This is the story of PCI to LAD from the customary bifurcation workshop for the budding experts, which ended up with a compulsive final OCT run-through, triggering a debate on what to do with the side branch.

What shall we do next?
  1. Just balloon dilate the distal strut
  2. Would consider a second stent. Maybe a TAP  depending upon LCX morphology
  3. At this stage, I would like to know the FFR or iFR across LCX Jail.
  4. Get rid of this OCT, Let me have look at regular CAG. I bet I can make a better decision.
  5. Leave it alone if the clinical status & profile is good

Leave it alone? Is it not an incomplete Job?

Definitely incomplete. Please realize, No job is complete in interventional cardiology. If we believe so, it exposes our Ignorance ( & some arrogance). Intentional side branch jailing is an integral part of  PCI techniques. Are we not ignoring day in and day out. 

Someone in the audience asked Why did you do OCT at all? 

The chief operator quipped “You can’t ask this silly question in a scientific workshop. We bought the OCT kit to improve the quality of PCI. We are proud of it. Really feel blessed to use it and I am sure my patients will benefit from it”. We have to agree with him. These new Imaging techniques though give us extra high-definition, but it comes with troubling revelations with their new vision. If you are pathologically honest and believe in empowering patients, it is absolutely necessary to convey the following facts in the discharge record as well. It would be something like this, “There was a 120-micron strut crossing the LCX ostium, that might continuously impede a chunk of platelets & RBCs every beat, for the rest of your life and might enhance the risk for thrombosis. (Of course, DAPT will take care of it and ask the patient not to worry)” 

OCT: One-minute review

OCT is Indeed a stunning Innovation. It can be useful in all 3 phases of PCI. 1. Assessment and preparation of lesion bed. 2. during stent deployment and optimization. ,3. Post-stenting follow up. The technology has grown so fast, now angiographic co-registration and longitudinal frame reconstruction comes inbuilt. It required 3 versions of LUMEN study and a 4 th one (LUMEN 4 ) is yet to come, expected in 2022  to prove the worthiness (or worthlessness)  of OCT. 

One attractively named DOCTORS study asked the specific question directly (Does Optical Coherence Tomography Optimize Results of Stenting)”  This is from NSTEMI patients .read yourself for the conclusion. It is not convincing to me.  Meneveau N.,  DOCTORS study (Does Optical Coherence Tomography Optimize Results of Stenting)”Circulation 2016134: 906.

Mind you, OCT is not only an expertise-dependent procedure, it also has important imaging limitations. It has low penetration max 2mm, can not differentiate lipids from calcium, shadowing behind red thrombus is an issue and most importantly it may miss the external elastic lamina (EEL) and measurement errors are real. 


If an imaging technique to assess a stent *(*Still waiting to prove its worthiness) could cost more than the device itself, realize how good our economic intellect is. Just because your lab has an OCT console, it need not transform into a technically perfect PCI. There are at least half a dozen factors other than Imaging that matters. 

Final message

OCT is a breakthrough technology that needs to be used judiciously and it definitely helps us understand the nuances of coronary stenting, especially in complex lesion subsets, and its mechanical and histological contents. However, let us not propagate a false message, that without OCT we can’t perform a perfect PCI. Give due respect to all those sharp-eyed interventional cardiologists with good techniques, who can do a better job, beating the HD vision of OCT, with their native blindness. 




Can you guess how many PCIs are done with OCT guidance globally?

It is less than 5 %. In India, it must be, I guess it is < 2% So, we are living in a terrifying world of coronary interventions, where  98 % of PCI is happening blindly, sub-optimally, and unscientifically., Data from CLI-OPCI registry adds more panic:  Centro per la Lotta Contro l’Infarto – Optimisation of Percutaneous Coronary Intervention (CLI-OPCI) registry:  It says device-oriented cardiovascular event (DOSE) is high with OCT detected sub-optimal  PCI.

So, what are we going to tell our patients who will undergo PCI (undergone) without OCT guidance in the past, present, and future?

Simply ask them to forget this OCT stuff. Just reassure them. Nothing will happen.

It brings a unique sense of greatness and gratitude to hear the voice of the father of Interventional cardiology decades after his demise.

The invention he made has evolved so much. Though, Dr. Gruentzig didn’t live to see any of them, the genius in him predicted most of them. This Interview was recorded a year before his small plane, which he loved next only to his pet balloons, crashed on the Atlantic coast along with his wife. That is history.

This is how the news was reported across US media on October 29th, 1985. (Reconstructed, click over the pic for high resolution)

It was a fact, that he defied the warning and flew in the adverse weather, what many of us were unaware of was, that he wanted to rush to Emory, only to see a patient whom he had done a PTCA, a few days earlier, developed some complication. This makes his death all the more poignant (Ref Dr. H.V. Anderson )

Here is a good account of the life history of Dr Gruentzig.  Link to the article 

Why didn’t you do it … for this patient?

 “I thought, he was not the right patient for the procedure. I believe, what I did was the correct decision. Why all this fuzz? after all, the patient is doing so well without that procedure,.. are you worried about that? 

“No, I need an explanation, we have a fully functional cath lab in our center. The patient came in the right window period. Still, you haven’t offered the best mode of treatment”.

“I can reiterate it again sir. Just because a lab is available 24/7, it doesn’t make all patients eligible for a  PCI. I think I didn’t commit a professional misdemeanor when I decided in favor of fibrinolysis. In fact, I would be guilty had I rushed him to the cath lab, just to satisfy the misplaced scientific position we have decided to adopt. If you think, I am culpable for successfully treating a patient without taking the patient to the cath lab, you may proceed with the penal action.

Before that, I would request you to please read the current edition of this book we all revere. (Which continues to mentor physicians all over the globe for the past 50 years)


The current edition of Harrison 2022 is just out. I thought, there is something great learning point in Cardiology chapter, specifically about the reperfusion strategies in STEMI

My hearty thanks to the editors of the chapter for the crystal clear expression about this much-debated procedure* and specifically choosing the word “PCI appears* to be more effective ” (even) if it is done in experienced persons in dedicated centers. The choice of the word used by the authors is Intentional and must be applauded. This message must be propagated to all our fellow physicians. What a way to convey an important truth pertaining to the management of the most common cardiac emergency, while many in the elite specialty are so dogmatic in their assertion without verifying the reality.

*  The verdict is still under the jury even after 3 decades, since the PAMI days of the early 1990s. Thank you, Harrison. What a gentle, but a righteous way to express an opinion about a procedure that is apparently enjoying a larger-than-life image based on a handful of studies and a flawed meta-analysis.

Final message 

Primary PCI is just an alternate form of treatment to fibrinolysis in STEMI. Both are equipoise in the majority of patients. Extreme care and diligence are required to harvest the small benefit the PCI seems to provide.  There are lots of ” if and buts” that decide the success of this procedure. Get trained, and do it selectively for those who really need it.


You may call yourself a super-specialist. But, please realize, If you have any doubt about key management strategies, never feel shy to take a cue from Internal medicine books. The greatness of these warrior books is that, it comes devoid of all those scientific clutters backed by premature evidence. 


AF is not only the most common cardiac arrhythmia,it is also an extensively researched entity in cardiology literature. We are trying to rein in, this arrhythmia for the past three decades with multiple strategies. Drugs, pacemakers, ICDs devices, surgical cuts, RF catheters, and the latest technique is trying to frostbite the atrial electrical circuits with ICE. ( Karl-Heinz Kuck,N Engl J Med 2016 )

It is believed that up 60% of AF originate from pulmonary veins. What does it mean?  So, when we blindly suggest PV Isolation routinely for all PAF,  there is 40% futility straightaway! Apart from the hugely variable anatomy of the pulmonary veins, there are prohibitive levels of recurrence due to  PV reconnections. Maybe, will find new technical solutions as we are now moving in 2nd or third generation cryo balloons, 4D imaging, contact force sensing, etc. But let us not forget there are other sources of focal electrical activity too  

Importance of non-PV ectopic beats initiating  AF(Ref 1,2)

  1. Superior vena cava (SVC),
  2. left atrial posterior free wall (LPFW),
  3. LA appendage
  4. crista terminalis (CT),
  5. coronary sinus ostium (CSO),
  6. Ligament of Marshall
  7. Interatrial septum (IAS) 

Ablation or no ablation, we need to reflect on two things in the management of AF.

1. AF can be triggered by totally different mechanisms like intermittent hypoxia, adverse electrolytic flux, diffuse atrial interstitial pathology or amyloid, etc. Before calling the appointment desk of the EP guy’s office please rule out all the systemic causes. This could be your last (lost) chance to save the atria from pulmonary burns.

2. This one is more important. Read carefully. It is not a divine protocol that demands us to restore sinus rhythm in all patients with AF. There is an excellent knowledge base, backed up by wonderfully done studies. (Need not mention the trial name, I think) that should effectively neutralize our compulsive &  misplaced urge to bring back sinus rhythm in all chronic AF.

With respect to the overall outcome, It hardly matters whether you treat the AF by rate control or rhythm control. While there is major technological leap in our fight with AF.It is heartening to know simple measures like regular exercise can control or reverse AF by atrial fatty mass regression.

Final message

We have played with fire for quite some time within the innocent lesser chambers of the heart  (RF ablation) and burnt our reputation considerably. Now, silently we have decided to fall for a more friendly weapon ICE. But we must remember our obsession with the pulmonary vein as the only source of initiation of AF is essentially flawed. Further, all these hyper-technology-based combat of AF is indicated only in a fraction of our patients (Maybe 5-10%) 


1.Chen SA, Tai CT, Yu WC, Chen YJ,  Right atrial focal atrial fibrillation: electrophysiologic characteristics and radiofrequency catheter ablation. J Cardiovasc Electrophysiol. 1999 Mar;10(3):328-35. doi: 10.1111/j.1540-8167.1999.tb00679.x. PMID: 10210494.

2.Lin, Wei-Shiang, et al. “Catheter ablation of paroxysmal atrial fibrillation initiated by non–pulmonary vein ectopy.” Circulation 107.25 (2003): 3176-3183.


If you think this write-up is too biased, please read the CABANA trial fully before ditching this post into the dustbin.

 1908, Going back on the time machine, more than 100 years ago, world war I was all set to begin, and the great Titanic was being built in the Belfast shipyard. A parallel histroy is being created in cardiology.

This is a brief story of Dr. James Mackenzie, a general practitioner from a remote Scottish village who ended up with the title of the father of British cardiology. Dr. Harvey might have invented circulation, but it was Mackenzie who taught the science of arterial pulse and wrote a classic on the topic to the new medical world. He was able to decode the secrets of the jugular venous pulse as well and diagnosed various arrhythmias including atrial fibrillation at the bedside. He used the polygraph to record his vast observations in pulse and JVP waveforms which were popularised later by Dr. Paulwood. ECG was just beginning to enter the scene in the 1920s. This makes his work all the more significant, as his treatise on pulse and JVP were based purely on clinical acumen.

                                                  Sir James Mackenzie, 1853-1925

Apart from his stupendously successful academic life, it was through his death, that he sent out an extraordinary message to the scientific community. His deep desire to know the truths about coronary atherosclerosis was astonishing. Since he himself was suffering from angina and possibly Infarct, he became his own subject of study. He became case number 28 in his own book on cardiology. When he was on his death bed, as a last wish he Insisted his colleagues do a learning post-mortem and keep his heart in the same hospital he worked. When he died in the early morning of January 25th, 1925, as per his wish, his students Dr. Parkinson,(WPW fame) and another pioneer Dr.Thomas Lewis did an autopsy on his heart.

It is tragic to know about the final days of Dr. Mackenzie’s life and how their beloved students performed the postmortem on their teacher and later published their findings in the British Heart Journal. (BHJ link )It is one of the poignant moments ever recorded in the history of cardiology, a doctor wishing to teach cardiology lessons to the generation next with his dead heart.No surprise, he is being conferred the title of father of British cardiology.


Final message

How could an unassuming GP practicing in a remote rural place reach the pinnacle of scientific glory?

Yes, it is possible. Today’s young (super) specialists must realize, that true scientific minds don’t require exotic research labs, tools, or conflict-ridded funds from Industry for the growth of science. All we require is a passion to teach, and the curiosity to learn. The rest of the things will follow… I think that was the message in the great life of Sir James Mackenzie.


Further reading


james mackenzie heart


            No one will disagree, this is the most celebrated medical quote of modern times 

It is so unfortunate, the quote has almost become a silly cliche for every one of us including the physicians, and patients. Preventive medicine always struggles to prevail over its starry-eyed colleague, curative medicine in spite of the fact that cure is an assumption in many illnesses. Classic examples are diabetes, hypertension, and atherosclerotic disease. Many of the chronic diseases that afflict human beings have no complete cure. At best we can control them. All that we do is symptomatic and supportive treatment.

Overlaps between preventive and curative medicine

Meanwhile, we must also understand preventive medicine is not only about sanitation, nutrition, and a good lifestyle. Most facets of curative medicine are actually preventing complications of the disease. So in reality curative medicine works by preventing events. There is a big overlap.

The cure is often a mirage except in treatable medical emergencies. Still, we strongly believe every disease listed in the ICD code has a cure. It would be unbecoming of a medical professional if we don’t try for a cure. We are repeatedly sensitized that cost (& effectiveness too )should never be an issue. The Insane world of medical merchandise does this propaganda perfectly. How many of us realize PTCA and CABG are essentially poor palliative procedures in our attempt to conquer atherosclerosis and CAD? No surprise, 90% of the global cost of medical care is spent on prolonging the last one month of human lives.

Preventive medicine is less popular, primarily because it demands more effort, perseverance, and also wisdom. On the other hand, curative medicine gives a sense of accomplishment and also the glamor of modern medical modalities. Of course, one of the new chapters to be added in the current preventive medicine books is the public health dysfunction due to incongruous tertiary care.

We are caught in a vicious cycle of poorly administered preventive medicine and indiscriminate usage of curative medicine, with the former under siege, by the latter with its bigger design. It is almost certain, that the malignant growth of curative medicine is indirectly preventing the“preventive medicine” to reach its desired goals. 

Preventive medicine has its own issues. One ingenious way to increase the glamor quotient in preventive medicine is to increase the cost and mode of administration of (Apple watch!) No, It didn’t work. What about five-star preventive master checks? Maybe, it works on an individual patient level, but still, a suspect value on a global scale. The problem with master health checks is their skewed priorities. It aims to catch the disease very early in the asymptomatic or subclinical stage and try to administer the cure on a large scale, with an illusion of an intervention. (Recall the PSA times on the prostate, now the breasts armed with BRACAs may end up in the same story.)


Final message


No doubt “Prevention is better than cure” will be an immortal medical quote. Two things are essential. 1. The term preventive medicine is to be understood in proper context. 2. We may need to clip the redundant wings of “curative medicine” and divert the wasted resources to resurrect the much-maligned specialty of preventive medicine, for human goodness.


There are fundamental gaps between the two limbs of treatment. It sounds like a crazy regressive statement to criticize curative medicine. Both shall grow and prosper on their path.

 But … why is it not happening?


When does the high blood pressure befriends blood sugar and instigates the LDL to initiate the vascular damage? Does it sound like medical astrology? Yes, welcome to a new world of network medicine, polygenic risk score & computational genomics. Experts believe this is going to be the future of medicine.

Dr. Jospeh Loscalzo, Physician-in-Chief  Brigham and Women’s Hospital, a leader in the field gives a brief introduction.

How to understand these complex subjects? 

We need not bother much in one sense. It’s all made to look complex by big data machines and modern scientific wordplay. It is true, that the power of computing and machine thinking will help us reach hidden secrets in our bodies. However, the bottom line is, If we live a simple. peaceful, worthy, active life we can afford to forget about this sophisticated risk predicting science, which comes loaded with unlimited anxiety. Let the science grow at its own pace.

Imagine the consequence of a powerful artificial intelligence algorithm telling us in advance all the possible future biological adversaries with 100% accuracy.

Final message 

Do you believe in astrology, an ancient Indian science?   No. Never!

Do you believe in network medicine: Yes for sure!


Two good review articles on Network medicine

1.Barabási, A.-L., Gulbahce, N., & Loscalzo, J. (2011). Network medicine: a network-based approach to human disease. Nature Reviews Genetics, 12(1), 56–68. doi:10.1038/nrg2918 




The 12-lead ECG is the single most important investigation that has withstood the test of time for over 100 years. I think it will never lose its relevance in cardiology. However, the traditional sequence of the 12 lead printout could have been a little more user-friendly, especially in its ability to convey the anatomical orientation. Expecting some Innovation in the ECG reporting format. 

This illustration helps us to understand, ECG lead orientation, and coronary arterial territory, IRA localization with reference to the various surfaces of the heart. (Courtesy of visible body-modified ) Always remember the heart is an organ, made up by a complex fusion and rolling of bundles of muscles over a fibrous skeleton. It has multiple surfaces. Please avoid calling various surfaces of the heart as walls (Request the young medical students to un-tune their brain, from the inherent tendency to Imagine the heart as a well-demarcated four-chambered concrete structure built with bricks !) 


Animated version


Currently, IRA localization with ECG may seem to be a redundant exercise, as we are straightaway seeing the coronaries if taken for primary PCI or at least within 24-48 hrs mostly.

  • But, IRA localization gives us a rough idea(still useful) of what we are going to deal with during the PCI.
  • More importantly, multivessel CAD during STEMI can be very significant in the elderly, diabetic, and in women, which can sometimes confuse us about the real culprit artery. (Recanalised IRA vs other chronic lesions). Similarly, CTOs can masquerade as ATO and vice versa. Here, ECG will come in handy to identify the true culprit.

One useful tip in IRA localization of LAD 

Lesions proximal to D1 will depress the ST segment in inferior leads. In other words, if reciprocal ST depression is seen in inferior leads it is most likely a proximal LAD lesion. Paradoxically, in distal LAD lesions, ST elevation occurs in 2,3,AVF. (What may look like a global MI, is in-fact less sinister since it is a distal LAD Infarct)

* The wrap-around LAD* can also mimic distal LAD lesion with simultaneous Inferior and anterior ST elevation. *The wrapping needs to be complete and reach almost the crux (Super dominant LAD ) to cause ST elevation in 2,3, AVF.

Final message

The limitation of surface ECG in localization is real

  • Multiple IRAs or diffuse lesions, and collaterals all can confound the ECG -IRA correlation.
  • There can be overlap between large diagonal, Ramus (or even a large OM) when they all try to converge on the curvey and imaginary slope between the anterior lateral wall
  • Localization of IRA (Rather Angina-related artery (ARA) is a different exercise altogether.
  • Experienced operators will agree  there have been many occasions, where multiple diffuse lessons with delicate collaterals interwoven make IRA identification so difficult, and ultimately primary PCI is abandoned, and the patient returned back into CCU for lysis (Fortunately, Tenekteplace, and streptokinase never need to bother about IRA localisation you know !)


A useful review on this topic

Rafl an S, Kamal A.  Localization of the occluded vessel in acute  myocardial infarction. J Cardiol Cardiovasc Med.
2020; 5: 029-033

It is likely, that the biggest Impact & influence in current medical research may not come from the IQ of our scientists, their concepts, or the sophistication of the laboratory. Then what? Can you guess? It is the man-made mathematic sub-specality called statistics. We are going to either ratify or reject any research work ( on which we toil) based on the quality of numbers we generate. Such is the critical value of this specialty. Just pause a moment, and think over. How much importance do we give to the credibility and “quality of the interpretation” of any study? We have conveniently left it to our esteemed mathematical colleagues and some other invisible forces for a proxy inference.

I don’t think we will ever find an answer for this. Whether facts are made by statistics or statistics are made by facts ?

In recent times, one technique called propensity matching and scoring is used to conduct medical research where multiple covariables and confounders play.

What does the word propensity mean?

Oxford defines this word /prəˈpɛnsət̮i(pl. propensities) (formala tendency toward a particular kind of behavior

What is propensity matching in medical research?

In simple terms, it is doing a study without a true control group. It is a statistical gimmick where in we create an Imaginary or virtual patient arm What a way to conduct a scientific study? Those days, if someone suggests a study without a true control arm, it will go straight to the dustbin. (Of course, the concept came into vogue because we can’t have controls for ethical reasons or the rarity of the condition ) We do have  many other conventional covariable analytical methods available A well-written reference  (Ellicott C. Matthay, SSM – Population Health, 2020,)

Who created this propensity score?

I thought It was a new concept.No, it was proposed by Rosenbaum et al in 1983. (Ref 1) The extreme popularity it enjoys today is unexplainable. I think it is the simplicity, joy of doing a study without a troublesome control population, and the subsequent herd behavior of medical researchers.

Read here the pros and cons

Final message

Only two questions need to be answered before crowning the “propensity score” to glory in the statistical world. 1. Who has the final authority to define, what amounts to a confounding effect?  2, What are the statistical chances of missing an important confounder in toto due to baseline ignorance? 

Most statistical methodologies are like Holywood movies, some strike gold for no reason in spite of a lot of flaws. A few examples are meta-analysis and non-inferiorly trials. Propensity matching with a synthetic control arm could be a useful methodology in very selected situations.  It is unfortunate it has become a fancy tool and doesn’t deserve the wholesome approval for doing away with the true control arm.

Statistics may be great science, but it seems to work fine, only in the absence of continuous, unpredictable biological interference with mathematics.

Lastly, can propensity score take into account of confounding effects of the non-academic mindset of many researchers in senior positions? What shall we do with many important therapeutic guidelines created apparently based on solid evidence created with poorly created virtual (propensity) matches?


Experience-based medicine, wild logical guesses, empiricism, and trial of error methods,  all these are unavoidable in medical care and research. We have to move ahead with all the uncertainties in-situ and take our patients to a positive destination. 


1.Rosenbaum, Paul R.; Rubin, Donald B. (1983). “The Central Role of the Propensity Score in Observational Studies for Causal Effects”. Biometrika70 (1): 41–55. doi:10.1093/biomet/70.1.41.

2.Wang J. To use or not to use propensity score matching? Pharm Stat. 2021 Jan;20(1):15-24. doi: 10.1002/pst.2051. Epub 2020 Aug 10. PMID: 32776719.

Propensity score in cardiology research 


Who is the guiding the guidelines, which have become omnipresent & omnipotent ?

I don’t know really. Some good people I guess. But, the doubt creeps in when they try to coerce it on us.