECG 

Here is an ECG, that was reported as AF, multiple APDs, or Possible AF, Pre AF. I suggested the term AF in transition. While few agreed, many said it is a straightforward SR with APDs, making it appear irregular RR. 

But, the fact of the matter is, ECGs are insensitive to pick all fibrillatory wavelets. It can selectively pick a few coarse F waves and make them appear as P. I think, in this era, we should not diagnose AF by proxy, ie absent P waves. Rather, we need to look actively for fibrillatory wavelets. (Imagine all sinus arrests will qualify for f fine AF with a slow ventricular rate  is it not ?)

The semantics of AF nomenclature is long. Intermittent AF, and paroxysmal AF, are well-known entities. It is now clear, AF can occur for a few seconds and vanish too. It seems we need to play some more linguistics with the most common cardiac arrhythmia. (Non-sustained AF,  evanescent AF, etc )

Some thoughts on this hide &  seek P waves 

  • Apart from the conventional list of absent P waves, one more example is repetitive APD can stun the atrial muscle for a few moments or minutes.
  • Then, we always have the issue( eluded to earlier) of sinus node paralysis, with irregular junctional escape mimicking AF.
  • Amiodarone can reduce fibrillatory rate, and (AF cycle length ?) Coarse F waves slow and stabilize it to mimic an organized P wave
  • P on Ta waves (Like R on T ) can trigger a nonsustained AF for a few moments in a functional manner without real pathology in atria.


A funny memory  brings back an EP truth 

During our student days, my Professor used to trap us with this question, Which atria would fibrillate in mitral stenosis?  Many of us blinked, and few had no hesitation to say, it is the LA that fibrillates. Now, after 50 years we realize, how fascinating the secrets AF has unfolded. Some organized activities are often in the right atrium, even as LA begins the process of AF. It is possible it may take variable time for the left atrial chaos to spill over to RA*. During these electrical uncertain times, some of the right atrial P wave activity refuses to die down.  Even more dramatic one Atrium alone can permanently fibrillate and others completely insulated by blocking the signal in the Interatrial pathways. (Ref 1 ) Ndrepepa’s paper in the JCE 2000)

Final message.

True scientists rarely bother about questioning a dictum. The concept of non-uniform AF was first thought of by (Schrmp et al Ref 2) 100 years ago in 1920, and Zipes(Ref 3) hypothesized this in 1973. now, in the Year 2000, Ndrepepa confirmed it with EP studies. The spotting of occasional  P waves is not forbidden in AF if the contralateral atria decide to block the incoming AF signals and keep generating their own P waves 

Young EP guys, now that you are equipped with the sophisticated intracardiac GPS,  please pursue this provocation in AF. One more piece of evidence we observed in the echo lab. Try to look at Tricuspid doppler A velocity waves in full-blown AF patients. You can see the surprise for yourself. This is very good research work to do. This is one of the ideas I gave to my fellows at MMC. Now, it is free for all to pursue whoever wants to do this. The clinical implication* will follow.

* A lingering query, how common is RAA clot in mitral stenosis with AF and the possible threat of pulmonary embolism?


1,Ndrepepa G, Zrenner B, Schreieck J, Karch MR, Schneider MA, Schömig A, Schmitt C. Left atrial fibrillation with regular right atrial activation and a single left-to-right electrical interatrial connection: multisite mapping of dissimilar atrial rhythms. J Cardiovasc Electrophysiol. 2000 May;11(5):587-92

2.Zipes DP. DeJoseph RL: Dissimilar atrial rhythms in man and dog. AmJCardioi I973;32:6l8-628.

3.Schrumpf P: De 1’interference de deux rythmes sinusaux. Preuve  du dualisme du nodule de Keilh. Arch Mai Qwur 1920;l3:168-173


The snapshot from Ref 1 . The term Isolated AF confined to one atrium could be a rare event, but, no one can deny we have plenty to learn from them


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LA dimension and volume have become vital parameters in recent times, especially, with the entity of HFpEF is becoming so common. LA not only acts as a live barometer, reflecting all that happens in LV, but it is also a chronic marker of LV diastolic function. (Funnily referred to as HBA1c of diastolic dysfunction) 

What is normal LA dimension & volume ? 

  • Normal left atrial diameter < 4.1 cm in men or < 3.9 cm in women
  • Normal left atrial volume indexed for body surface area (BSA) is 34 ml/m2 for both women and men 

Which part of the cardiac cycle do we measure? 

Ever since Wiggers introduced the overwhelming concept of LV systole and diastole, most of us ignored the fact that atria do have a separate contraction relaxation cycle, independent of what happens in the ventricle. Of course, atria and ventricles act as a single chamber in diastole. In reality, atria lack true boundaries when it acts as a conduit. The LA dimension varies considerably during the atrial cardiac cycle. Look at the  LA pressure-volume loop, which can frighten anyone, with its horizontally lying figure of 8 pattern. During every cardiac cycle, the volume reaches atleast two troughs and one peak.

Don’t get frightened with this graph, spend some time, and you will get it right, Begin at  “3” o clock position with the onset of diastole with a downsloping green loop, that continues as the red line of atrial contraction to end up in systole. The entire black loop, that happens during ventricular systole depicts the true reservoir function. with MV closed. ,


As of now, we have a consensus, LA volume is measured typically in LV end-systolic frame. ( Rather, we measure it at maximum LA volume ) However, we have 4 different LA  volumetric components to assess, as this article excellently depicts. (Hoit BD. Left atrial size and function: role in prognosis. J Am Coll Cardiol. 2014 Feb 18;63(6):493-505.)

What could be the limitations of the traditional end-systolic measurement?

No single measurement will give an overall LA function assessment. But still, Somehow, we have measured the maximum LA  volume as a reference of true diastolic function. This happens in LV end-systolic point where atria reach the maximum size. But, here is a catch, we assess the left atrial function before its main physiological function of emptying takes place.

How about assessing  LA efficiency after it completes its job, ie end diastole? 

In LV function end-systolic dimension has pride of place as it is devoid of influence from loading condition. If applying the same logic, the “end atrial” systolic dimension(Which is the same as LV end-diastolic point/or post A ) should be perfect. It can also help measure the residual LA volume after its systole.

A potential advantage of LV end-diastolic dimension (The Heart & Soul study )

Maybe, this is less affected in the presence of MR systolic jet will spuriously elevate LA volume. In AF also this parameter is less likely to be influenced by LA preload.

Final message

Suddenly, we are debating a fundamental Issue, ie timing of LA measurement. While the end-systolic size/volume is the current standard, the LA dimension in the end diastole also provides useful info. There are at least 4 different LA volumes, at different parts of the LA cycle that need to be studied for a proper understanding of diastology (Unlike LV which has only two).

Now, we may need to ponder, if there is a mean LA volume, measured with the 3D volumetric analysis or MRI, that could be representative of the global LA function. 


Thadani SR, Shaw RE, Fang Q, Whooley MA, Schiller NB. Left Atrial End-Diastolic Volume Index as a Predictor of Cardiovascular Outcomes: The Heart and Soul Study. Circ Cardiovasc Imaging. 2020 Apr;13(4):e009746. doi: 10.1161/CIRCIMAGING.119.009746. Epub 2020 Apr 20. PMID: 32306763; PMCID: PMC8846436.


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Myocardial infarction, a gross pathological entity renamed now as STEMI for clinical purposes, continues to be the most famous medical emergency that triggers a series of calls, right from 911 to the ER, that eventually ends up in CCU or a 24/7 cath lab. The heart, can’t wait for all these external responses when it is challenged with a vascular accident. The moment ATO occurs, two things happen. The endogenous fibrinolytic led by native tissue PA (Tpa) tries to get rid of the thrombotic plug by all its means. It succeeds in 15%. We call it spontaneous lysis or aborted MI. Many lives are lost in the remaining before they reach the hospital..

Meanwhile, the immune high-command deputes scores of neutrophils to the ground zero Fig 1) to supervise what is happening and try to heal the injury. It is worth, understanding, that activated WBCs, sort of convert myocardial infarction from a vascular event to inflammatory pathology, as the hour progress.


Fig 1  Infarcted myocardium Invaded by neutrophils



What do these neutrophils do?  

It will be our ignorance, if we think, they simply crowd around the myocytes helplessly, that is hit by ischemia. They are sent with a specific purpose to protect and heal the myocardium. Very often it fails in its mission is a different story. These fighting neutrophils send a subtle signal  of their presence with a mild increase in temperature during ACS  ( Patel  Prognostic usefulness of white blood cell count and temperature in acute myocardial infarction  Am J Cardiol. 2005 Mar 1;95(5):614-8. )

Is neutrophil invasion good or bad for the myocardium?

These are pro-inflammatory cells. meant to promote healing and mitigate Injury. Interleukins and Leukotrienes do have a healing power as well. But, what happens, in reality, is, still a mystery. As of now, it is tempting to think, it does more damage than good. Its role changes over time. 

 Acute reperfusion Injury in Primary PCI 

Neutrophils are quiet obedient cells generally, but once activated, their behavior can’t be predicted. It may start attacking the host cells, We know reperfusion injury is real and poorly understood. Delayed reperfusion, is well known to cause myocyte softening and lysis. What we know for sure is, primary PCI, induced accelerated flushing of these angry neutrophils is definitely related to no flow, microvascular plugging, and cardiogenic shock.  (The fact that no-reflow and reperfusion injury is less of a problem in fibrinolysis  demands introspection)

Diagnostic & prognostic value of neutrophilia 

Neutrophilia is such a nonspecific response, faces ridicule for its clinical utility. But, In reality, it can be a worthy parameter, to time the age of the infarct (or even confirm* the ACS ) in otherwise equivocal clinical presentation.(Ref 2) More importantly, it provides prognostic information. One more potential use is Neutrophil count to guide the timing of surgery post-MI (as in VSR) A neutrophil count could help avoid the active phase of inflammation.

*I recall my surgical professor’s emphasis on leukocytosis to confirm acute appendicitis during the first clinical year. 

Final message 

There is no academic by-law, that forbids full-blown interventional cardiologists from having an affair with basic science. Unless the core science is irreversibly bonded to the bedside, we can never reap the true benefits of translational research. Hematological aspects in STEMI is one such underrated discipline. Also, we must encourage every postgraduate student in pathology/biochemistry/physiology to visit the CCUs or sit in the cath lab gallery more frequently. Watching the cardiology stalwarts plowing through the blocked coronary arteries, racing against time, is sure to kindle young minds, for a potential molecular breakthrough in cell survival and healing following myocardial hypoxia.


1.Ma Y. Role of Neutrophils in Cardiac Injury and Repair Following Myocardial Infarction. Cells. 2021 Jul 2;10(7):1676. doi: 10.3390/cells10071676. 

2. Thomson SP, Gibbons RJ, Smars PA, Suman VJ, Pierre RV, Santrach PJ, Jiang NS. Incremental value of the leukocyte differential and the rapid creatine kinase-MB isoenzyme for the early diagnosis of myocardial infarction. Annals of internal medicine. 1995;122:335–341. [PubMed] [Google Scholar]

3.. Cannon CP, McCabe CH, Wilcox RG, Bentley JH, Braunwald E. Association of white blood cell count with increased mortality in acute myocardial infarction and unstable angina pectoris. OPUS-TIMI 16 Investigators. Am J Cardiol. 2001;87:636–639. A610. [PubMed] [Google Scholar]

4. Bhatt DL, Chew DP, Lincoff AM, Simoons ML, Harrington RA, Ommen SR, Jia G, Topol EJ. Effect of revascularization on mortality associated with an elevated white blood cell count in acute coronary syndromes. Am J Cardiol. 2003;92:136–140. [PubMed] [Google Scholar]


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Pardon ,this video is nothing to do with cardiology. It is from the archives of the United nations library .This can teach some important lessons in art of communication , sharing to all folks, especially medical students. It was recorded in 1959 in Newyork, UN head quarters.Four 17 year old school girls & boys were invited for a debate on a complex topic. Does God exist ? How do you pray ? and what is the purpose of different religions ?

I keep wondering , how these youngsters accumulated so much wisdom and express it in such a polite manner too. Mind you, this was recorded , when learning happened with out any digital aids.The word Internet was unheard off. No ego, no bluntness, no diatirbes that has become a norm in many debates now. I got a punching lesson from this clip, be gentle when taking extreme views in any topic.

I wish, every medical debate in class rooms should happen this way.The key to succesful debate is, to accumulate knowedge, willingness to question the convention, and respecting the oppositie point of view.

The highest point of talk show, (for me) was, when the Brazilian girl(due respects, she should be nearing 80 years now) tell us casually some things are not meant to be understood in life .I tell the same when some patients ask too many questions about their illness which may not have an answer.

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Management of recurrent ventricular tachycardia has developed a lot in recent times. Anti-arrhythmic drugs(AADs) were a cornerstone for most recurrent and refractory VTs till recently. Surgeries including CABG,  repair of the aneurysm, and subendocardial resection has helped to control many post-MI ischemic VTs. Soon they became obsolete. Realistically, PCIs had little impact on post-MI VT for some unknown reasons. However, with the advent of ICDs and RF, ablation, a new dimension is added to this field. 

ICDs, though an attractive device, don’t prevent a VT but vow to nullify the consequence of VT. This is problematic. ICDs in spite of their ability to prevent SCD effectively, it has little say in preventing non-sudden deaths of in any form of cardiomyopathy. (In fact, there is some evidence ICDs might increase myocardial damage with inappropriate shocks )

Hence, RF ablation can be called as true curative therapy by extinguishing hot spots of VT genesis. Still, we need to understand ablation is technically creating new dead myocardium (in alreadly  damaged myocardium) and hence, can’t avoid a consequence. More importantly, ablation as a modality is technically more demanding. We have accumulated huge experience with the help of electro-anatomic imaging and cutting-edge hardware in the last few decades. Still, we find it difficult to zero in the target area of RF ablation, with all available techniques of mapping (Activation, substrate, entrainment, and pace mapping) The reason is,  VT circuits can be really complex ones. Not only different loops but also it can travel deep into the myocardium (Intramural or epicardial) making a single approach endocardial often futile. Success rates vary between 60 -70% (Some may claim 90 +)

This post wants the young fellows to take on this fundamental issue and learn in-depth about the arrhythmia circuit.(Get Inspired by Dr. Samuvel Asirwatham of Mayo clinic work )

What is the best site to ablate ventricular tachycardia?

  1. Exit point 
  2. Central isthmus
  3. Entrance 
  4. Inner loop
  5. Outer loop
  • Though logic would tell us we can intercept an arrhythmia by ablating anywhere in the circuit. But the issue here is we need to permanently ablate it. not just interrupting. 
  • The best site to ablate is the exit point or entry point. Maybe isthmus. I am not really sure. But, one thing is clear, the outer and inner loops are not important. Further, live tissues are the culprits and not the scars and infarcted zones. 
  • One more possible answer is to try to ablate all (or maximum) points in the circuits.

How to identify entry points and exit points?

Not a simple answer .EPs apply their life experience to do that, assisted by technology. Not everyone who has a Carto -GPS can do that.

One simple answer for the fellows is, in entrainment mapping,  critical sites can be somewhat arbitrarily labeled as exit, central isthmus, or entrance on the basis of the Stimulus-QRS interval relationship to the TCL. Exit sites will show an S-QRS interval < 30% TCL (QRS onset shortly after pacing), central isthmuses will show an S-QRS interval of 30% to 50% TCL (some delay in QRS onset after pacing), and entrance sites will show an S-QRS interval of 50% to 70% TCL 

Ruairidh Martin et all Circulation: Arrhythmia and Electrophysiology. 2018;11:e006569

Final message 

Key to the successful ablation of VT is the accuracy in choosing the target site. Locating the target is meaningless if we can’t reach that site. Reaching the site is again futile unless we are able to deliver adequate burning or icing with sufficient contact.

Meanwhile, AADs can never be ignored in spite of the apparent side effects, for the simple reason they reach the VT circuits without any fuss. The Pharma industry has almost lost its interest in AAD research and the hyper-talented EP guys are squarely responsible for this unintended consequence.

Future directions

RF energy modification and newer catheter designs will help. While cryoablation shows a promising advantage over RF, it is still to prove its sustained efficiency. Meanwhile, other ablation modes are being tried. Transvascular ethanol ablation and stereotactic radio ablation have both shown promise for arrhythmias that fail other ablation strategies.

Some more questions

  • What is the difference between arrhythmia focus of origin and entry point? 
  • Once the VT is set in, what is the relevance of its origin? 


One of the very good reviews on the topic.

1.Gustavo S. Guandalini, Jackson J. Liang, Francis E. Marchlinski, Ventricular Tachycardia Ablation: Past, Present, and Future Perspectives,
JACC: Clinical Electrophysiology, Volume 5, Issue 12, 2019, 1363-1383,
2;,W.G. Stevenson, H. Khan, P. Sager, et al.  Identification of reentry circuit sites during catheter mapping and radiofrequency ablation of ventricular tachycardia late after myocardial infarction Circulation, 88 (1993), pp. 1647-1670

3.M.E. Josephson, L.N. Horowitz, H.L. Waxman, et al.Sustained ventricular tachycardia: role of the 12-lead electrocardiogram in localizing site of origin Circulation, 64 (1981), pp. 257-272

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EHJ has listed the top 10 papers in cardiology in the year 2022 in its current issue. 

Kindly go through this when free. While each of the 10 has its own importance, one meta-analysis, I thought was a  real bright spot. Though the message it conveys is nothing new,  it reaffirms an important management principle in ACS. Getting curious? Before going into the paper, a mini pretest

What is your take on these 4 statements on ACS?  True or False

1. STEMI is an emergency, NSTE-ACS* is not an emergency

2. Both are true emergencies.

3. STEMI is definite, yes, but  NSTE-ACS may or may not be (Mind the GRACE score dude !)

4. Even STEMI can be a non-emergency if the patient reports after 24 -48 hours.

(Remind you, NSTEACS = UA+NSTEMI , still often used interchangeably)

Hope we don’t have difficulty in identifying the wrong response. Whatever the answer to this somewhat insulting question to our intellect, forget it. Now, read this paper, which is listed as one of the most read last year. It is about the impact of early invasive strategy in NSTE-ACS.

Kite TA, Kurmani SA, Bountziouka . Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

Conclusion is pasted for the busy guys.


  1. What is overall NSTEMI in-hospital mortality? (Everyone knows for STEMI it is around 4-8 %, no one seems to be sure about NSTEMI. I think it can’t be estimated accurately, guess it is 1 -2% )
  2. Is there a primary PCI equivalent situation in NSTEMI?  What are they? (Left main UA with AVR ST elevation comes first on the list)
  3. Based on the urgency to treat how does the ultimate outcome change? (This is what this meta-analysis by Kite et all proved.It is not a new revelation though . Recall the landmark ICTUS study  of 2010 which was largely kept in the dark )

Final message

One lay definition of STEMI is, It is a mass of myocardium under fire. True UA/NSTEMI is, a mass of myocardium, that is threatening to go on fire. When firefighters are able to reach a smoky building before the onset of a fire, no doubt, it looks like a great & awesome response, Isn’t it? Unfortunately, the myocardial landscape is different and NSTEACS is such a heterogenous entity that doesn’t welcome unsolicited aggressive, emergency rescue missions. That’s one of the messages we get (at least I got )from this top-read paper in 2022. 


1.Emanuele Barbato, Margaret McEntegart, Tommaso Gori, The year in cardiovascular medicine 2022: the top 10 papers in interventional cardiology, European Heart Journal, 2023;, ehac778https://doi.org/10.1093/eurheartj/ehac778

2.Kite TA, Kurmani SA, Bountziouka V, Cooper NJ, Lock ST, Gale CP, Flather M, Curzen N, Banning AP, McCann GP, Ladwiniec A. Timing of invasive strategy in non-ST-elevation acute coronary syndrome: a meta-analysis of randomized controlled trials. Eur Heart J. 2022 Sep 1;43(33):3148-3161.

3.Damman P, Hirsch A, Windhausen F, et al. 5-Year Clinical Outcomes in the ICTUS (Invasive versus Conservative Treatment in Unstable coronary Syndromes) Trial. J Am Coll Cardiol. 2010 Mar, 55 (9) 858–864.https://doi.org/10.1016/j.jacc.2009.11.026

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