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There is no simple answer. We hide behind two terms, adaptive and maladaptive RVH. While the former is beneficial for an unknown period of time, the latter rapidly goes into a downward spiral.

  • Adaptive RVH (A-RVH) occurs when the RV responds to chronic pressure overload by increasing muscle mass concentrically. This adaptation maintains RV contractility and cardiac output despite increased pulmonary vascular resistance. RVH is typically concentric with less chamber dilation, preserved coronary perfusion,
  • Mal-adoptive RVH (M-RVH)occurs If afterload is excessive, prolonged and the RV cannot maintain sufficient contractile function . For some unknown reason, in M-RVH, the impact of PA pressure is not uniform the chamber dilates asymmetrically this leads to wall stress increase, fibrosis, ischemia, and contractile failure.

I am unable to find the exact incidence of the above two entities. In COPD, it is more adaptive; in cardiac conditions, it is more maladaptive. A new thinking is that the LV plays a significant role in determining RV function, as both are interdependent. (Both arms of Bernheim effect)

The third entity is acute RV dilatation to sudden elevation of PA pressure as in PE. (Recall the 60/60 sign) Though we think it is purely a hemodynamic response, there are reasons to believe an ultra-rapid predetermined genetic response is also possible by recruiting messenger RNA and growth factors.

*It is worthwhile to note the complexity of RV dynamics. Chronic RV dilatation, (without pressure load)need not be a major pathology, as they are meant to dilate with excess venous return (We also see ASD patients live their entire lives with baggy right ventricles.)

Various shapes of RV in PH .Image source : Llucià-Valldeperas A, de Man FS, Bogaard HJ. Adaptation and Maladaptation of the Right Ventricle in Pulmonary Vascular Diseases. Clin Chest Med. 2021 Mar;42(1):179-194.

Mechansims of adoptive RVH

The following mechanisms are believed to be responsible.

  • Concentric hypertrophy with preserved contractile function involving mainly fast myosin heavy chain (MHC) α isoform expression.
  • Metabolic remodeling with a switch to glycolytic metabolism but preserved energy supply through compensatory mechanisms like increased GLUT-1 expression.
  • Maintenance of angiogenesis and oxygen supply through vascular endothelial growth factor (VEGF) signaling.
  • Self restricting fibrosis and balanced extracellular matrix remodeling.

Is there any Clinical and echocardiographic clues to adoptive RVH ?

Of course yes. But all are common sense related.

  • Patients with adaptive RVH often maintain higher exercise tolerance.
  • Elevated levels of BNP or NT-proBNP correlate with maladaptive RVH.
  • In echocardiography , Adoptive RVH is characterized by increased RV wall thickness (>5 mm) with relatively preserved RV chamber size and function. TR is less common as shape is preserved and annular distortion is minimal.

How long the Adoptive RVH phase can lasts ?

Law of Laplace states, wall thickness will reduce the after-load, balance out the RV-PA coupling mis match. How long this can last? A wild guess is that it can last even up to a decade. Studies in conditions like surgically repaired congenital heart disease and Eisenmenger syndrome have shown adaptive RVH with preserved contractility and normal chamber size for many years. However, this phase eventually transits to maladaptive state.

Can we Induce adaptive RVH as a therapeutic measure ?
As of now , this possible only on paper .Research should target therapeutically, controlled pressure overload and neurohormonal modulation can promote beneficial RV hypertrophy. Strategies to support favorable metabolic pathways, enhance angiogenesis, and reduce oxidative stress are under investigation

Final message

Whether the RV is going to fight or flight the raising afterload of pulmonary HT is not in our hands. It is pre-programmed and switches are controlled by destiny. We can only do whatever, to lower the PA pressure and PVR by treating the primary cause if any. Though, the pharmacological strategies in PH has shown tremendous progress in recent times , the behavior of RV will define the outcome.

Reference

1.Khassafi, F., Chelladurai, P., Valasarajan, C. et al. Transcriptional profiling unveils molecular subgroups of adaptive and maladaptive right ventricular remodeling in pulmonary hypertension. Nat Cardiovasc Res 2, 917–936 (2023). https://doi.org/10.1038/s44161-023

2.Ren X, Johns RA, Gao WD. EXPRESS: Right Heart in Pulmonary Hypertension: From Adaptation to Failure. Pulm Circ. 2019 Apr 3;9(3):2045894019845611. doi: 10.1177/2045894019845611. Epub ahead of print. PMID: 30942134; PMCID: PMC6681271.

3.Llucià-Valldeperas A, de Man FS, Bogaard HJ. Adaptation and Maladaptation of the Right Ventricle in Pulmonary Vascular Diseases. Clin Chest Med. 2021 Mar;42(1):179-194. doi: 10.1016/j.ccm.2020.11.010. Epub 2021 Jan 12. PMID: 33541611.

4.Magoon, Rohan; Dey, Souvik; ItiShri, ; Kashav, Ramesh. Evolution of Ventricular Interdependence Concept: Bernheim, Reverse-Bernheim Effect and Beyond!. Journal of the Practice of Cardiovascular Sciences 6(1):p 90-91, Jan–Apr 2020. | DOI: 10.4103/jpcs.jpcs_55_19

Post-amble : How the new age interventions help tackle the RV failure

TR clips, and tricuspid valve reconstruction, either surgical or percutaneous, RV assist devices are THE interventions done in a failing RV before the last resort of heart/Lung transplantation.

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Who are we ?

Where are we from ?

What is the purpose for us , being the part of this world ?

Why time , space, mind are almost one and the same ?


Spend few minutes here in this video. Not every one is blessed to reach the space station .But thanks for this effort by Sen , we can see the astronauts eye view of our lovely planet . Do you see any unrest ? How many of you are seeing 5 million life forms here, other than human beings ?

As cardiologists , we are struggling round the clock ,to salvage even few milligrams of myocardial damage. Meanwhile, how could the world be a mute spectator, to all those fights for silly things in life , and allow, war, violence, poverty, greed & commerce, take more lives than diseases ? It is very very clear , doctor’s role in alleviating human suffering is far less than, what we Imagine.

To know more about Sen click here

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Breaking the science of Heart failure :

Heart failure (HFrEF) remains a gigantic clinico-pharmacological entity. In the last decade, pharmacological strategies to tame HF turned out to be a multi-billion global block buster. Industry constructed multiple evidence-based pillars to lift the drowning patients from HF. To be precise, there were four (Some wanted to insert a fifth pillar : Riociguat a sensitizer of soluble guanylate cyclase (sGC) which play mimicry with Nitic oxide ). All sounds good and right on paper .

But, what was hidden from the public was, that they were built displacing the foundation on which heart failure was managed for centuries if not decades. Yes, it’s about the foxglove-derived grand old drug Digoxin, a Na+ /K+ATPase blocker in the myocyte cell membrane, that exchanges calcium for stable Inotropy. Digoxin is only positive Inotropic with vago -mimitic action that calms the heart. Though the efficacy to safety margin is low in terms of pro arrhythmia , if used properly Digoxin had been a key drug in HF especially if AF is associated. Over time, we have developed RASS sympathetic blockade system in various forms. One poorly done study in 1990s, DIG-Trail, was enough to paint black on the wonder drug.

Now, In 2025, it seems apparent, lack of that vital foundation might shake the pillars, built with ornamental ARNI’s and the flimsy Flozins (Which are essentially renal glycosuric agents also playing a diuretic role , in the process partly stealing the benefits from time-tested diuretics)

This post was written in this site about long back, questioning the DIG trial conclusion (Click here)

Delighted to note , the observations were ratified today.

Now in 2025, the ESC congress in Madrid, some sensible study group from Germany and France found Digoxin indeed saves lives, confirming the suspicius results of DIG trial results done in 1997.(Which claimed no mortality benafit )

The NEJM article ACC website

Back to Catch 22 situation

This time, in DIGIT -HF they used Digitoxin instead of Digoxin. Why ? again, something sounds fishy. Digoxin is the true universal generic available for a peanut price. I am not sure about the availability and price of Digitoxin. This trial is is really kick all those modern cardiologists who get humiliated to write this old drug.

Meanwhile, a near foolish argument is already on , questioning Digitoxin cannot be compared with Digoxin as the former is more stable, has a hepatic route to eliminate if HF patients are renally compromised, etc. I checked with the pharma guys. Digitoxin is difficult to get. My fear is someone may patent this new improved German Digitoxin that was used in this study. (Digitoxin -Trade Name Crystodigin)

Final message

It is glad to see Digoxin continue to defy the death sentence passed by modern day scientists. Though DIGIT-HF is a good come back, we need to allow more truths to come out from the secret scientific cupboards.

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There is a list of conditions that come under cono-truncal anomaly(CTA) in CHD. TOF is the classical example. CTA are group of genetically determined fusion defects between developing right ventricle , septum and the outflows .Many components of outflow are outsourced from cranially located neural crest . In fact, improper migration and fusion of this secondary heart field to the primary is most common cause of many complex heart disease. Microdeletion on chromosome 22, specifically in the 22q11.2 is a major documented gene defect. Traditionally CTA list often includes PA with VSD. This table compares the anatomical and embryological basis of TOF & PA with VSD. You can decide whether to call both as part of cono-truncal anomaly or not.

Add on content.

One important difference is missing in the above table. It is about presence and absence of PDA. In TOF true PDA may be present in early days or months . In PA with VSD , PDA or (MAPCAS mimicking a PDA ) can be part of collateral .A persistent controversy is, how to differentiate a PDA from MAPCAS .That can be challenging. Further, to label a vessel as PDA it should drain into normally formed left pulmonary artery, which is rarely likely.

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This a transcript of a mini-cardiology consult happened in a routine office practice of a physician.


I am Mr. S. I just went for a preventive health check, specifically to rule out hypertension . I got my BP checked by a physician who is also an experienced cardiologist.

“How is my BP doctor ?

“Its fine , It is 120/76

I asked him, “Is my blood pressure normal doctor?

I thought, the doctor sort of frowned at me for a moment and said , “Oh sure, technically yes , it is normal BP , but academically it is not.” 

Doctor, make a pardon , I didn’t get it . You mean to say my BP is abnormal ?

No, not really, it is not abnormal either.”

Then, why you said it is academically not-normal doctor ?

I would love to call it normal, in fact it is normal .

I am confused doctor. What prevents you to call it as normal BP doctor ?

Let me tell the truth .The current scientific guidelines (ESC) which we revere , doesn’t allow me to call it as normal BP . It wants to get rid of the term normal BP from the cardiology literature. It asks us to call you guys with perfectly normal BP as having non elevated BP. I want to be loyal to the science and also should not feel out-dated with my peers.

I understand doctor, the compulsion to respect science more than your conscience in your day to day practice and admit it too .You are a very rare & frank Doctor I have, ever come across

Thank you, Mr S. for your complements very kind of you .But, let me go little personal. My colleagues consider me otherwise . They don’t consider me as a normal doctor , because I am frank.

Doctor, please don’t bring that normal curve stuff again. If you are called abnormal, then who is normal , doctor?

Sorry, I don’t have an answer .We shall meet on our next visit. Bye & thanks


Those who want to dwell deep please go through this 107 page document.

Trying to find out the word normal BP in the latest ESC 2024  Hypertension  guidelines .

What is the logic for removing the term Normal BP in the new ESC guidelines ?

BP is a continuous variable . People with any level of BP can develop cardiovascular events. So there can’t be strict normal.

Why such a classification could be dangerous ?

By avoiding the word normal, are we trying to suggest non-elevated BP is also a potential risk factor? These guidelines misleadingly and unintentionally took a cue from the LDL analogy: i.e., lower is better. They conveniently forgot the J-curves and U-curve of BP. This classification is meant to keep every adult human being as a potential candidate to get ready for elevated BP or HT. Can’t suspect the true intentions, though, as these guidelines stress the importance of good lifestyle choices to keep the BP in control without drugs.

The fact that the new guidelines is avoiding the word normal , implies it hesitates to reassure our public .This, by itself, will make our public anxious, push up the BP, and end up as drug-consuming hypertensives later. Principles of the practice of medicine hinge on trust and reassurance. In the name of scientific preventive medicine, we are unable to call a normal person normal. That is the wages for the sins we pay for the explosive growth of knowledge (Pseudo) and technology.


Post-amble

Who am I ? to question the credibility of a 107-page document prepared by the best of all experts in the field of cardiology? Just a reminder to mind , what happened to the term pre-hypertension and the fate of JNC across the Atlantic a decade ago.


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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.

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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.

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.


Post-amble

Are you a professional physician doctor ?

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


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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.

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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,

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