How can we use AI as a tool of knowledge distillation ?
Here is a deep discussion with Grok 3, on the merits, limitations & validity of DANAMI 2 and PRAGUE 2 , the two old studies on pPCI. Curiously , we don’t have any other studies to quote. As on 2025 , superiority of pPCI hangs precariously on these two decade old studies, which has some serious omissions in the primary end point and its Interpretation. To get into the facts , please go through the following link.
Since, we can’t sue science for its impurity , or a misbehaving bacteria , an inadequate imaging machine or manipulated health care system,poor doctors have become, the only visible targets.
Every day, 100s of physicians and cardiologists are asked to report ECG either physically or on-line .In India, they do it for some paltry benefits from stand alone labs , hospitals , institutional protocol or by sheer compulsion.
When only ECG is reported ,the physicians are often blind to the indications for which it is taken . The symptoms of the patient or the past history is rarely available. It is a sorry state of affairs and many of us do this, fully aware of the consequences – a normal ECG can’t rule out an ACS in at least 10 % of times.
Now, here is an ECG of a 40 year old male, on my table for reporting. No other info is available.
How should I report it ? Can I refuse to report ?
There were five options
A.ECG Normal
B.ECG within normal limits, with non specific ST/T changes
C.ECG shows ST elevation Infero- lateral leads. To rule out ACS
D. Early repolarization pattern
E. I refuse to report, until clinical data is made available.
My report: ECG within normal limits. (Shows ERS pattern with non specific ST elevation in Infero-lateral leads.To correlate clinically, and adviced a physician consult. )
One of my colleagues commented, that I lacked the guts to comment the above ECG as normal. The contention is, ERS pattern occurs in up to 20% of the young population, and it evokes unnecessary anxiety. How do I know he is pain free ?However, I agreed with my colleague. It is indeed ERS by all means. But,how long ?, we can be carriers of proxy anxiety, for the sake of our patients. Further, by no means ERS gives immunity to ACS. (What happens to the ST segment of ERS during ACS is a different query to be answered.)
(*Later on I came to know this guy had epigastric pain, and was simultaneously evaluated for CAD which was excluded . Mind you, mistaking ERS pattern for ACS is an age old problem. About 5% of thrombolysis in ISIS -2 study(1988) turned out to be in patients with possible ERS)
Final message
Can we report an ECG without knowing the patient and his symptoms ?
It is a foundational question in clinical medicine. The answer to which can shake the way, we practice cardiology. It is indeed unprofessional* of a physician to report an ECG without knowing the patient status. But we do it every day , can’t avoid it. But ,let us at-least insist the ECG lab guys to note down the symptoms or /the purpose for which it is taken (like a regular health check or pre-op evaluation, etc).
*Of course , to escape from a potential miss, we should atleast write, ECG to be correlated clinically and with past records.
Post-amble
We are in the AI era. ECGs are read by data-hungry machines. If you think there are AI models that can match a million ECG patterns and detect an ACS in milliseconds, sorry, you are sadly mistaken. Unless and until patients’ entire history is fed into humanized machines, (that had undergone 8 years of rigorous cardiology training) the risk of missing a diagnosis is significant.
The following table was created , when there was a dispute in one of my lectures , when I told self expanding valves has more” Net-radial force”on the annular arena. It was pointed out, I was wrong and contrary to the published literature . Yes, may be, but could agree only partly on this. The physics of radial force/stress can be under stood only, if we classify it with reference to time , ie at the time of deployment vs long term stress. Also,the type of metal and the intrinsic potential energy stored in self expanding stent.By the way, this enhanced radial force is supposed reduce the PVL in SEV.
Note : One curious fact is often ignored. All self expandable valves, can be balloon expanded further, if there is a need. While, a balloon expandable valves can never acquire the properties of a self expanding valve.( Toutouzas K, The DIRECT Trial. JACC Cardiovasc Interv. 2019 )
TAVI : Current status
TAVI is considered by many (not all) as the revolution of this century ,in the field of Interventional cardiology .More than a million valves are implanted so for .TAVI as a concept is sustaining and trying to prove the test of time (Of course with lots of ifs and but)
The indications for TAVI has come down drastically ,from very high risk subsets to even low risk patients, without corresponding reduction in complications. (Consider this : Para valvular leaks in surgical AVR can be low as 1-3% while it can be as high as 40% ) Still TAVR has that magnetic attraction for a simple reason it avoids surgery.
Unfortunately, the technology has not seen much innovation beyond the PARTNER .We get to see so many clones of self-expanding and balloon-expanding platforms are crowding the market ,with extra skirts , sleeves, design for coronary access etc. Meanwhile, we have vastly improved in expertise, delivery hardware and managing complications.
However, until we develop methods to remove the native valve debri from the aortic root , it is very hard to bring an outcome, that is equipoise to surgical valve replacement. Future designs will look into active fixing valves with polymer-based leaflets to increase the longevity of the valve, which is, currently less than 50% of mechanical valves.
Simple answer : If one leaflet is absent (True embryonal agenesis of anlagen) then corresponding sinus also fails to germinate. So number of leaflet is equal to number of sinus.This implies,In normal Tricuspid aortic valve there are three Aortic sinuses. In Bi-cuspid Aortic valve there are two Aortic sinuses depending on the absent leaflet (Generally R & L sinus present)
But, reality iscomplex : (Apparently , there can be no relation between the leaflet and cusp) Here, a distinction is made between truly absent leaflet to fused BCAV. In fused BCAV (ie with or without raphe )the number of sinus can be three like a normal Aortic root .
Is fusion line same as Raphe ?
Usually yes. Raphe is a raised ridge which is a marker of fusion plane But, cardiac morphology never allows us to take things easy. To complicatt our thinking, the fusion can be smooth and perfect without a ridge or raphe. This raphe less fusion makes it difficult whether we are dealing with true geno-phenotypically BCAV or simply fusion phenotypes of what should have been a genotypic- tricuspid valves . There is a simple clue in this complex scenario .In the later case it is identified by presence of three sinus. Does this make simple our understanding right ?( I am not sure, the above understanding is correct , this is how I Interpreted. (Please, clarify if some one finds it wrong)
The two famous classification of Aortic leaflet 1.Siever 2.Micahlena
Why is the number of cusps important ?
It decides the type of TAVI valves and location of implant.
Fortunately, we have a consensus nomenclature system for Aortic valve leaflets
BCAV types are defined as fused BCAV,
Two-sinus BCAV,
Partial-fusion (or forme fruste) BCAV.
The fused BCAV type is the most common type (90-95% of BAV cases); and is characterized by two of three cusps appearing fused within three distinguishable sinuses of Valsalva; frequently but not always with a congenital fibrous ridge (raphe) between the fused cusps.
Right-left fusion is most common (70-80%). The right-left phenotype also is most common across all variations of aortic valve dysfunction (AS or AR) and aortic phenotypes (normal aorta, dilated root, dilated ascending aorta, dilated arch).
Right-nonfusion is second most common (20-30%), and in adults is associated with a higher prevalence of AS and of progressive AR.
Left-non fusion is least common (3-5%).
The two-sinus BCAV type is uncommon (5% of BAV cases), with two cusps of roughly equal size within two sinuses of Valsalva.
Laterolateral (side-to-side) two-sinus BAV has one coronary artery arising from each sinus.
Anteroposterior (front and back) two-sinus BAV can have one coronary artery arising from each sinus or both coronaries arising from the anterior sinus.
The partial-fusion BCAV ( forme fruste) type is more recently recognized and of unknown prevalence. The appearance is similar to a typical tricuspid aortic valve, but with <50% fusion between two cusps at the commissural base forming a mini-raphe.
Next query :
What are differences between raphe and commissure ?
No doctor will want any disease to progress in their patients. But, coronary revascularization is an enigma. Cardiologists take every step to regress the atherosclerotic process and be meticulous in maintaining antegrade flow across the left main and proximal LAD or LCX. They double up their caution after PCI in left main or proximal segments.
Meanwhile, our cardiac surgeons do enjoy a unique liberty. In fact it is a luxury, i.e., they can afford to forget the status of proximal disease. What they want is the patency of the graft, integrity of the anastomotic site, and distal vessel status. Atherosclerosis being essentially a proximal disease, surgeons have all the more reason to be blessed. Of course, it should have been disciplined well-done CABG.
Do they ever wish for proximal vessel disease progression ?
What a non-sensical question, dude ?. Don’t get shocked. I was told, many of surgeons would, indeed be happy with that, as it tends to divert more flow to the graft, and long term patency is better. There are many instances when they close the antegrade flow, if it is interfering with graft flow during the surgery itself. .
Final message
Cardiologists strive hard to heal at ground zero where vessels are traumatized. Worrying day in and day out, after putting a scaffold. Surgeons simply fly over it, laughing at the lesions. So, what is the lesson from this post? When making critical decisions on coronary revascularization, think twice .Make a learned decision for every given patient.
Counterpoint
Native vessel progression do have adverse outcomes even after CABG, provided it occurs in the non by-passed vessel or when it occurs distal to the bypass circuit. Please ,don’t take a wrong message that progression of atherosclerosis is welcome post CABG. Every post-CABG patient should follow the same OMT and lifestyle modifications to reduce the burden of atherosclerosis in a larger sense. What this article refers to, is mainly about the influence of disproportionately high antegrade flow on graft survival. Surgeons do prescribe statin after CABG routinely , not withstanding the results of ACTIVE study (Ref 2) which showed high Intensity statin following CABG, had little influence on graft patency.
Dyspnea is one of the commonest symptoms in medical practice. Whatever be the trigger, ultimately, it is a sensory perception, felt at the level of the cortex (to be specific, the Amygdala nucleus) decides the intensity . The initiating receptor usually arises from the muscle spindles , due to mismatch in the length and tension . These spindles are located widespread in intercostal and other respiratory muscles. The afferent pathways are complex, as are the brain stem processing centers and cortical modifications—all matters.
(* A proposed definition with mechanism :Both physiological and pathological dyspnea are the unpleasant breathing awareness (In time), till for the oxygen debt is repaid to the depleted mitochondrial, ATP treasury , for the cost of excess respiratory work done, is one popular definition )
The complexity of the neural circuit for dyspnea can be judged, even if the cranial or spinal pathways i.e., vagus or spinal transection, dyspnea is not fully relieved (experiments on post-vagotomy, quadriplegic patients, and transverse myelitis). The answer might look simple in one way. Please mind, we don’t need an intact nervous system to carry afferent dyspnea signals to the brain centers. It can simply be carried by blood, to the central chemoreceptor in biochemical form.
The uniqueness of this symptom is , it can be entirely physiological , or a harbinger of Instant fatality as in acute pulmonary embolism or LVF. Resting dyspnea is always a concern, unlike exertional which has more benign cause. As a cardiologist, we always equate dyspnea to elevated LVEDP and possible LVF . Though RV failure can also cause dyspnea.
Generally, young fellows might ignore non -cardiac non- pulmonary cause of dyspnea. It is better to reemphasize ,the commonest cause of dyspnea missed in ERs and ICUs are metabolic or systemic in nature . (We have seen Kusmaul’s breathing of DKA raising false cardiac alarm )
Systemic causes of dyspnea (With normal PCWP)
Metabolic dyspnea*
Bio-chemical dyspnea*
Anemia*
Most lung diseases
*Chemo receptors are as important as baro- recptors of heart and J receptors in lungs
Is cardiac dyspnea possible with normal PCWP ?
Pre capillary Pulmonary HT (Isolated Arterial PH)
RV infarction.
Classical Hypoxic dyspnes in cyanotic heart disease (TOF,)
Any RV failure , can trigger RV baro-receptors(similar to LV but less concentrated)
Final message
Dyspnea: is it from the heart or lungs? This popular debate has been going on for decades and was answered in a landmark review published four decades ago.(JAMA 1982).Every one of us, must go through this to understand critical cause of dyspnea that arise from heart and lungs.
However, if the question is, which is the commonest cause for exertional dyspnea? Is it from the heart or lungs? The answer is neither of the two. The commonest cause of dyspnea as a whole is neither from the heart nor lungs. It is probably anemia, physical deconditioning, fragility, or sluggish systemic skeletal muscle respiratory status due to a sedentary lifestyle. This explains why a marathon runner can run 42 km without stopping, while a healthy middle-aged man struggles to climb even three floors because of sedentary activity.
Paclitaxel: Is a highly lipophilic, and rapidly absorbed by vessel walls and retained for days to weeks, making it ideal for DEBs, which deliver the drug during brief balloon inflation (30–60 seconds). Its cytotoxic action, disrupting microtubules and arresting cells in the M-phase, effectively inhibits neointimal hyperplasia without requiring prolonged drug release.
Sirolimus: Less lipophilic, sirolimus requires sustained release to achieve therapeutic levels, as it acts cytostatically by inhibiting the mTOR pathway, arresting cells in the G1 phase. This suits DESs, which provide continuous drug elution over weeks via polymer coatings. Its lower tissue retention makes it less effective for short-contact DEBs.
Paclitaxel hurts the endothelium with DES, but it heals with DEB ? How is this possible ?
Paclitaxel’s association with delayed healing and inflammation raised concerns about long-term safety in DESs, particularly after reports of late and very late stent thrombosis. It is abandoned in DES platform.
Paclitaxel born again as DEB avatar
It is claimed, Paclitaxel’s rapid uptake and lipophilicity make it suitable for DEBs, while sirolimus’s need for sustained release and favorable long-term profile suits DESs. It is very hard to believe, the published evidence, however robust they are. Only thing I can guess is, Paclitaxel enjoys a safety net in DEB , as the drug disappears so quickly before any useful effect or side effect could manifest. Ongoing research into sirolimus-coated balloons may shift this paradigm. Till then, we have to trust Paclitaxel, that remains the standard for DEBs due to pure scientific reasons.
Final message
Paclitaxel, which was at its crowning glory during the SYNTAX times , was phased out in DES due to various/ serious untoward effects.
Please bear with this highly biased opinion. I suspect, as a face-saving measure, the industry accommodated Paclitaxel into the DEB platform when it was chucked out of DES. I think we must learn to find truthful pathways of research.
Understanding sympathetic nervous had never been easy. (It doesn’t in any way mean, we have mastered para-sympathetic !). As physicians and cardiologists, we are expected to know the updated adrenergic, dopaminergic, imidazoline receptors etc. We need to know at-least an overview of its current nomenclature, area of distribution, benefits of blocking and stimulating them. Unfortunately, many of us consider it as student stuff and too theoretical for a busy cardiologist.
A realistic scenerio
Then one fine day, an I-pad wielding ,medical representative would come, late in night and teach us about a new drug called Moxonidine. “Sir this is a combined alpha and Imidazoline-1 agonist. Just .2 mg is enough sir to treat any refractory HT” We nod our heads sheepishly, wondering what is that Imidazoline ? Why is this guy is saying alpha agonist* ?
*So far I had been thinking only alpha blockers, have anti-hypertensive action. It took few moments to make some sense . Oh, okay, I got it, Clonidine and Prazosin are entirely different groups of drugs, though they act on alpha receptors—one stimulating and other blocking at different sites.
This post is meant to avoid such embarrassing situations.
Final message
Let us learn new things every day , but never think, reviewing what we read in the past is a mean academic activity.
The contents of the this blog is being published as Kindle E book , as per the request of many of the readers. Every article will continue to be open source in this site. Again I shall reiterate the book format is not aimed at any commercial intent. It is only to facilitate learning in a single book format Here is the link to book https://amzn.in/d/euhL5vu
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Please Note
The author acknowledges all the queries posted by the readers and wishes to answer them .Due to logistic reasons only few could be responded. Inconvenience caused is regretted.
Dr.S.Venkatesan MD 