Dr.S.Venkatesan MD

Pre-operative cardiac fitness : No, it is not acceptable , you are not authorised to do this !

April 3, 2023 by dr s venkatesan

A 62-year-old man who is being scheduled for prostate surgery with no cardiac risk factors or comorbid status came for surgical clearance. I examined him and took an ECG, everything was fine and gave him clearance for surgery.

 I was surprised to spot him the very next day, waiting in the lounge of my office. He said, his anesthetist was not happy with my pre-op-cardiac assessment report, suggested it was incomplete, and sent me back for echocardiography to know the LV ejection fraction.

I wanted to clarify with the patient, what exactly happened when he met his anesthesiologist.

“I am not sure doctor, the moment he saw your report, he called my urologist. I overheard his call, they were discussing the need for an echocardiogram and they were also wondering,  how could a cardiologist give a  surgical clearance without even an echocardiography”.

I wasn’t really surprised by the turn of events and told the patient. 

“I am experienced enough to say, your heart is 100 % normal without an echocardiogram”.

“I understand doctor, but sorry to bother you. Can you please take it for the sake of my anesthetist and urologist, after all, right now I am worried about their peace of mind” 

“You are absolutely right. This is a topsy-turvy world. Investigations are dictated to me in my own field of expertise. Anyway, I am not a fool, to expect a patient’s help to guard my principles of practice. Please check in, let me do the echocardiogram as they wish” 

“Thank you so much, Doctor“.

I showed him, the vigorously contracting ventricle and taught the student trainee who was nearby, a simple clinical tip ie, a loud first heart sound on auscultation is good enough to tell you, the EF is beyond 60% in most situations. (A forceful AML movement is a direct auditory marker of EF %)

Final message

It is getting more & more clear,  physicians will face huge hurdles in applying their clinical skills to practice. They may even be unauthorized to do so. It seems, in our misplaced quest for perfection, we have fallen into a scientific trap, that every clinical decision must be authenticated by some objective lab-made obsession. The word clinical acumen could soon become a laughing stock, as AI-powered medical zombies are waiting to join our consultation suits.

(Meanwhile,  the guidelines are very clear. (Read below)  Do echo only in high-risk surgery, if patients’ functional capacity is poor. But, let me confess, at least in our part of the world,  we are happy to violate standard guidelines  without any degree of guilt )

Reference 

ESC Scientific Document Group, 2022 ESC Guidelines on cardiovascular assessment and management of patients undergoing non-cardiac surgery: Developed by the task force for cardiovascular assessment and management of patients undergoing non-cardiac surgery of the European Society of Cardiology (ESC) Endorsed by the European Society of Anaesthesiology and Intensive Care (ESAIC), European Heart Journal, Volume 43, Issue 39, 14 October 2022, Pages 3826–3924, https://doi.org/10.1093/eurheartj/ehac270

 

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Posted in cardiac surgery | Tagged Cardiac fitness for non cardiac surgery, preoperative cardiac risk assesment, surgical clearance and cardiac fitness |

AI, is not risk free in medical science !

March 25, 2023 by dr s venkatesan

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Posted in Uncategorized |

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 |

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