Dr.S.Venkatesan MD

“Professional etiquette” need not be misplaced

November 29, 2022 by dr s venkatesan

 

 

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Posted in Uncategorized |

STEMI secrets : Honesty is still Intact in “Harrison text book” of medicine

September 1, 2022 by dr s venkatesan

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.

Postamble

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. 

 

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Posted in acute coroanry syndrome, Cardiology -guidelines, Cardiology -Therapeutic dilemma, Cardiology -unresolved questions, cardiology-ethics, Primary -PCI, Thrombolysis, Thrombolysis -Tips | Tagged euro pcr, Harrison principles of internal medicine, management issues in cad, Primary PCI vs Fibrinolysis, scai acc aha esc guideliens, stemi secrets, tct md, tips and tricks in priamry pci, tips in acs |

Can we mix philosophy with science in medical teaching ?

May 14, 2020 by dr s venkatesan

I think it is an Invalid question. Whether you like it or not , medical science and philosophy are always bonded together and its relationship is eternal. It doesn’t make sense to separate them. I think we have misunderstood the meaning of philosophy. While science is presumed truths, philosophy is trying to believe in unknown truths. Philosophical truths are built-into every decision a medical professional takes.

                                                         Rudolf Carnap A German philosopher

If the expected natural history of any disease is science, unexpected deviations are philosophy. (RT PCR testing for diagnosing  Corona is science, why 90% of them are not infective and don’t transform disease is philosophy) When something is not seen or quantifiable like human immunity, it is a perfect example of concealed science or manifest philosophy.

Taking about what we think we know is science, Talking about what we really don’t know is philosophy. The term Idiopathic syndrome finds a  proud of the place in every specialty in medicine, Isn’t? 

 What will be your answer when your patient wants an assurance that a stent, you had just implanted will not get occluded in the next 6 months or so.“I don’t know, I cant assure you about that”  will be your most likely answer. (Though, we do it in style, hiding behind  the scientific hyperbole decorated with numbers,  also referred to as statistics) Please realize, this is the expression of medical philosophy in the finest form.

Final message 

My Impression is, philosophical truths should be liberally used in a regular fashion right from the first-year medical school to advanced specialty teaching. This seems essential as science in the current times suffers from too much sanctity. This has spilled over to the doctor population as well, and make them appear invincible. 

If only we realize science often trails behind the philosophical truths at least by a few decades, our patients will not be injured inappropriately and prematurely. Mixing science with philosophy in the right composition ( a perfect academic cocktail ) will bring out the best from the noble profession.   

Postamble

Can anyone guess, why scientists are given a doctorate in Philosophy degree  (PhD ) ?

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Posted in Uncategorized | Tagged ethics in medicine |

Who killed Starr -Edwards valve ?

January 15, 2011 by dr s venkatesan

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

• Almost unheard in our population.
• The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
• Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
• A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion .  Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .

http://www.heartlungcirc.org/article/S1443-9506%2810%2900076-4/abstract

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Posted in cardiac surgery, Cardiology - Clinical, cardiology -Therapeutics | Tagged ball valve, cardiommc, departemnt of cardiology, dr sadasivam madras medcial college, dr sadasivan, dr vasudevan, mitral starr edwards, portland hospital, prosthetic heart valve, solomon victor india chennai madras medical college, starr edwards valve, www.cardiommc.com, www.cardiommc.org | 5 Comments »

Learning targeted IAS puncture in 20 minutes

March 10, 2023 by dr s venkatesan

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. 

Reference 

One more good read

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

 

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Posted in Anatomy of heart, Uncategorized | Tagged anatomy of heart, ias puncture, right vs left atrial anatomy |

P wave spotting in AF is not forbidden

March 8, 2023 by dr s venkatesan

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?

Reference

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

Postamble

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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Posted in Uncategorized | Tagged cardiology research topics for fellows, causes of absent p wabes, p vs f waves in af, p waves in atrial fibrillation, research topics in atrial fibrillation |

LA volume assessment : A critical parameter with a time trouble !

February 8, 2023 by dr s venkatesan

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. 

Reference

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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Posted in Cardiology Illustrations, cardiology physiology, Left atrial enlargement, Uncategorized | Tagged LA end diastolic dimension, la end diastolic vs end systolic dimension, LA end systolic dimension, la pressure volume loop, LA volume by mri, normal LA dimension, normal la volume, When do you measure LA dimension volume |

Primary PCI and its silent encounter with “myocardial neutrophilia”

February 1, 2023 by dr s venkatesan

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.

Reference

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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Posted in Uncategorized | Tagged myocardial neutrophilia |

Furore over FOURIER is (un)warranted : Evolocumab is an Innocent molecule !

January 16, 2023 by dr s venkatesan

Welcome back to the big molecular science of PCSK and its antagonist Evolocumab, a monoclonal antibody designed to target and prevent the LDL receptor catabolism inside the lysosomes. Evolocumab was approved by FDA for aggressive lowering of LDL, following a  customary study published in NEJM 2017, that released this double-edged anti-lipid molecule into the human domain with all fanfare.

It aimed to reduce the LDL as low as possible in selected patients with familial LDLemia & and those who don’t tolerate statins.  Now, a study was silently released in BMJ open, at the fag end of 2002, which is causing ripples in the pharma world in the new year.

BMJ Open 2022;12:e060172. doi: 10.1136/bmjopen-2021-060172

In fact, this paper can’t be called a study. It looks more like an FIR. It questions the missing death counts, which were not included in the landmark trial, that led to its approval.  It took time for the news to sink into the world lipid community. 

Final message

I am surprised at the reactions to the reanalysis of FOURIER data. Any reasonably experienced cardiologist will agree, getting regulatory approval with manipulated data and analysis is more of a norm and not an exception (Ref 1). In a trillion-dollar pharma industry, do you think hiding deaths is a big crime? Is there a solution to this menace?  Yes, let us hope so, with movements like this one (Doshi P et all, Restoring invisible and abandoned trials: A call for people to publish the findings BMJ 2013; 346 )

 

Counterpoint (Q&A)

Q  

Damn this post. Don’t blame a phenomenally successful scientific breakthrough that intercepts the immune destruction of LDL receptors. Instead of being cynical, try to come up with a scientific analysis of the FOURIER study. Please read this rebuttal from the TIMI group, https://www.tctmd.com/news/study-alleges-mortality-miscount-fourier-trial-timi-group-disagrees

 A 

I agree, let us not blame Evolocumab. It is an innocent and intelligent molecule. Culprits are elsewhere. It is a reserve drug in a highly selected population with refractory LDLemia.The lesson from the FOURIER  to all the clinical trialists is, when credibility is lost every thing is lost, even truths can become a casualty. We have to live with that. 

Reference

Marcia Angell,the former NEJM editor’s  book

 

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Posted in lipid metabolism | Tagged evolocumab, fourier study, how low ldl can go, inclisiron, lipid guidelines acc aha esc csi |

Which is the Ideal site to ablate VT circuit ?

January 12, 2023 by dr s venkatesan

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? 

Reference

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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Posted in Uncategorized | Tagged acc aha esc guidelines, cryoablation, exit site of vt, exit vs entry site, icd vs rf ablation, RF ablation, scar induced vt |

An unpalatable medical quote

January 11, 2023 by dr s venkatesan

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Posted in Ethics in Medicine, medical quotes | Tagged drsvenkatesan, hippocrates ethics, medical ethics, medical practice, medical quote, primum non nocere, voltaire |

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