Posted in Uncategorized, tagged AI in cardiology, artificial intelligence, dr s venkatesan, drsvenkatesan, madras medical college on June 11, 2024|
This is a condensed video version of PPT slides of my recent presentation.Please pardon, there is no audio as of now. Will make a voice-over and post soon.
Topic : AI in cardiology
Occasion: Prof Rathnavelu Subramanian memory oration. Cardiological Society of India Chennai.
Date : 8-06-2024
Acknowledgment & Courtesy: Images and videos from open source
Posted in Uncategorized on May 26, 2024|
“Half-baked knowledge is not better than fully-baked Ignorance“
LDL is portrayed as villain de-chief of Atheroscerlois and CAD. But, LDL with a 100 to 160 mg concentration, is in constant circulation, in a smooth manner serving other physiological vascular functions.
The forcible evidence that LDL can pierce an Intact endothelium is so huge no one can have the courage to dispute it. But, it doesn’t happen in the majority is the mysterious truth.
Electron microscopic picture of 20nm sized LDL molecules in circulation. They are not as frightening molecules as they are portrayed
What factors induce LDL to enter the endothelial gap junctions.?
Some facts
The diameter of LDL particles is about 20–30 nm which is much larger than that of gap-junctions (3–6 nm) between adjacent cells in continuous endothelium (Iuliano, Micheletta, & Violi, 2001). Hence, the only way for LDLs to cross the endothelium is through a process called caveolae-mediated transcytosis.
Contrary to the shout-out, LDL is not a true villain in all patients with CAD. It is something else, we aren’t aware of that keeps the LDL either passive or promotes its penetration.
There are at least five important factors.
1. Baseline Endothelial Integrity & vascular aging
2. Accelerated caveolae formation,
3,The shear stress of flowing BP .
4 .The associated diabetic basement membrane dysfunction.
5. Finally, the aggressiveness of native LDL molecule (Absolute levels of LDL are less important than we think . Please note, the much-researched South Asian metabolic syndrome has near normal LDL )
What we fail to acknowledge is the fact that our understanding of endothelial lipid interaction is based on poor-quality data . Meanwhile, the concept of endothelial-friendly LDL can’t be eliminated totally.
Final message
How many molecules of LDL enter endothelial breakpoints?
I am sure, no one can answer this question. In fact, this question need not be answered. Still, the PCSK blockers, the Inclisirons are the new armed weapons in anti LDL industry waiting hungrily to Invade the vasculature. What if these agents swallow good LDLs ?
Let us first clarify, the true invading potential of LDL before falling for these costly semi-annual subscription-based drugs. Meanwhile, HDL dysfunction with its Apo A2 interaction defects may be a more concerning issue than LDL-mediated injury is coming up.
Reference
Posted in Uncategorized on May 16, 2024|
Leriche syndrome (1948, Annals of Surgery, College de Paris, France) is a famous eponym in Aortic vascular emergency, where a saddle-shaped thrombus folds across the Aortic bi-furcation resulting in bilateral lower limb vascular insufficiency.
Though such vascular emergencies can occur in any bifurcation point in a vascular tree, it is not often thought about in acute coronary syndrome.
Large thrombus burden in LAD or LCX is so commonly visualized, while in a stump left main, we often fail to recognize the fact, that it is almost the same as “saddle embolus” sitting across both LAD & LCX bifurcation.
Most such patients do not reach the hospital. If the thrombus migrates to one of the branches, it might evolve either as LAD STEMI, LCX STEMI, or a combination of both. We have seen a few lucky Left main STEMIs in the cath lab, with some spontaneous canalization.
Final message
De-novo Coronary Leriche syndrome is a real entity. For many of us this may appear, just an acute coronary curiosity, since most of the time it results in silent sudden deaths and escapes from our vision. However, primary PCI Interventionalists need to be aware of this concept, as meddling in this critical arena with high thrombus load can rapidly evolve into an acquired Leriche syndrome, for which the operator becomes squarely responsible.
Reference
Posted in Uncategorized on May 16, 2024|
1. Wrap around LAD true Global MI
2. RCA-dependent LAD circulation through collaterals
3. True bifurcation STEMI with static thrombus (Carinal trapping of thrombus ,Coronary Lerish sydrome )
4. Embolic STEMI with showers of emboli into both LCX and LAD
Simultaneous or sequential Anterior and Inferior STEMI
5. Mid or Proximal LAD lesion with proximal thrombus build-up
Further possibilities
Mimickers: Distal LAD lesions -Inferior ST elevation due to sparing of diagonal
Wrong diagnosis -ERS pattern, pericarditis etc.
Posted in Uncategorized on May 15, 2024|
We have more than solid evidence, that rate control is good enough or even better than rhythm control in the management of AF , for more than two decades. Studies that showed either equipoise or rate control was marginally superior in certain clinical parameters are.
1.AFFIRM (2002)
2.RACE
3.STAF(2003)
4.HOT-CAFE (2004)
Now, in 2020s with modalities like ablation, the choice is being pushed toward Pro-rhythm control. (Of course with evidence).Some of these studies are,
1.EAST-AFNET (2020)
2.CASTLE AF(2018)
3.RAFT AF (Again equivocal)
With emerging new technologies, scientists are trying whether more safer methods like cryoablation or pulse-filed ablation would beat the rate control with drugs. Still, rhythm control strategy is finding it tough to win over the apparently less scientific rate control strategy. (Why? The reason is discussed elsewhere )
“How can rhythm control be inferior or non-superior? Something is wrong. We can’t leave it like that. Let’s do a meta-analysis”
Even meta-analysis couldn’t help out rhythm control strategy.(Caldeira, Daniel et al. “Rate versus rhythm control in atrial fibrillation and clinical outcomes: updated systematic review and meta-analysis of randomized controlled trials.” Archives of cardiovascular diseases 105 4 (2012): 226-38 .)
Now, what shall we do? , Let us do another meta-analysis. A fresh one is released just a few days ago in 2024 . This mega meta-analysis with almost similar data, clearly vouchs for the superiority of early rhythm control with some form of ablation. It is gratifying that, with this study, we could sustain some confusion, in the management of this most common cardiac arrhythmia.
When will this fight for Rate vs Rhythm control in AF end?
Answer: It will not stop as long as an entity AF exists. Research, as the name implies, we need to search again, & again for truth. However, In the case of AF, I think, a different game is being played in the EP arena. It looks like, we are fighting with an established truth, not fighting for the truth.
Reference
Posted in Uncategorized, tagged atrial cardiomyopathy, atrial fibrillation, biatrial enlargement in af, dispropotinate atrial enlargement in af, left atrial cardiomyopathy, left atrial fibrillation, left atrial vs right atrial fibrillation, lone af, non pulmonary vien focus in af, pulmonary vein ablation, right atrial focus in af, selective atrial cardiomyopathy on April 28, 2024|
(This is supposed to be a poll. Sorry, readers, you can’t select the answer. WordPress is not kind enough and suddenly made the poll service payable extra. I am already paying nearly a $100 fee to maintain this site. I can’t afford any more.)
We have been taught Bi-Atrial enlargement is the rule in AF .It is still true in most situations. But, we rarely dispute it , & ask which atrium dilates more in AF ?
Let us see few factors.
Implications for electrophysiologists.
In contrast to other tachycardias, with atrial fibrillation (AF), the focus is often speculative, and ablation attempts are made accordingly. Pulmonary veins have been the primary target for ablation for many years, yet the success rates remain inconsistent. To determine if the AF focus is non-pulmonary venous, such as right atrial, septal, or involving the inferior vena cava (IVC) or superior vena cava (SVC), several techniques are employed to provoke and localize these non-pulmonary vein triggers
Localized atrial fibrosis and interatrial blocks can result in differential fibrillatory counts across the atria. (RA fib-rate can be more than LA, and vice versa.) Is there proof for this, or just an academic gossip? We know atrial flutters can be confined to one atrium. (Pierre Jaïs Circulation 2000) When such flutters transform into fibrillation, how does the spillover of signals occur to the contralateral atrium? On a personal note, we have recorded good E & A Doppler signals across the tricuspid valve, in RHD mitral stenosis, and AF. No published proof as such. I strongly suspect the right atrium can resist the tsunami of approaching fibrillatory waves from engulfing its chamber in at least some patients. An appeal to the new generation EPs who have special flair in AF should look into this and either prove or disprove it.
Final message
My answer to the question is either D or E. Atrial size in AF is not a trivial thing to ignore. This question pushes a simple idea. In primary or lone AF, just by having a look at the RA to LA size ratio, one might get a reasonable guess,about the Initial focus, trigger & pathology of the AF.
A request to all the high profile stake holders involved in the science of PV ablation (either with Ice or fire). Think about all the possible right-sided or septal focuses, before going overzealously for the jugulars of Pulmonary veins, especially if the RA significantly larger than LA . This will save time, effort & of course our reputation.
References
Nil
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Posted in Uncategorized, tagged acc aha esc guidlines, dilemma in cardiology, drsvenkatesan, ethics in medicine, high senstivity troponins, jama network, nstemi, pci, stemi, troponin on April 25, 2024|
As the medical literature expands exponentially, the quality and intent of the research questions sound awry. There are only a handful of journals like JAMA that are bold enough to ask some tough and pragmatic questions in this glitzy world of medical extravaganza.
The current issue wants to set the pace for an important debate, on a topic that is rarely discussed.
The question is
Check whether your answers concur with this crucial query from Harvard Medical School and Massachusetts General Hospital. Three questions this article wishes to address.
1.What is the reason it is happening?
2. What are the implications?
3. What can be done for it?
My thoughts
“It is indeed over diagnosed. Once labeled, a chain reaction is set in. The cost, and resource consumption that follow a misdiagnosis are nearly identical to that of a true MI. More than that, the adversities of the tense investigative protocol can convert a misdiagnosis into a real one because that sadly includes even an overzealous poking right at the mouth of the coronary artery just o exclude a non existing MI . and ICU-related anxiety stand apart in this scientific comical game of ruling out a cardiac emergency.
The paper seems to blame mostly on the powerful screening test high sensitivity Troponin, Everyone will agree it has a major role in this. But, the more important reason is the cardiology community’s vigorous adoption of a universal definition of MI criteria (which is never intended to apply at the bedside) .Next factor is probably more important. The fear of missing a potential MI and legal consequences thereafter. I wish, the experts who sit on medical juries need to learn few extra lessons in the art of medical uncertainties.
Medical jurists, need to take some Intellectual cues from their criminal courts. How is it that, even well-planned criminal murders are successfully allowed to be argued and won in courts,…while inadvertent events such as missing an inconsequential MI by doctors are rarely pardoned?
How to avoid over diagnosis of MI ?
In this scenario, It is sad, that only very few cardiologists have the guts to ignore this omnipotent molecular sub-fraction of cardiac muscle Troponin, with their clinical skills. What we can do, at our level is to incorporate a new term “benign or micro myocardial Infarction” – akin to lacunar infarcts or TIA equivalents of the brain in the heart. We need to de-list the vast majority of chronic ischemic,non-ischemic, or systemic causes of Troponin leaks from the myocardial infarction chart. Physicians must realize, that protocol violation should not be deemed a crime always, rather it has a sure potential to benefit your patient if it is done properly and intelligently.
Final message
Recently one cardiologist in a sub-urban center was thrashed both physically and in social media ,for missing an ACS , which was subsequently recognised and treated well and good.
“Doctors should be legally allowed,* (rather forgiven) to make permissible levels of errors in the medical decision-making process ” like any other profession .However, we must ensure our constant pursuit towards zero error, which may not be possible always. This should include overlooking apparently positive lab results if they have reasonably applied their clinical acumen. *Until this happens, the unquantifiable suffering of our patients* due to over-diagnosis and inappropriate interventions can not be reigned in.
*Maybe, this sounds more controversial statement in my 15 years of writing. Beloved patients shall note, it is a rare for me to make what probably, look like an anti-patient statement. Till now, I have been blamed my many of our colleagues, as self slandering my own profession for too many errors in many of the posts. Nothing can be done for this. When you search for truths , you need to tolerate all these.
Reference
Posted in Uncategorized, tagged chb after tavi, chb risk with tavi, core valve vs sapien, how to use a permanent pacemaker as temporary ?, how to use a ppm as tpm?, mechansim of chb after tavi, tavi, TAVR on April 22, 2024|
This image comes with courtesy of the Journal of SCAI Jai Parekh, Vikram Sharma, Jared Robl,et al Journal of the Society for Cardiovascular Angiography & Interventions 3 (2024) 101310
What is your diagnosis ?
I thought, it was pacemaker extrusion. It was indeed a close answer, still terribly wrong. It is an intentional exterior placement of a permanent pacemaker generator mimicking an extrusion due to pocket infection. Here is a patient, where a permanent pacemaker was kept temporarily for a few weeks or a month in high-risk reversible complete heart block situations. This typically occurs after an inferior posterior myocardial infarction, drug-induced CHB.
Currently, with the arrrival of TAVR, CHB has beceome a glamorous complication and is getting wider attention. This happens due to the anatomical uncertainties where the inferior landing zone of TAVI is pre-destained and is beyond our control. This is more true in the self expanding Core valve platform . When the lower edge treaspass the non-coronary cusp- membranous septal junction, it hits perfectly the compact post-penetrating bundle of His, confering a high risk of CHB.
Still, the good thing is some of them recover as the pressure edema regress .Putting a PPM in all such patients was considered mandatory or even a vanity in the past. Now we realise it is an additional metallic luggage in an already strained heart, Temporary-PPM the oxymoronic innovation is perfect option in this setting.
Final message
A typical external temporary pacemaker can be kept for up to 2 weeks maximum. (We have kept it for a month or so) It’s done via the jugular, subclavian, or even femoral. If the underlying condition demands more time for recovery of CHB, many do a regular permanent pacemaker.
Now , we have this unique option of using PPM as TPM. This is not a new concept though. It was used few decades ago .Has come back in more centers .Thanks to TAVI and its specific complications.
Reference
1.Rodés-Cabau J. Ellenbogen K.A. Krahn A.D. et al. Management of conduction disturbances associated with transcatheter aortic valve replacement: JACC Scientific Expert Panel. J Am Coll Cardiol. 2019; 74: 1086-1106.
2. Leong D, Sovari AA, Ehdaie A, Chakravarty T, Liu Q, Jilaihawi H, Makkar R, Wang X, Cingolani E, Shehata M. Permanent-temporary pacemakers in the management of patients with conduction abnormalities after transcatheter aortic valve replacement. J Interv Card Electrophysiol. 2018 Jun;52(1):111-116. doi: 10.1007/s10840-018-0345-z. Epub 2018 Mar 12. PMID: 29532275.
Posted in Uncategorized, tagged best quote on medical ethics, bio ethics, british journal of medical ethics, ethical dysfunction, future of noble profession, Hippocratic oath, indian journal of medical ethics, journal of medical ethics, Lown Institute, medical education, medical ethics, modified hippocratic oath, taboo topics in medical science on April 22, 2024|
Posted in Uncategorized, tagged acquired asd in hfpef, atrial flow regulator, corvia atrial shunt system, decompression of left atrium, hhpef, lutembacher syndrome on April 18, 2024|
Lowering the raised LA mean pressure is a major therapeutic goal in any severely symptomatic left heart disease, whether it is valvular or myocardial disease. It is prudent to understand, that even in systolic LV failure; it is the raised LVEDP that causes the symptoms and marks the limits of exercise capacity. Drugs like inotropes, pre-load , afterload modulators like diuretics and vasodilators can take care to a certain extent.
When symptoms are refractory and the underlying condition has no primary correction , we need to intervene with some extreme procedures. We know a small ASD decompresses mitral stenosis, and the combination of ASD and MS, Lutembacher, is a well-known syndrome called Lutembacher. The concept of LA flow regulator or decompressor came from this .
When the left ventricle is stiffened and restrictive, and LA mean pressure is prohibitively high,we have a viable option now. This is to create a small regulatory orifice in the IAS ( A complicated term for a small ASD) to decompress the LA and reduce pulmonary congestive symptoms. Curious minds might ask, can’t we decompress LV it self by creating a small VSD. Probably in the thin membranous area. May be, it will come soon in the innovative lanes of cardiology.
As of now, we have an important human study REDUCE LAP-HF II , from Chicago with a 2-year follow-up up .The device used here was Corvia atrial shunt system.
The study finds the device can be beneficial without compromising much on RV side function.
Animation Courtesy: Corvia website; The procedure looks simple when compared with other procedures inside the LA .The device looks like an octopus, and sits on either side of IAS, like a stapler and maintains the orifice.
Here is an audio podcast from the primary author published in JAMA network.
Interview with Sanjiv J. Shah, author of Atrial Shunt Device Effects on Cardiac Structure and Function in Heart Failure With Preserved Ejection Fraction: The REDUCE LAP-HF II Randomized Clinical Trial. Hosted by James E. Udelson,
Final message
This device’s core concept lies in requesting the right ventricle to help its bigger brother LV at its difficult times. You can call this an artificially created interventricular dependence. Though it might help, we need to watch the right heart’s dynamics closely. Maybe, if RV is experiencing difficulty, we can have external control over the IAS orifice and flow as and when required. (This is not new, a remote-controlled switch regulation was done for pulmonary banding in children with congenital heart disease who needed regulation of pulmonary flow by a device FloWatch-R-PAB (Ref 2)
It is logical to expect the same device would be useful to decompress RA at high pressures as in severe primary pulmonary hypertension. If you think backwards, it looks the same as a life-saving, reverse Rashkind procedure variant in adult
Reference
2.Antonio F Corno, et al JTVS 2003 Remote controlled pulmonary artery banding
Dr.S.Venkatesan MD 