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Archive for April, 2026

The inferior vena cava (IVC) rim is the most critical rim for successful transcatheter ASD device closure due to its role in preventing device embolization and prolapse. Absence or deficiency of the IVC rim is often a contraindication, as it leads to higher rates of procedural failure compared to other rims like the aortic or SVC.

Anatomical Reasons

The IVC rim forms the posteroinferior border of the secundum ASD, measured in the bicaval TEE view as the distance from the defect’s inferior margin to the IVC ostium. Without ≥5 mm of adequate IVC rim, the device’s right atrial disc lacks stable septal anchorage inferiorly, allowing slippage toward the compliant, funnel-shaped IVC-RA junction. This contrasts with superior rims (SVC), where the SVC-RA junction provides firm foundation.

A dislodged device Video source : APCIS 2016 Jae Young Choi (Yonsei University, Korea) 

Physical and hemodynamic forces at IVC:RA junction

High-volume IVC blood flow (2-3 L/min, 60-70% of venous return) directly strikes the inferior septum and device, exerting continuous shear force that can dislodge a poorly anchored disc, causing left disc prolapse into the RA or embolization. SVC flow (1 L/min) is less voluminous and angled favorably, reducing its destabilizing effect.

If there is good rims on all other sides (270 degreees) can we proceed with ASD device ?

Some cardiologst believe so. Some institiosn have reported ASD device closure in deficnet IVC rims as well . That is not respecting the evidence (Ref 4,5) But, the fact seems to be different. The IVC’s perpendicular, high-momentum jet amplifies fluttering of floppy rims. Thus, even ample superior/anterior rims fail to counter this inferior “pull,” as the device pivots around the waist under dyanmic atrial pressures and flow. Hence IVC deficiency uniquely predisposes to instability despite the availablity of 270° of other rims.

One caution : A common mistake done is eustachian valves is taken as false IVC rim and the device is implanted and later facing issuers. So, a meticulous TEE imaging is neccessary .

Reference

  1. Amin Z. Considerations for ASD closure. Cardiac Interventions Today. 2014;7(2):1–8.
    Link: https://citoday.com/articles/2014-mar-apr/considerations-for-asd-closure
  2. Amedro P, Bayburt S, Assaidi A, Kreitmann B, Habib G, Fouilloux V, Fraisse A. Should transcatheter closure of atrial septal defects with inferior-posterior deficient rim still be attempted? J Thorac Dis. 2019 Mar;11(3):708-716. doi: 10.21037/jtd.2019.02.89. PMID: 31019758; PMCID: PMC6462671.
  3. Song J. Comprehensive understanding of atrial septal defects by imaging studies for successful transcatheter closure. Korean J Pediatr. 2014 Jul;57(7):297-303. doi: 10.3345/kjp.2014.57.7.297. Epub 2014 Jul 23. PMID: 25114689; PMCID: PMC4127391.
  4. Remadevi KS, Francis E, Kumar RK. Catheter closure of atrial septal defects with deficient inferior vena cava rim under transesophageal echo guidance. Catheter Cardiovasc Interv. 2009 Jan 1;73(1):90-6. doi: 10.1002/ccd.21756. PMID: 19089959.

Postamble

Can we create a neo IVC rim by some means?, (Ex by agumenting the lower end of the IVC with stent , that can protrude clost ASD and act as a rim . We have strated closing the complex sinus venosus ASD, so , this might also be possible)

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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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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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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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STEMI and STEMI Equivalents, i.e. Who Needs the Cath Lab Now! — Taming the  SRU

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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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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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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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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