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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%) 

Reference 

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.

Postamble

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

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 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

http://www.dundee.ac.uk/museum/exhibitions/medical/cardiology/cardiology1/

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            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.

Counterpoint

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?

 

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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!

Reference

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 

 

 

 

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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 !)

Reference 

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

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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?

Postamble

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. 

Reference

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 

 

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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.

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A brief conversation between an elite consultant and his fellow. (Caution: Grade 2 harsh language) 

Hey Doc, why is this guy’s name not found in today’s angiogram list? Any Insurance issues?

No sir, he has every requirement. Thrombolysis was very successful, ST has regressed well and it is nearly isoelectric and only T is inverted. His LV function is normal. In fact, I am not able to pick up any WMA.

Aren’t you aware, that being fine is never a contraindication for a PCI ? Which book teach you like that?

No sir, It’s already beyond 48 hrs sir. What is the purpose of knowing IRA status now? If it is open, well and good.If it is partially closed, again little to gain, right? 

Don’t expose your Ignorance. … haven’t you heard of the pharmaco-invasive strategy & open artery hypothesis. Always learn to respect science.

But sir, then why does late PCI of IRA in otherwise stable patients come under class 3 recommendation, if I understand the guidelines correctly, it is a contraindication, am I, right sir? But, this patient got stabilized by us still, why he is compelled to undergo another procedure exposing and adding further risk?  

That shows your immaturity. Doing an angiogram is never forbidden. It is the inappropriate late revascularisation of IRA that is the issue.

 Agreed sir, how confident are we, that we will stop just with an angiogram after visualizing a tempting lesion in either IRA or non-IRA? (My brief experience as a fellow doesn’t tell a fair story) 

 Now, you are trespassing into prohibited non-academic zones of cardiology practice. Instead, talk about FFR, OCT, multivessel angioplasty, and ( deferred or instant ) complete revascularization. Think like a true scientist don’t get spoiled at a young age in your career with all this ethical stuff. 

Final message 

Never allow an ACS to stabilize by medical management, if he is otherwise eligible and affordable for a procedure. You are not authorized to do that. 

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CPR with BLS and ACLS is time tested method of cardiopulmonary resuscitation. The automatic external defibrillator(AED) was a real breakthrough. Still, complete recovery eveN in “in-hospital cardiac arrest”  is at best 10-15 % . (Brindley PG, CMAJ. 2002. )Here is a technology in-progress story, now I understand FDA has approved this device for emergency resuscitation in cardiac arrest.

The principle is simple. In the early minutes following cardiac arrest, it is the survival of the myocardium and brain that matters. So, occluding Aorta transiently and continuing CPR infuses more life into the brain and heart, and the possibility of revival they say is significantly increased.

Mind you, this is not for the layperson or public but can become a game-changer for the ER crew and in ambulances or even in the cath lab. Emergency insertion of ECMO is never easy and a Neurescue balloon may come in handy in the meantime.

 

The attraction is the simplicity of the device, just inserted through the femoral artery. Don’t know how successful we would be, in centering the collapsed femoral artery though. The balloon actually doesn’t really impede the lower limb flow.It senses and relaxes as and when necessary. 

Final message

The concept behind neurescue looks like a bedside emergency partial IABP-like (IABO-Intra aortic balloon occluder rather) but appears promising. What I understood grossly is, that potential extremity Ischemia is acceptable if it’s going to save a life! Also realize, it is not a magic device that brings back life in every cardiac arrest. It gives us more time to act so that we can do other measures to bring back circulation. 

Reference

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Bifurcation PCI is a modern-day Cardiologist’s fascinating professional adventure within coronary arteries. Of course, one of their Intentions is to do good for the patient. Bifurcation lesions (BFL) are a special subset of lesions, that looks challenging, more because of the potential biological aftermath following the delicate construction of a grade separator at a critical site. Mind you, it’s done within a live flowing artery and subsequently needs lifelong maintenance.

Strategies for BFL

  1. Strictly committed* single stent strategy (Irrespective of what may come, LCX or LAD  pinching let me take care . Don’t worry strategy *May sound dangerous, but still, it doesn’t make other strategies less ominous) 
  2. Provisional single stent strategy with elective cross-over for truly poor result /cosmetic/peer satisfaction  purpose
  3. Provisional single stent with bail-out cross-over. Often happen as an emergency  (Not all techniques are amenable for this)
  4. Elective planned two stents (Still, flexible  to revert to single stent if the situation allows)
  5. Elective, strictly committed, prefixed  two-stent strategy  (No going back strategy/ Not really a professional PCI )
  6. Always remember, SYNTAX or no SYNTAX CABG is the safe & best bet for many severely symptomatic patients, with complex as well as non-complex BFL lesions esp in diabetic patients.

Wait, there are two more.

7. Please note, there is one benign strategy, that is always available, but hiding deep in the interventional cardiologist’s sub(non)conscious minds. It is a zero radiation, zero contrast, and almost zero cost strategy. Yes, It is “No stent strategy’ also called exclusive medical management, currently referred to as OMT/GDMT. In our analysis of symptom- lesions significance at least 30% of BFL are eligible for exclusive medical management.(FFR & IFRs ? Less we say about it, is better!) 

8. One more option for those patients (&cardiologists) who wants to travel the middle path is POBA or a Glorified POBA ie DEB  (Ref  Corballis NH,. PLoS One. 2021)

Whatever the treatment, bifurcation PCI  cannot be taken lightly. One exclusive club is debating this topic in Europe every year (EBC) for the past 10 years. Currently, Double kiss and crush (DK crush) is considered superior to others. Mini crush and Culotte are good alternatives in specific circumstances (Definition 2, NORDIC, BBC 2)

Something about DK crush (Shao-Liang Chen Nanjing, China first modified mini crush to DK crush)

Best video resource for DK crush 

 

In DK crush every step appears to be double. Apart from the double stent, it is a double wire cross, double crush, double kiss, and double POT (or even more). All must happen in a specific sequence. One may add double Imaging (Pre and Post PCI IVUS or OCT) to the list.  Finally and funnily not to miss the realistic possibility of double complications over the provisional strategy.

I am not sure which of the 10 steps in DK crush is most important. When we go through the physics of  BFL intervention it appears, that proper crushing and kissing may be the key to success. Though kissing is an integral part of any two stent strategies, in DK crush it happens in a unique interface between balloons /balloons with a stent and finally between two stents. In fact 

The physics of bifurcation kissing includes balloon hugging diameter, area, and pressure. Added to that is the intervening metal layer.

Can’t take the kissing in a casual manner. The Morino & Mitsuda model tells us more about the physics of kissing. In BFL interventions, kissing can happen with various layers that include one layer of the balloon with a crushed and non-crushed stent, carina. While we are mastering the techniques, we must realize, Kissing is aimed at stabilizing the carinal basement, still, there is a distinct possibility, that what may appear as innocuous kissing may undo all the good work we have done in previous steps. I guess, no harm in missing the final kissing if everything is ok in OCT.

Dr. Anonio Colombo’s take on kissing 

 

Final message

So, we have both simple and complex modalities for BFL. Evidence and experience reveal that 90 -95 % of patients with BFL would be eligible for the easy path. In one sense, we are indeed wasting our energy and resources in tackling this negligible CAD burden located at the summit of the global CAD pyramid with a gigantic base. However, we can feel scientifically happy, that we have gained considerable expertise in tackling complex lesions with multiple stent strategies in recent times. Still, we are far away from a true vision, of what really might follow such a niche & expertise-intensive procedure.

Let us hope, that modern metallurgy in combination with physics & hydrology would ultimately beat Biology.

Reference 

1.Dr Colomo article (For personal use only)

2..Morino Y, Yamamoto H, Mitsudo K, . Functional formula to determine adequate balloon diameter of simultaneous kissing balloon technique for treatment of bifurcated coronary lesions: clinical validation by volumetric intravascular ultrasound analysis. Circ J. 2008 Jun;72(6):886-92. doi: 10.1253/circj.72.886. PMID: 18503211.

Postamble

Does evidence create expertise?

Looking at the whole issue of complex PCI philosophically, no technique may really be superior based on accrued evidence. In fact, when expertise becomes the key determinant, the evidence goes to the background. It is really surprising we are too much dependent on hasty and often biased evidence to ratify our expertise, technique, or hardware. I know, one of my colleagues can cross any lesion with one or 2 wires.

To insist, that a particular technique must be followed may not be academically correct always. It is similar to telling a coach driver in advance when to apply a brake or accelerator when he is negotiating multiple hairpin bends in hilly terrain on a rainy day, based on clinical trials done with different drivers on different routes. Ultimately, the outcome is decided by the expertise of the driver, the condition of the vehicle, the road, and not least, the destiny of the passenger.

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