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Good bye to Gruentzig … the mercurial genius and the father of Interventional cardiology. The swag attached to PCI has become a bygone era. Percutaneous structural heart disease interventions, though in Infancy, is ruling the world today. Tans catheter heart valves is the new mantra. (THV).We can say Aortic stenosis has been conquered without surgery.(*Note : we means cardiologists, not patients) . Pediatric cardiologists have done the same in percutaneous pulmonary valve delivery in children. However, our quest for percutaneous AV valve implantation is facing tough challenges that sans meaningful outcomes.

It is heartening to witness huge technological innovations in arena of native TMVR*. Still, Mitra clip (TEER ) is the only non surgical solution for MR as of now. We know, It is a terrible alternative for an surgical MVR. The key issue with TMVR is the absence of good native foundation and tackling the extremely dynamic AV ring , which are in continuity with LV/RV muscle (unlike Aortic valve ) Mind you ,the AV valves should withstand the force of TAPSE/MAPSE for tricuspid and mitral valves respectively. May be a dysfunctional left ventricle might co-live with a TMVR with more peace. (Fortunately ,LV dysfunction is common in patients who are considered for TMVR)

*Valve in valve in TMVR is being widely used .The issue discussed here will be for TMVR . native mitral valve diseae.

Here , an attempt is made to differentiate the basic differences in the science of between TAVR vs TMVR . (Not comprehensive, but has compared three promising TMVRs , Intrepid, Tendyne, M-3 and Alta-valve.

Final message

Though TAVR and TMVR share a word ‘transcatheter’ they live in different anatomical and physiological worlds. TAVR is often successful because calcium is mostly friendly , the annulus is near circular, and landing zone is fairly predictable. Implantation of TMVR demands extreme diligence because the annulus is dynamic, calcium is an unstable ally, and of course there is always the fearsome LVOT nearby.

Post-amble

Meanwhile, the inability to dispose of the native disease leaflets is a the common issue in both TAVR and TMVR .( which our surgical colleagues will laugh at) May be we need to wait until an new avatar of BASILICA or LAMPOON, which might have a valve bioptome , to cut and extract native leaflet ,safely through a dedicated port without the risk of embolization.

TAVI is becoming like PCI equivalent of aortic valve. The procedure is nothing but stenting and plastering the aortic prothesis ,with all the native diseased aortic leaflet in-situ. Pre procedure CT aortic valve mapping (rather the entire Aorta) is the key to successful outcome.

While the calcium is the essential bonding force of the valve to the aortic annulus, it can also play some serious spoilsport, along with native leaflet debri . Many times, the hardened calcium are like like sharp 3 dimensional knife hanging over there in root of aorta.

Every TAVI operator has this ligering fear . Will that speck of calcium “ice berg”, hiding 2 mm above the NCC, hit the AV node, when I deploy the valve ? Will the distorted leaflet jump few mm above and hit the coronary ostia , however high it may be. (After all , the exact final landing zone is not determined by the operator , but by the ROC curve)

Every severely calcified valve experiences a Titanic effect , fortunately most valves escape.

Realise how important the accuracy these softwares are .It is just a matter of few mm error . . Apart form calcium distribution pattern , more fundamental parameters like the annular size, shape, and optimal imaging angle are critically important. Here is brief report on various software packages available for pre procedure planning of TAVR.

Image courtesy : Thoracic Key  Assessment of aortic valve calcification.The stretch view shows dense calcification of the right coronary cusp, noncoronary cusp, and left coronary cusp. The stretch view (A), angiographic overlay (B), cross-sectional view (C), and “hockey puck” view (D) allow quantification of the calcium in the aortic valve.

The following table was curated from the respective company websites. Any further details can visit them.

SoftwareVendor/DeveloperKey Features for TAVR Pre-Planning
3mensio Structural HeartPie Medical ImagingDedicated TAVR module for automated aortic root analysis, valve sizing, and access route planning. Provides 3D visualization, calcium scoring, and virtual valve implantation. Widely used for precise measurements and procedural simulation.
OsiriX MD / HorosPixmeo (OsiriX) / Open-source (Horos)DICOM viewer with 3D multiplanar reconstruction (MPR) tools for manual valve sizing, annulus measurement, and aortic root analysis. Horos is a free alternative. Supports plugins like ProSizeAV for semi-automated sizing.
syngo.via CT Cardiac Function – Valve PilotSiemens HealthineersSemi-automated workflow for aortic valve assessment, angulation prediction, and device sizing. Includes valve pilot tools for efficient CT analysis.
HeartNavigatorPhilips HealthcareAutomated or semi-automated CT processing for TAVR, including aortic root segmentation, access route simulation, and procedural guidance. Often compared for reliability in measurements.
Valve Assist 2GE HealthcareAI-assisted tool for valve sizing, CT analysis, and planning efficiency. Focuses on automating measurements to reduce manual effort.
Mimics Enlight / Mimics PlannerMaterialiseCloud-based 3D modeling software with automated workflows for structural heart interventions, including TAVR-specific measurements, virtual valve implantation, and 3D printing support. Includes AI for segmentation.
cvi42Circle Cardiovascular ImagingAdvanced CT tools for interventional planning, including TAVR, with automation for aortic valve assessment, flow quantification, and structural heart disease management.
Intuition TAVR PlanningTeraReconComprehensive package for aortic root segmentation, centerline extraction, and pre-operative measurements. Supports advanced 3D/4D visualization for TAVR workflows.
Vitrea CT TAVR PlanningCanon Medical (Vital Images)AI-leveraged application for automated TAVR assessment, including valve sizing, access planning, and post-operative evaluation. Integrates deep learning for efficiency.

Some questions

1.Which one is most popular ?

With out doubt 3mensio is top software because of its neutrality between various TAVR valve and wide spread usage and comparisons.

2.What is the cost of these software ?

They are substantial has a monthly subscription model. 3Mensio pricing starts at approximately $500/month for 1 user, $4,000/month for 10 users.

3.Is there any Freeware for assessing Aortic root ?

Yes . OsiriX MD / Horos is a free ware, but not getting sufficient attention.

4.What is the error rate of these software ? since they are offline and often images are machine extrapolated ?

Error rate in software are well not reported. (Can’t expect the vendors to do it !) However, It must be acknowledged they are real because of the offline nature of image processing .These tools process DICOM data, in pre-trained algorithms. Errors can arise from poor CT input (e.g., motion artifacts) or extrapolation in 3D reconstruction (e.g., interpolating between slices), but studies show minimal impact with high-quality scans.

Common Error Sources: User variability, calcium blooming artifacts, or phase-specific differences in dynamic CT.

Clinical Implications: Errors in sizing can lead to complications like paravalvular leak (if undersized) or embolism (if oversized), but validation shows risks are low (e.g., <2 mm differences rarely affect outcomes). Multi-reader or expert double check is encouraged to improve accuracy.

.


Post-amble

Are you a professional physician doctor ?

Honestly I am struggling to become one , it is still a long way to go.


Open artery hypothesis

The open artery hypothesis was first postulated by Eugene Braunwald in 1993 (Ref 1). He suggested that restoring blood flow in an occluded coronary artery, has time independent benefits. beyond the acute phase of myocardial infarction. The proposal was, it could improve left ventricular function, reduce remodeling, and potentially decrease mortality by mechanisms beyond myocardial salvage, such as reduced ventricular arrhythmias and improved healing and also potential channels of future collaterals.It was a great concept and sounded very logical and got world wide attention.

Is it really valid now as a therapeutic concept in CCS ? If so, why we struggle to show benefits in asymptomatic CTOs ?

The fact that, opening a CTO is not bringing the expected benefits is one of the most intellectual questions in coronary physiology. Most of us are not keen to go deep into this question.

Could Opening a CTO Confer More Risk Than Leaving It Closed?

Now get ready for some nasty truths. There are plausible mechanisms by which opening a CTO might increase the risk of recurrent events compared to a stable, closed artery.

1.Procedural Risks:

CTO-PCI is technically complex, with risks including periprocedural myocardial infarction ,coronary perforation, stent thrombosis, restenosis, and contrast-induced nephropathy. In this context , it is worth noting the DECISION-CTO trial reported a 2-3% rate of major procedural complications, which could of offset benefits of PCI in asymptomatic patients.

2.Restored Flow and Plaque Instability:

Opening a CTO restores blood flow to a previously ischemic territory, but the downstream vessel may have unstable or vulnerable plaques that were previously “protected” by the occlusion. Sudden reperfusion could trigger microembolization, increasing the risk of acute coronary syndromes (ACS).

3 .Stent-Related Issues:

CTO-PCI often requires not only long procedure times, it often requires long stents , or multiple stents, increasing the risk of stent thrombosis compared to a naturally occluded artery that has adapted with collaterals. Dual antiplatelet therapy (DAPT) post-PCI introduces bleeding risks, which may outweigh benefits in asymptomatic patients.

4.Collateral Regression:

CTOs often develop robust collateral circulation, which may provide adequate perfusion to the myocardium. After successful PCI, collaterals may regress, leaving the myocardium dependent on the newly opened vessel. If restenosis or reocclusion occurs, this could lead to ischemia or infarction, potentially worse than the pre-PCI state fed by the caring collaterals.

5. Inflammatory Response:

PCI also induces an inflammatory response in the vessel wall, which may promote neointimal hyperplasia or accelerate atherosclerosis in the treated segment, increasing the risk of future events. All these, bring a curious and serious assumption close to reality. (That is, opening a CTO could, in some cases, disrupt a stable, quiescent milieu into, potentially un-predictable terrain and lead to more events than leaving the artery closed.)

Why CTO-PCI May Not Outperform Medical Therapy in Asymptomatic Patients

The lack of clear benefit from CTO-PCI in asymptomatic patients, as seen in trials like the Occluded Artery Trial (OAT) and DECISION-CTO, may partly stem from these risks. Key reasons include:

  • Stable Collaterals: In asymptomatic CTOs, well-developed collaterals may provide sufficient perfusion, reducing ischemia-driven events. Opening the artery may not add significant benefit but introduces procedural and stent-related risks.
  • Optimal Medical Therapy (OMT): Advances in OMT (e.g., statins, beta-blockers, SGLT2 inhibitors) have significantly reduced event rates in stable coronary artery disease (CAD), making it harder for PCI to show incremental benefit.
  • Lack of Ischemia or Viability: Most importantly ,In asymptomatic patients, the absence of significant ischemia or already viable myocardium. reduces the potential for PCI to improve outcomes.

Squeezing the landmark studies on CTOs for some data

While no study has explicitly tested whether closed arteries are better than open ones , several trials and analyses have explored whether CTO-PCI increases event rates compared to leaving the artery closed.

Occluded Artery Trial (OAT)

  • Design: Note : It randomized 2,166 patients with an occluded infarct-related artery (post-MI, >24 hours) to PCI or OMT. OAT is not a strict CTO study.
  • Findings: At 4 years, there was no significant difference in major adverse cardiac events (MACE: death, MI, or heart failure) between PCI (17.2%) and OMT (15.6%) However, there was a trend toward more nonfatal MIs in the PCI group (7.0% vs. 5.3%, ) suggesting a potential for increased events post-PCI, possibly due to procedural complications or restenosis.
  • Implication: This supports the idea that opening an occluded artery may not always be beneficial and could introduce risks.

DECISION-CTO Trial

  • Design: Randomized 834 patients with CTOs to PCI + OMT vs. OMT alone.
  • Findings: At 3 years, there was no difference in MACE (death, MI, stroke, or revascularization) between groups. However, periprocedural complications (e.g., perforation, tamponade) occurred in the PCI arm, and there was a non-significant trend toward higher restenosis-related events.
  • Implication: The trial suggests that PCI does not consistently outperform OMT and may introduce risks that offset benefits in asymptomatic patients.

EXPLORE Trial

  • Design: Randomized 304 patients with STEMI and a CTO in a non-infarct-related artery to CTO-PCI or no PCI.
  • Findings: No significant difference in left ventricular ejection fraction (LVEF) or MACE at 4 months. A subset analysis showed a trend toward more revascularization events in the PCI group, possibly due to restenosis or reocclusion.
  • Implication: Opening a CTO did not improve outcomes and may have increased event rates in some cases.

A provocative proposal

Thanks to the absolute democracy in science , I can propose a concept, however crazy it may appear. Yes, it is the Closed artery hypothesis . It can be defined as follows: In asymptomatic patients with chronic total occlusions and well-developed collaterals, leaving the occluded artery closed may result in fewer recurrent cardiovascular events than opening it via PCI, due to the stability of the collateralized system and the risks associated with intervention.

The closed artery hypothesis could turn out to be a compelling concept that merits further investigation

Reference

1.Kim CB, Braunwald E. Potential benefits of late reperfusion of infarcted myocardium. The open artery hypothesis. Circulation. 1993 Nov;88(5 Pt 1):2426-36. doi: 10.1161/01.cir.88.5.2426. PMID: 8222135.

2.Kimmelstiel CD, Salem DN. The Open-Artery Hypothesis: An Overview. J Thromb Thrombolysis. 1997;4(2):227-237. doi: 10.1023/a:1008842917403. PMID: 10639257.


Postamble

What makes coronary blood flow dynamics so fascinating ?

A cardiologist’s primary job is to open the artery when it is closed in an emergency . This rule goes topsy-turvy when it happens in a chronic fashion**. Think about the two contrasting behavior of the same myocardium. In Stemi, it bounces back to life with emergent opening of the artery, while in the other, myocardium simply doesn’t bother about total shut down and possibly enjoys* the protection conferred by a closed artery.

*Objection my Lord. The word enjoys is brutal .Are you aware CTOs can be responsible for Stemi too ? ** But, Is it not Intriguing to note, OAT study included primarily ACS population and it looks so true , even acutely occluded coronary artery need some rest from reperfusion Injury.

It is often said, If you are not able to answer a question, in a single line, or if the explanation is too long, then the answer is likely to be vague and difficult. So does this question.

It is a very practical probelm in day to day cardiology practice faced by every one of us. Still, it is often taken for granted during echo lessons in cardiology schools.

Here is a big table of differences listed. Read it if you have time.

There are only three words important. Find it out.

Final message

Look beyond septum, concentrate both systole and diastole. Normal systolic thickening and beaking in M-mode, clinch the diagnosis as LBBB

A query for advanced readers.

If LBBB and CAD /DCM co-exists, (a common scenario ) Which component of wall motion defect dominates ?

The answer to this question becomes important, as only the electrical component is correctable by CRT (or CSP now). No surprise, there is huge chunk of non responders, where myocardial component of de-synchrony prevails over the electrical LBBB,

History beckons… once upon a time, assessing severity in valvular heart disease was gloriously simple. We used to just a pullback pressure gradient across the aortic valve . Now, history repeats itself, as the same philosophy returns to coronary arteries, offering a surprisingly elegant solution amid a chaos of physiological indices. That is PPG .

What Is PPG*?

Pullback Pressure Gradient (PPG) is a physiological mapping method that evaluates the pressure gradient across a coronary artery using a gradual pullback of a pressure wire . It helps to:

  • Localize ischemia
  • Differentiate focal from diffuse disease
  • Guide a more logical PCI strategy

Rather than a strict binary verdict (ischemic or not), PPG gives us a gradient map — revealing how pressure falls, where it falls, and whether intervention makes sense.

*I would love to call it as plain old PPG. POPP-G . (Sort of POBA equivalent in PCI)

How to Measure It ?

  1. Essentially it is a less glorified iFR or FFR .Same hard ware is used.
  2. Pull back happens in both .But ,here thats is only that happens, that’s devoid of the clumsy Adenosine protocols, Incomplete hyperemia, patient anxiety, or microvascular dysfunction etc.
  3. Apart from measurinng pressure drop the rate of fall the gradient slope is also analysed. PPG = ΔP / pullback distance (mm) .If the slope is steep the lesion is probably stentable . If the rate of fall is slow or flat we may avoid stenting.

PPG is a dynamic, localized, gradient-based insight into coronary disease. A focal ΔP over small length ΔL would be a perfect PCI candidate. A flat gradient over long ΔL , would suggest medical therapy .(May be CABG in few)

PPG in bifurcation Lesions

How do you FFR in bifurcation or trifurcation lesions . If you ask this question to any cardiologist, will try to get away from the scene. Such is the complexity involved. Here comes the savior. PPG helps you out in a smart fashion.

  • PPG allows branch-specific physiological localization, Can be used selectively in each branch to map the true pressure loss. This is contrast to the crude FFR that may falsely elevate due to competitive flow or tandem disease.
  • PPG can avoid the unnecessary double stenting and of course make the make the bifurcation club members unhappy in the process. PPG also can help detect ostial branch disease (by inching technique we do in cardiac auscultation,) by very slow pull back.

Image courtesy : Daniel Munhoz CARDIAC INTERVENTIONS TODAY MAY/JUNE 2021 VOL. 15, NO. 3

Is FFR really problematic ? Be aware of conflicting studies

FFR was a great concept when it came in. FAME I study adored It. FAME II questioned PCI’s benefit despite FFR-positive lesions. Then came DEFINE-FLAIR and iFR-SWEDEHEART, questioning the need for hyperemia at all. Still, residual ischemia post-PCI in up to 20% of cases (DEFINE-PCI) even when FFR said “normal.” Confused? So are most cardiologists.

Modern cardiologist’s dilemma: How to cross coronary jungle infested multiple flow Indices ?

The list is long . FFR , iFR, FFR-CT, QFR, RFR, dPR, NHPR, µQFR (there are few more I might have left ) . None are perfect. Some contradict. Some cost too much. Many need drugs. All add layers of complexity to what should be a simple clinical question: Should I stent this lesion? Now, we have the simple plain PPG.

Why should, we fall for PPG ?

Let’s be honest. PPG is not flawless. After all, we take pressure drop as a surrogate marker for restricted flow . Every Indices does that. But unlike other indices It’s intuitive. It’s visual. It tells you where to treat. It gets the pressure data on the spot from ground zero . It can bring reliable info without the need for intracoronary medication , or costly software. Finally, it restores some simple sense in us ,without great knowledge in coronary hemodynamics.

Reference

  1. Kobayashi Y, Johnson NP, et al. “Physiological Assessment of Residual Ischemia After Coronary Stent Implantation Using Instantaneous Wave-Free Ratio.” JACC Cardiovasc Interv. 2019;12(19):1996–2007. https://doi.org/10.1016/j.jcin.2019.04.040
    PPG-based residual gradients predicted poor outcomes post-PCI even when angiographic results looked fine.
  2. Collet C, et al. “Stress myocardial perfusion imaging vs coronary functional assessment with PPG and FFR: A physiologic map approach.” Eur Heart J. 2021;42(10):926–938.
    PPG superior in identifying focal lesions amenable to PCI compared to binary FFR thresholds.
  3. van Belle E, et al. “DEFINE-PCI: Residual Ischemia Post-PCI Detected by PPG and iFR Pullback.” JACC Cardiovasc Interv. 2019;12(20):1991–2001.
    Post-PCI ischemia often missed by angiography alone — PPG reveals it.
  4. Davies JE, et al. “Use of the Instantaneous Wave-Free Ratio or Fractional Flow Reserve in PCI.” N Engl J Med. 2017;376:1824–34.
    iFR non-inferior to FFR .Suggests resting physiology-based PPG.

5.Munhoz D, Collet C, Mizukami T, Yong A, Leone AM, Eftekhari A, Ko B, da Costa BR, Berry C, Collison D, Perera D, Christiansen EH, Rivero F, Zimmermann FM, Ando H, Matsuo H, Nakayama M, Escaned J, Sonck J, Sakai K, Adjedj J, Desta L, van Nunen LX, West NEJ, Fournier S, Storozhenko T, Amano T, Engstrøm T, Johnson T, Shinke T, Biscaglia S, Fearon WF, Ali Z, De Bruyne B, Johnson NP. Rationale and design of the pullback pressure gradient (PPG) global registry. Am Heart J. 2023 Nov;265:170-179. doi: 10.1016/j.ahj.2023.07.016. Epub 2023 Aug 21. PMID: 37611857.

Recently , a young celebrity lost his life during gym session suddenly . The media erupted as expected .Every TV channel became a temporary schools of advanced cardiology . It seemed anchors knew more cardiology than us.

Among the peers, so many hypothesis were going around. The loudest one was prolonged QT. We are discussing a relatively new, (rather les popular ) entity for the potential cause of SCD. What is it ? DID is the new buzzword in electrophysiology . Next to Long QT, Brugada, DID is looked upon as a new marker for SCD in young as well as elderly .

What is DID ?

Delayed Intrinsicoid deflection. (DID) Mind you, Intrinsicoid deflection ( ID ) is nearly 100 year old concept, being rediscovered. ID is the time it takes for the electrical impulse to travel from the endocardium to the epicardium directly beneath the recording electrode.

Macleod, A. G., Wilson, F. N., & Barker, P. S. (1930). The form of the electrocardiogram; intrinsicoid electrocardiographic deflections in animals and man. Proceedings of the Society for Experimental Biology
and Medicine. 27(6), 586–587


1.How to measure, what is the normal ?

Variable in each lead.

2. Which lead it is measure ? Is ID relevant in Limb leads ?

V5, V6. Normal less than 50 ms

3.When do you call Intrinsicoid deflection as prolonged ?

>50ms

4.What is the Ionic basis of ID ?

Sodium

5.Is there both congenital and acquired forms?

Yes

7.Is it different over RV vs LV ?

Yes

6.How does a DID trigger an arrhythmia ?

Not clear

Two more questions

7.Why it is called Intrinsicoid deflection rather than Intrinsic ?

Intrinsic was the original term coined by Sir Thomas Lewis in 1914, To get this “intrinsic” measurement, an electrode had to be placed in direct contact with the epicardium . Measuring it from surface ECG leds make it Intrinsicoid.

8. Is Intrinsicoid deflection and ventricular activation time (VAT) both are same ?

Yes. Both are used inter changeably , though one denotes time other the wave as such. While VAT is the same time , specifically look at time to R wave peak. However , ID can be applied to the leads where there is no R wave. Then it becomes time to peak of Q

9.Is it true, in every LBBB, ID is prolonged by default ? Then what is the risk of SCD in LBBB ?

For the first part of the question, the answer is Yes. The second part , we don’t know the true risk yet.

10. …………………………………………………………………..(Question left for the readers to ask)

Final message

As cardiologists, we have given disproportionate importance to the QT interval and gets the blame for many SCD. It is time, the 100 year old ECG parameter Intrinsicoid deflection (ID,) seems to be equally important. Much of the secret ionic codes, for many SCDs are believed to hide behind this eerie deflection.

Reference

Here is an important review

1.Aiken AV, Goldhaber JI, Chugh SS. Delayed intrinsicoid deflection: Electrocardiographic harbinger of heart disease. Ann Noninvasive Electrocardiol. 2022 May;27(3):e12940. doi: 10.1111/anec.12940. Epub 2022 Feb 17. PMID: 35176188; PMCID: PMC9107081.

Once the Noble and pride profession, practicing medicine is becoming fearsome. India’s healthcare system is facing a silent emergency, not of disease, but of distrust. A worrying wave of rising intolerance among patients has led to an alarming surge in verbal abuse, threats, and physical assaults on doctors. Once revered as lifesavers, doctors now work under the looming shadow of mob rage, fueled by unrealistic expectations and social media-triggered misinformation. Emergency rooms have become battlegrounds. This is not just a law and order crisis—it is a near collapse of the doctor-patient relationship, once sacred, now strained to the breaking point. Urgent systemic, legal, and cultural interventions are no longer optional they are are matter of survival.

While the issue looks monstrous, if we dwell a little deeper, it is clear case of miscommunication, over-expectations, low tolerance, and sheer ignorance about human biology and illness . With the destructive mass of information explosion , every patient tries to think more than a doctor, about his or her illness.

This curious thought popped up during a debate with my colleagues . Why not propose a Hippocratic-like oath for every patient and their close family members as they enter any public or private hospital .Hippocrates would have never Imagined , there would be need for such an oath from patients.

Here is the Hippocratic Oath : Patient version 2025 : *Disclaimer : The content is never meant to underestimate the freedom and rights of the patients. While the patients are becoming hyper educated , with various resources , this oath is an attempt to enlighten them some simple but Invisible truths in our profession.

I am sure, this might look harsh, provocative, and even belittling of patient rights. But, to my conscience, it looks like, we the doctors have failed the whole patient population, by behaving, as if we are doing the job of a God. (at least in India) In the process, we have hidden many errors and systemic malfunction that are built into the system. We hesitate to tell the truth .For example . the true medical risk is dynamic and can vary moment to moment, even with an apparently simple procedure. (1% risk can become 100% risk in a flash ( A minor lapse of concentration* during a complex surgery or procedure can lead to… )

No surprise, patients expect 0% error and 100% success. Think for a minute and reflect. When did you last admit to your patient, “Yes, it was a mistake or error on my part?” That’s where the seeds of problems germinate. In spite of the dedication (& sacrifice) of our entire lifetime to our patients, we stand sorry. We must ensure and sensitize our patients, that complications and errors are irreversible attachments of disease and the treatment process. (As of now, so called informed consent document in India, doesn’t even receive the respect of torn rubbish in the dustbin.)

Reference

1.Jain P, Singh K, Piplani S, Gulati S, Kour H. Beyond Scrubs: Understanding the Root Causes of Violence Against Doctors. Cureus. 2023 May 27;15(5):e39559. doi: 10.7759/cureus.39559. PMID: 37378246; PMCID: PMC10292170.

*Full time sports professionals like Messi or Ronaldo can miss a penalty kick in a most crazy fashion, Virat Kholi can see his middle stump flying on the first ball, but Doctors can never err* … they need to be perennially precise, 24/7 X 365 .How fair it is ? Wish, God shall answer this query for our beloved patients.

** But, the truth is , they err quite often is the untold story .The day our beloved patients realize this, medical profession will be released from the clutches of distrust from the patients.

An Awakening Call to the Guardians of Medical Science

Dr. Venkatesan Sangareddi MD, Former professor of cardiology, Madras medical college,Chennai .India

Medical science remains a cornerstone of human progress, and what we have achieved in the last 100 years is unprecedented. Every one of us is aware that the trust placed in medical research is sacred. Also, the medical profession is expected to remain noble as long as human beings exist. However, as in all walks of life, there must be trade-offs to any positives. Yes, this trust has increasingly become vulnerable, threatened by the pervasive and often subtle influence of conflicts of interest (COI). This is especially explicit in the current medical research landscape.

While the scientific community has made strides in acknowledging and requiring disclosure of COIs, particularly from authors , the measures are proving insufficient. There is a big irony sitting right across us. It is made to look, as if conflicts of Interest (COI) exist only with the authors.

The following article written by the author (Ref 1) calls for an  awakening to every medical journal publishers, regardless of their prestige or impact factor, to recognize their vulnerability . We are expected to adopt a new paradigm of transparency in declaring COI, that extends to every participant in the publication process, including the scientific or ethical committies that approve the study ,the peer reviewers, the publishers and finally to the industries that fund the research.

Reference

1,Click here to download the full paper: A caution: It is a fairly lengthy article. (15 minutes read) Hope the suggestions made in the article are not labeled as unrealistic and possibly crazy as well.

Measurement of pulmonary vascular resistance (PVR) is traditionally done by cardiac catheterization. It remains the (un)disputed gold standard, despite numerous assumptions, errors in measurement, and lack of reproducibility.

PVR by Echocardiography

Recently, echocardiographic calculation of PVR gained importance. Resistance is pressure divided by flow. Pressure is measured by Doppler, flow is measured by the cross-sectional area of RVOT times the TVI. We can arrive at PVR quickly. As simple as that.

Still, many institutions and purists ( Who have huge trust in cath derived, Oxygen diluted data) ) won’t accept this as standard . They fail to realise echo methodology carries less limitation, if not similar limitations as in traditional cath method. However, a significant advantage is, it is more real -time, can be repeated any number of times, and documents a baseline PVR, and at least is useful for follow-up.

There are two formulas used.

1.Abbas Formula

PVR = (TRV / RVOT VTI) × 10 + 0.16

2.Haddad formula :

PVR= (TRV²/VTI_RVOT)

*TRV = Tricuspid Regurgitation Velocity (m/s)

*RVOT VTI = Right Ventricular Outflow Tract Velocity Time Integral (cm)

Comparing Abbas vs Haddad

The Abbas formula is better validated and widely used in clinical practice, as it was specifically designed to correlate with catheter-based pulmonary vascular resistance measurements. It provides reasonably accurate estimates, especially for screening pulmonary hypertension, though it tends to under-estimate PVR at higher values (>8–10 Wood units).

In contrast, the Haddad formula ) is simpler but less rigorously validated and is more commonly applied in research settings focused on right ventricular-pulmonary artery coupling rather than direct PVR estimation.

Haddad’s method may be less reliable in patients with significant tricuspid or pulmonary valve abnormalities. Therefore, Abbas remains the preferred formula for routine clinical application. There is still hope to improve Haddad equation.

How to improve upon Haddad equation* ?

The Haddad equation for estimating PVR (TRV²/RVOT VTI) lacks calibration and overlooks key hemodynamic variables. It can be improved by introducing empirically derived correction factors to correlate with catheter-based values. Incorporating right atrial pressure (RAP), RV functional indices like TAPSE or RV strain, and adjusting for heart rate or rhythm variability can enhance accuracy. Averaging VTI across multiple cardiac cycles could also stabilize measurements. Additionally, machine learning on large datasets and AI-enhanced model could outperform the current linear Haddad formula for non-invasive PVR estimation.

* This is a fresh area of study , young fellows should come forward to do.

Final message

As discussed earlier, Abbas remains the preferred formula. But, the real issue is cardiologists refusing to accept any Echo-derived PVR and incorporate it, in the day to day practice. We have accepted EF % as the gold standard for LV function in spite of some serious lacunae. PVR carries the same story. Cath-derived data, in all likelihood, is enjoying pseudo-sanctity. It is time we should embrace one of these Echo formulas regularly and make life simple for both ourselves and the patients (who are often tiny babies or children). I think it can be done without compromise on scientific purity.

Reference

1.Haddad F, Zamanian R, Beraud AS, Schnittger I, Feinstein J, Peterson T, Yang P, Doyle R, Rosenthal D. A novel non-invasive method of estimating pulmonary vascular resistance in patients with pulmonary arterial hypertension. J Am Soc Echocardiogr. 2009 May;22(5):523-9. doi: 10.1016/j.echo.2009.01.021. Erratum in: J Am Soc Echocardiogr. 2010 Apr;23(4):376. PMID: 19307098.

2.Abbas AE, Fortuin FD, Schiller NB, Appleton CP, Moreno CA, Lester SJ. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am Coll Cardiol. 2003 Mar 19;41(6):1021-7. doi: 10.1016/s0735-1097(02)02973-x. PMID: 12651052.