Dr.S.Venkatesan MD

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Mitral valve anatomy : Why AML lacks scallops, while PML has ? What are the clinical implications ?

Posted in Uncategorized, tagged 3d echo tee mitral valve, clincail implications of mitral leflet scallops, does aml has scallops, mechansim of mitral regurgitation, mitra clip, Mitral valve anatomy, mitral vlave replacement, p2 a2 scallop, scallops, tee mitral valve leaflet terminology on April 24, 2026|

When discussing the anatomy of the mitral valve, many of us get a confusion regarding these A 1, 2, 3 , P 1,2,3 stuff . Is the mitral leaflet really has sub-cm clefts or interuptions , that form the popular terminology mitral scallops .If so how long , these clefts go ? If it goes deep. will it not potentially the mitral valve look a tricupid ? Yes, every thing is possible . But ,It is very important to realise AML has no scallops and indentations, while the PML has distinct sub-commisures that make the well defined three scallops. The so called A 1, 2, 3 are just corresponding segments with reference to PML. Current day cardiologists are supposed to specify , segment or scallop orieneted MR jets . 3-D echo makes it possible. Also live, online TEE( with a good interperator) in cath lab has become essential in cath lab during mitra- clip procedure

3D echo showing the well defined scallops in PML, while the AML appears as single sheet.

A brief review on this topic

The PML has scallops because it develops as three distinct segments separated by indentations (subcommissures), with chordae attaching focally at these inter‑scallops to reinforce and stabilize the scalloped architecture, whereas the anterior leaflet (AML) forms as a single, broad, continuous sheet without clefts and is pulled by chordae in a broad, basket‑like pattern that does not create scallops.

In MR the PML’s scallops are prone to malcoaptation when annular dilatation or tethering pulls them apart, often producing focal jets at P1–P2 or P2–P3, while AML‑driven MR tends to be more diffuse when the entire leaflet is involved.

During MitraClip deployment, the PML’s scallops provide a useful roadmap to target graspable segments (e.g., A2–P2), whereas the smooth AML complicates precise alignment and raises the risk of eccentric residual jets if the clip captures non‑opposite segments, making the PML’s segmental architecturea vulnerability.

Final message

Understanding these mitral leaflet segments in TTE, TEE, are crtical if you are doing a mitral valve repair or mitra clip procedure. However, we need not waste much time in delineating these complex mechansims of MR , if you contemplate a definite mitral valve replacement.

Postamble

Can AML have true scallop ?

Yes , but it is abnormal can be observed in 2 to 3 % . (Ref : Muraru D, Cattarina M, Boccalini F, Dal Lin C, Peluso D, Zoppellaro G, Bellu R, Sarais C, Xhyheri B, Iliceto S, Badano LP. Mitral valve anatomy and function: new insights from three-dimensional echocardiography. J Cardiovasc Med (Hagerstown). 2013 Feb;14(2):91-9. )

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Let us go back to the golden age of simple clinical trials & get rid of    big, motivated RCTs.

Posted in Uncategorized, tagged bmj, clinical trials, evoultion of clinical research, jam network, lancet, medical education, medical ethics, nejm, rct on April 19, 2026|

Very soon, blogs and independent writing will be the only source of unadulterated truths. One such article is shared here written by Adam Kroetsch , formerly in the FDA

A review and comments

The above article compellingly recounts how clinical trials evolved from ad-hoc, investigator-led efforts in the mid-20th century to the bureaucratic behemoths of today. It highlights the “golden age” of the 1980s-1990s, when academic “trialists” pioneered large simple trials like ISIS and GISSI. These mega-trials enrolled tens of thousands with minimal protocols ,one-page forms, no routine monitoring or source data verification (SDV), proper randomization, and focus on clinical hard endpoints and mortality delivering transformative, low-cost evidence on treatments like streptokinase and Aspirin.

The decline followed the rise of Contract Research Organizations (CROs) in the 1990s, global Good clinical practice -GCP guidelines (1996), and FDA missteps. Trials are now industrialized and bureaucratized: extensive on-site monitoring, exhaustive adverse event reporting, data audits, and risk-averse compliance layers inflated the costs (rising 10% annually). Academic and NIH-funded large trials plummeted .Pharma shifted to smaller, often useless biomarker-driven studies instead of clinical outcome. (Eg Drug X reduce NT-pro BNP by this,and it is crowned in glory ). The irony is ,the trialists are crying “foul” at GCP, and call it unscientific as they interupt the industry.

Who is responsible for this chaos?

Primarily commerce and greed in a profit-driven ecosystem .Alos pharma’s risk aversion and demand for speed and volume. Other factors were, heavily empowered CROs, Perverse incentives and Industry balance sheets, dictated the how science should behave. No surprise , true academics and genuine funders retreated amid prohibitive costs.

Final message

GCP  is not a taboo subject,  as some non- academic forces would like to envisage. Let us bring back the golden age of simple trials—even observational ones will bring the truth when done appropriately .Let us stop this big commercialised RCT nonsense  with ultier motives.

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How Important is LA pumping function in LV filling ?

Posted in Uncategorized, tagged la conduit, la function assessment, LA pressure volume lopp, la pressure volume lopp animation, la resorvoir strain, la strian on April 10, 2026|

LA has three important functions, namely reservoir, conduit, and pumping. Which among the three is the most and least important?

Find out the answer yourself. One clue: Atrial systole is very brief, hardly lasting for 120 ms (equal to P wave duration). The rest of the period, the atria are taking rest. You think so? No, It gets ready to receive and deliver the entire stroke volume meant for the next LV contraction. Note the green path; it is not only long, it has to be less steep. For this, we require an agile LA (technically good compliant LA). If the LA is stiff, the LA struggles to form a good V loop, and it depends more on its pumping function. That is, the A loop contribution is more than the physiological 25%. So, as of now, the most critical function of LA seems to be its reservoir function, which is often measured by LA strain; normal values are -18 (luckily the same value as LV strain, easy to remember).

By the way, coming to the least important functional component .Even a 65-year-old elderly person just walks to your office with AF and a rapid rate. He just complains of some palpitations. Nothing else. His BP is normal. What does this mean? It would mean, most healthy adults do not really depend on the atrial booster pump for hemodynamic stability .The early ssytolic suction force of LV effectively compensates for this lack of atrial pump assistance. This is a very provocative statement and needs clarification from experts. One more piece of evidence comes from the long standing debate over rate vs. rhythm control in AF. With almost equipoise between rate and rhythm control, I wonder when exactly this atrial booster pump matters? Understanding LA pressure volume loop may look complex. When we spend some time, it becomes less fritetning.Think about how, MS, acute and chronic MR or LV dysfucntion modify this loop.

Final message

William Harvey might have discovered the circulatory system, but it is Carl Wiggers, the father of cardiac physiology and hemodynamics, whose wisdom taught us that the heart plays a silent  hemodynamic orchestra called systole and diastole. We, the current generation of cardiologists, are happy to stop with that. Do we need to have a separate cardiac cycle dedicated to the atria? Which would mean we need to know the nuances of the isolated atrial cardiac cycle (atrial systole and diastole) in and out of sync with the LV. Maybe someone who carries the same passion as Wiggers will soon emerge and do it.

Postamble

One point, I am yet to understand fully is, why should the LA pressure goes up during the conduit function (See the the blue line going north) as the LV fills. Maybe LA is restricted and trying to get equilibrated with the rasing slope of LVEDP, as the LV is getting filled rapidly.

Reference

1.Thomas L, Marwick TH, Popescu BA, Donal E, Badano LP. Left Atrial Structure and Function, and Left Ventricular Diastolic Dysfunction: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019 Apr 23;73(15):1961-1977. doi: 10.1016/j.jacc.2019.01.059. PMID: 31000000.

Link 2

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Forbidden quotes in medicine : Healing shall prevail over harming

Posted in Uncategorized, tagged bmj, british journal of medical ethics, dr s venkatesan, ethics in medicine, famous quotes on medical ethics, Hippocratic oath, indian journal of medical ethics, lancet, madras medical college, medical education, modern medicine, nejm, venkatesan sangareddi, world health organisation on April 9, 2026|

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Why different cut-offs for diagnosing STEMI in men and women ?

Posted in Uncategorized, tagged stemi gender difference in defintion on April 6, 2026|

In healthy people, some J-point/ST elevation in V2–V3 is normal. This physiologic elevation is greater in men than in women Using the same cutoff for everyone would cause many false-positive STEMI calls in men (over-diagnosis) while missing true ischemia in women (under-diagnosis).

Molecular and Ionic basis

The difference is not because gender based difference in ischemia response . It is because ventricular repolarization differs between men and women due to sex hormones acting on cardiac ion channels. These differences appear at puberty and are belived to be driven by androgenic hormones.

Mechanism

Transient outward potassium current (Ito, carried by K+channels) is higher in male ventricular epicardium than in females. Testosterone up-regulates Ito density and function. In the action potential (AP) of epicardial myocytes higher Ito produces a deeper phase-1 notch This creates a larger transmural voltage gradient (epicardium vs. endocardium during phases 1–2 of the AP. This transaltes in the surface ECG as J-point elevation reflecting early-repolarization voltage gradients. Greater gradient steepr the J-point and higher ST takeoff .This is called the the classic “male-pattern early reppolarization.”Women have a shallow j point.

Image source : Blinova, Ksenia (2020). Sex and Cardiac Electrophysiology Atrial and ventricular tissue electrophysiology.

Why this difference is not seen in limb leads ?

Note : This J point difference is more prounuced in chest leads only because they are unipolar , and very close to epicardium and picks up the difference

Final message

Whenever we have trouble identifying the true mechanism in any gender-related difference, it is easy to blame it on either testosterone or estrogen. As in the atheletic filed , men are naturally a little faster to fly off from the start-boots in the early phase of repolarization. This also has some connection with why women have longer basal QT intervals than men. The whole repolarization process is slow but steady. We can alos realise, in spite of longer QT, women have less incidence of primary ventricular arrhythmias even during ACS, implying better reslience and stress handling. (Ref 2)

Reference

1.Blinova, Ksenia (2020). Sex and Cardiac Electrophysiology || Atrial and ventricular tissue electrophysiology. , (), 39–48. doi:10.1016/B978-0-12-817728-0.00004

2.Weizman O, Marijon E, Narayanan K, et al. Incidence, Characteristics, and Outcomes of Ventricular Fibrillation Complicating Acute Myocardial Infarction in Women Admitted Alive in the Hospital. Journal of the American Heart Association. 2022;11(17):e025959. doi:10.1161/JAHA.122.025959.

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IVUS says good bye to complex PCI & left main :  Cardiologists, are yet to blink !

Posted in Uncategorized, tagged ivus oct, ivus-chip study on April 6, 2026|

How many conferences, live workshops, where elite cardiologists, thought leaders (rather, academic influncers) , were projecting glittering power points about IVUS guided stent optimization, the sacred MLA’s , high precision POTS.They , sort of seduced us to believe , that these are going to rule the next generation PCIs .

In fact, some them warned us (with the company brand on the background) it’s a crime, to do any left main interventions without imaging.

Now, two back to back papers has come in NEJM* , exposing the futility of routine IVUS (after exhausting the market, and seeing no further scope for this deciet market ) . It simply unserscores the fact , that the good old luminogram  is good enough for most PCIs including the complex ones *

Ironically , we should thank the same old  companies, who for some reason , decided to stop this futility, by funding these studies.

Final message

The message from this study is , we should concentrate on the treatment of the whole burden of atherosclerosis. Let us not waste our resources to optimize the stent with exotic imaging , which can be done by conventional means.

Further, Cardiologists are obliged to apologize to their fellow physicians as well as the patient community for hyping up these unnecessary tools causing financial excess and promoting pseudo-science. They should also take an oath , they will not embrace the future technologies, prematurely and blindly.

Postamble

Waiting for OCT to go the same way as IVUS very soon. *By the way, I want to ask NEJM one question: Do you have any mechanism to identify these futilities earlier? Because you guys only publish and lift up the Iniital hypes.

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Why Superior Scientists, will never rely on Non-Inferiority trials?

Posted in Uncategorized, tagged bmj, data torturing, fake science, fake stastistics, jama network, lancet, medical stastistics, nejm, non inferiority trials, stastistics, who is superior scientists, why rcts are riggged on April 4, 2026|

Statistics is the most advanced form of mathematics by which predictions about the future can be made with some degree of surety.  It is a vital cog linking biology with  maths. However, since the last few decades, an abnormal man made bio-mathematical mutation is being spotted in the field of medical statistics.

Why superior scientists avoid Non Inferiority (NI)trials?

They avoid relying NI -trials due to fundamental statistical, interpretive, and ethical weaknesses that undermine rigorous evidence and patient benefit.

Superiority trial models , reduce bias  towards the null hypothesis and proactively protect against false claims. NI trials just do the opposite. The same issues dilute differences, biasing toward falsely concluding the new treatment is “not unacceptably worse” than the active control by a pre-specified margin . Without a placebo arm, sensitivity cannot be confirmed, and the assumption remains tentative.

Key vulnerabilities In NI trials include arbitrary, manipulable margins that may permit clinically meaningful inferiority. High success rates (>85–95%, especially industry-sponsored) suggesting bias, and risks ( Biocreep) where successive approvals erode standards. “Non-inferior” does not mean equivalent .It can mask statistically significant inferiority. Reporting often deviates from guidelines, with inconsistent margin justification and analyses (ITT vs. per-protocol).

Ethically, NI designs accept potential efficacy loss for unproven gains (convenience, cost, safety) without direct proof, exposing patients unjustifiably in high-stakes areas. They place disproportionate proof burdens on de-escalation or alternatives while entrenching suboptimal standards.

A Lancet Oncology piece highlights this as “the tyranny of non-inferiority trials”:. The authors propose abandoning superiority/NI distinctions for simple “comparative” trials.

Final message

Superior scientists prefer superiority or hybrid designs, or direct comparisons of net patient-centered outcomes .They never go for the NI shortcuts driven by regulatory or commercial pragmatism.

Reference

1.Tannock IF, Buyse M, De Backer M, et al. The tyranny of non-inferiority trials. Lancet Oncol. 2024;25(10):e520-e525. doi:10.1016/S1470-2045(24)00218-3.

2.Beryl P, Vach W. Is there a danger of “biocreep” with non-inferiority trials? Trials. 2011 Dec 13;12(Suppl 1):A29. doi: 10.1186/1745-6215-12-S1-A29. PMCID: PMC3287743.

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SMART- DECISION : When big science tries to disrupt our Intellect,what shall we do ?

Posted in Uncategorized, tagged abyss action trial, acc aha esc, beta blckers post mi, comet trial, drsvenkatesan, esc guidlines, euro pcr, GDMT, jama cardiology, jama network, lancet, nejm, non inferiority trial, omt, reboot trial, reduce ami, secondary prevention of cad by beta blockers, smart decision, tct md on April 1, 2026|

Caution: Harsh language & Unscientific truths

It is a pattern out there, rolled out periodically in cardiac- pharma literature . It happened for Digoxin. They have been trying to do this to beta blockers for quite some time. They successfully ditched beta blockers in systemic hypertension with synthesized evidence. Mind you, BBs are the only drug that received a Nobel Prize for its invention, and its role in post-MI protection is well established.

The script is well written. Trying to ring a death knell for cheap and established medical therapeutic norms, citing lack of evidence. It is done based on some non-sensical study designs called Non-Inferiority Trials. (Tannock I, Buyse M, De Backer M et al.The tyranny of non-inferiority trials The Lancet Oncology, 25, e520-e525 Now, powerful cartels want to get rid of BBs in  post-MI ecosystem. REBOOT, REDUCE-AMI, ABYSS all were done with fixed ideas. Of course, ABYSS didn’t follow their agenda. Now, a  the latest trial has come out with a magical name SMART – DECISION.

Read this paper https://www.nejm.org/doi/full/10.1056/NEJMoa2601005

One famous statistician said, non-inferiority study concept is foundationally flawed. Hence, it is generally not worth reviewing them, as most conclusions are deemed to be wrong and not scientifically consumable. Still, looking beyond the trial design, three important flaws are obvious in SMART-DECISION’ trial , which argues for beta-blocker discontinuation after MI.

The study population is highly selected (median 4.7 years 98% revascularized; median LVEF 59%). The study advocated discontinuation among long-term accrued beneficiaries of BBs rather than typical 6–36-month post-ACS patients. Physician-driven HF hospitalization amplifies open-label bias. A wide non-inferiority margin (HR upper CI <1.4) plus low events (132 total) leave it underpowered, unable to exclude modest 15–25% harm (7.2% vs 9.0%).

Final message

In science, we need to be right first … being polite is optional.

When big science tries to corrupt our minds, what should we do? Let us continue with our conscience and follow the instinct and work for the welfare of our patients. We know the healing power of BBs. Let us be cautious and alert. Never allow wayward science to intrude upon our minds to take STUPID DECISIONS and defame the OMT in CAD.

Postamble

A newchallenge to take on

Fact : There is no published RCT that proves diuretics improve mortality and survival in heart failure.

Action requested : Let all evidence-based cardiologists withhold injections of Furosemide or Torsemide when they encounter their next patient with acute heart failure and pulmonary edema.

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How often PV ablation converts AF to AT ?

Posted in Uncategorized, tagged atrial fibrillation, pulmonary vein ablation, pulse field abaltion pfa, rf vs cryo ablation on March 31, 2026|

PV isolation or ablation is considered as an ingenious modality in tackling chronic recurrent AF. Still, it is too invasive and complication-prone, with less than desired success rates. EPs are struggling to mitigate the adverse events. Hardware has vastly improved. We have since moved from RF , cryo , to pulse field ablations.

Whatever said, AF is a chaotic arrhythmia. When we try to take on the chaos head-on with more force, considerable damage, mostly invisible, is expected in the atrial battlefield. One such thing is post-ablation atrial tachycardia. The exact incidence is under-reported. Many times EPs don’t consider this as a complication at all. It is funny, some percieve it as a partial success as  the chaos has become less intense. The fact of the matter is, an AT can be more unpredictable and carry electrical morbidity, whike the risk of further AF always remain.

Zakeri R, Van Wagoner DR, Calkins H, The burden of proof: The current state of atrial fibrillation prevention and treatment trials. Heart Rhythm. 2017

Incidence of AT post AF ablation

Organized atrial tachycardias (ATs) occur in 5–40% of patients after catheter ablation for atrial fibrillation (AF), with the exact rate depending on the index procedure strategy, AF duration, LA size, and follow-up duration.

• With pulmonary vein isolation (PVI) alone: Incidence is lower (5% or less). When AT occurs, it is frequently focal, most often originating from reconnected PVs
• With additional substrate modification (linear lesions, complex fractionated atrial electrogram ablation, etc., common in persistent AF): Incidence rises to a prohibitive 20–50%.
• Macro-reentrant ATs also occurs due to gap-related peri-mitral or roof-dependent circuits.

Final metssage

Both focal and non focal ATs  are much common after PV ablation, than we realise.Very often, they require another procedure or more intensive drugs . Realistically, the original purpose of treating the chronic AF is lost , if AF is likely to be transfomed to some other form of  AT.There is nothing called 50% chaos reduction in AF treatment.

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What is the purpose of “24-hour” upper limit cut off in the pharmaco invasive strategy ?

Posted in Uncategorized, tagged acc, dr s venkatesan, esc, extended pharmaco invasive strategy, fast mi trial, madras medical college, pharmaco Invasive strategy, primarypci, stemi, stemi nstemi guidelines, stream trial, why 3 to 24 hour time window in pharmaco invasive strategy on March 30, 2026|

Why 3-24h ?

The famous & popular 3-24 hr time window for pharmaco-invasive strateg(PIPCI) was adopted blindly from STREAM (prehospital tenecteplase + PCI <6-24h in <3h presenters) and FAST-MI trials  assuming uniform IRA patency. It fails to stress the importance Initial time window to lysis, and its response . This makes the distinction between rescue vs routine pharmaco invasive PCI  a hazy excercise . Thus, both inappropriately  delayed or a hastily-routine PCI becomes all too common.

The 24-hour upper cutoff in pharmacoinvasive strategy serves to prevent reocclusion, or to address any residual stenosis . It is not meant for myocardial salvage, which is irrelevant if lysis was successful.

Mind you, IRA optimisation  is not a time bound emergency in a well recannalised vesseel. In fact,  PCI is not an absolute neccesity for long term IRA patency. With TIMI 3 flow ,and in the absence of any ischemic substrate , there is no need to chase the 24 hr time window. If lysis achieves complete( or almost complete) IRA patency, PCI can safely extended to 48-72 hours, or even permanent deferral (No-PCI , stand alone thrombolysis’ ) in stable patients with optimal medical therapy.

An intresting study is published , from my institute in the current issue of AJC with a title.  Extended Pharmacoinvasive PCI Compared to Primary PCI: Insights From Madras Medical College STEMI Registry . This study argues for extending the time window for pharmacoinvasive strategy to 48 hrs. (It could still be higher.) It suggests , this flexibility suits the LMIC, due to logistical realities. ( Glad to be listed as a co-athour)

Link to the PDF of the article

I am sure, this study, demands to reset the 24 hr upper limit of cut off for pharmaco invasive strategy.Looking beyond this study, there is an urgent need to clarify the specifc purpose of the generalised time window of “3 to 24” hr time window in pharmaco invasive strategy.

A call for new sub defintions in the time windows in PIPCI

1.Successful Lysis* (TIMI 2-3, in about 70%): Routine angiography/PCI 3-24h (prevent reocclusion/residual stenosis) .Extendable to 48-72h + is possibel. Permanent deferral if the pateint and myocardiumare , with a patent IRA . (Implying no need for further salvage at all , we should allow a green corridor for patients with successful standalone thromolysis to exit the hospital without a PCI ) Doing a PCI onlu t0 prevent fear of reocclusion in the first 30 days is not backed with good data.

2.Failed Lysis* (TIMI 0-1, 30%): Rescue PCI immediately (<3-6h post-lysi, like PPCI) Here the time window should be hastened and can never afford to extend it, at any stretch of imagination.

* Ironically, the 24hr cut of has no place in both the above subsets. (May be in failed lysis , 24 hr cut off might apply , again it is 12 hr longer than primary PCI )

Final message

Time is no longer the muscle , if the Intial lysis is suscessful .

What is the purpose of “24-hour” upper limit cut of time in pharmaco invasive strategy ? The 24 hr is not universally valid. Pharmaco Invasive  strategy time windows need to be  based on timing and  efficacy of the Initial  lysis.

Postamble

Commenting this paper as a third person : (With due respect to all the authours )

One limitation in this study is to be admitted. I think, the generalised comparative efficacy of extended PIPCI with primary PCI can not be made, for the simple reason, the extension of time window is possible only in patients who had successful lysis. This study may ideally be concluded as  “3-24h pharmacoinvasive PCI can be extended to 48h if the initial lysis successful” . Further, If initial lysis fails (30% TIMI 0-1), any extension is contraindicated and requires immediate rescue PCI akin to PPCI. Also, data regarding non-IRA intervention might help understand the importance of the extension of the time window better.

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