Archive for the ‘Uncategorized’ Category

Aortic dissection : False lumen stenting is not forbidden

Posted in Uncategorized, tagged acc, aortic dissection, AORTIC DISSECTION GUIDELINES, esc guidlines, FALSE LUMEN STENTING, FALSE VS TRUE LUMEN on May 29, 2026|

Some truths about True & False lumen :

Aortic dissection splits the aorta into a true lumen (TL) and a false lumen (FL) at  different planes of aortic media. True lumen often retains* all the three wall layers (intima, media, adventitia), providing structural stability. Conversely, the FL outer wall consists only of outer media and adventitia. This thin wall can be fragile. Persistent, un-thrombosed FL flow may maintain organ perfusion but it carries a risk of aneurysm or late rupture. The false lumen has less elastin, in long term more likely to to replaced with fibrosis. In spite of this , there are occasions were false lumen can by exploited for a good circulation. (Click here for more eloborate True vs false lumen difference)

Image source : Anna M H Sailer Circulation Cardiovascular Imaging 10(4):e005709

*A significant portion of wall of true lumen faces the false lumen .So technically true lumen also lacks three layers in its entire 360 degrees. But the risk of rupture is internal not in the aortic wall.A comforting truth about false lumen.The fragility of false lumen is highly variable, depending on the thickness of media .However, adventitia , the toughest layer of of Aorta is always there to limit the risk of rupture in the outer curvature.

Situations where false lumen Stenting is only way out.

Image source : Zaidan L, . TEVAR Stent to the False Lumen of a Chronic Type B Aortic Dissection With Aneurysmal Dilatation, When no Other Options Are Left. Ann Vasc Surg. 2021 Jul;74:523.e19-523.e25.

While standard endovascular repair aims to stent the TL and obliterate the FL, stenting the FL itself is utilized in two distinct scenarios:

• Intentional Organ Salvage: In chronic or severe dissections, vital branch arteries may arise solely from a dominant FL. If the TL is too crushed or severely calcified (or porcelain like ), we need to intentionally stent the FL to preserve critical organ perfusion.
• The STABILISE Technique: This aggressive strategy uses a TL stent followed by heavy-duty balloon inflation. The balloon deliberately breaks the internal dissection flap, obliterating the FL space and fusing both channels into a single, stable lumen.(Ref 2)

Inadvertent false lumen stenting

This is more common than we realise.Some times it is not never recognised ,if the entry and exit paths are clean. But more often it creates immediate hemodynamic issues.A guidewire can accidentally enter the dynamic FL . Deploying a stent here can catastrophically crush the TL, requiring immediate rescue fenestration or secondary TL stenting to restore flow.

Conclusion

Identifying entire morphology of true and false lumen is critical. Restoring true lumen flow, and trying to obliterate false lumen is the default strategy in majority of aortic dissections. However, it is good to recognise , false lumen stenting is not forbidden, if situations demand. It can be life-saving in some complex anatomy or acute organ malperfusion.

Reference

1. Simring D, Raja J, Morgan-Rowe L, Hague J, Harris PL, Ivancev K. Placement of a branched stent graft into the false lumen of a chronic type B aortic dissection. J Vasc Surg. 2011 Dec;54(6):1784-7. doi: 10.1016/j.jvs.2011.05.053. Epub 2011 Jul 23. PMID: 21784607.
2. Hofferberth SC, Nixon IK, Boston RC, McLachlan CS, Mossop PJ. Stent-assisted balloon-induced intimal disruption and relamination in aortic dissection repair: the STABILISE concept. J Thorac Cardiovasc Surg. 2014;147(4):1240-1245. Available from: The Journal of Thoracic and Cardiovascular Surgery or via PubMed Central.
3. Resch TA, Kölbel T, Dias NV, Rohlffs F, Carpenter SW, Heidemann F, et al. Intentional false lumen stenting for complex chronic aortic dissection: te

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South Asian Lipid paradox : Chasing a wrong culprit in Atherosclerosis

Posted in Uncategorized, tagged acc esc lipid guidlines, bempidoic acid, cad with normal ldl, dyslipedimia guidlines, inclisiran, ldl, ldl targets in cad, lipid assocaition, pssk blockers, south asian metabolic syndrome, statins in cad, verve 120 on May 28, 2026|

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We know south Asians (who constitute about 2 billion people) consistently develop premature and severe atherosclerosis despite largely normal or only mildly elevated LDL-C levels. This “Lipid Paradox” is driven by small dense LDL particles, elevated ApoB, high triglycerides, low HDL, and insulin resistance not classical high LDL cholesterol.

This reveals a fundamental flaw in the current LDL-centric model of atherosclerosis genesis. When one-quarter of humanity develops CAD without high LDL, we must question whether LDL reduction is the primary target or merely a convenient proxy. A broader focus on ApoB, metabolic health, and visceral fat may be more scientifically honest and cost-effective.

Further, HDL molecule has its own problems in being a savior. At a level more than 60 mg/dl, it loses its protective value; rather, excess dysfunctional HDL is harmful as well. Since we have failed to increase HDL by pharmacological means, LDL reduction has gained more attention.(Franczyk B Et all , 2021)

Forget the patient .. target the LDL

Yet, aggressive marketing promotes expensive drugs like, PCSK antagonists, SiRNAs like Inclisiran and ATP citrate blocker Bempedoic acid to target ultra-low LDL levels (<55 or <50 mg/dL) in a population where LDL-C is often a weak tentative target. The latest to join the LDL rat race is the VERVE* 102 yearly Injection , a dramatic temporary RNA editing drug by the pharma giant Eli lilly.

*VERVE-102 consists of a messenger RNA encoding an adenine base-editor protein and a guide RNA targeting PCSK9, which are encapsulated in a lipid nanoparticle incorporating N-acetylgalactosamine (NEJM 2026)

Final message

LDL is definitely one of the culprit in human Atherosclerosis , but it is very difficult to prove , it is a major, universal, risk factor in isolation.This is not mocking the science. This is true at least in our part of the world. To treat a South Asian patient exclusively on standard LDL lowering protocols and projecting it as villain de chief, is not a scientically sound cardiology practice.

Reference

1. Volgman AS, Palaniappan LS, Aggarwal NT, et al. Atherosclerotic Cardiovascular Disease in South Asians in the United States: Epidemiology, Risk Factors, and Treatments: A Scientific Statement From the American Heart Association. Circulation. 2018;138(1):e1-e34.
2. Agarwala A, Satish P, Al Rifai M, et al. Identification and Management of Atherosclerotic Cardiovascular Disease Risk in South Asian Populations in the U.S. JACC Adv. 2023;2(2):100258.
3. Bilen O, Kamal A, Virani SS. Lipoprotein abnormalities in South Asians and its association with cardiovascular disease: Current and future perspectives. J Clin Lipidol. 2016;10(3):543-552.

Postamble

The word “wrong culprit” in the title is intentional. It actually means “not a primary culprit”

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Don’t fall for newer MCS devices in cardiogenic shock: A call for continued, “Guilt-free” usage of IABP

Posted in Uncategorized on May 19, 2026|

The rise of percutaneous mechanical circulatory support (MCS) in cardiogenic shock is phenomenal.  This has happened inspite  of the fact no RCTs proved, that they are superior to the humble IABP. For most patients, IABP remains a simpler, safer, and often sufficient.

How did we fell into the trap?

Cardiogenic shock is a setting where technology can appear decisive even when evidence is uncertain. Devices that generate more flow and better filling pressures naturally attract attention, but physiology is not the same as prognosis. The real question is whether a device improves survival, organ recovery, and quality of life. Newer MCS devices have not convincingly reached that end point over IABP.

What do the evidence for Impella and Tandem heart tell us ?

Though IABP-SHOCK 2, trial pulled the IABP down,  there were significant flaws in the design. In ISAR-SHOCK, Impella improved early hemodynamics, but 30-day mortality was unchanged. The Tandem Heart trial showed better hemodynamic support than IABP, but no survival benefit. Meta-analyses show the same pattern, better hemodynamics, no clear mortality gain. This the shocking truth from Shock trial, still not good enough to touch the conscience of most of us.

Where is the Disconnect ?

This disconnect comes from the fact that, cardiogenic shock is much more complex than simple interruption of blood flow from the heart. Timing of onset of shock , infarct size, right ventricular dysfunction, inflammation, renal failure, bleeding, and access complications all shape outcome. A device that improves pressure may still be too late or too harmful to change survival. Hemodynamic superiority alone is not enough.

Are the advantages of IAPB real ?

IABP retains practical advantages. It is easier to implant, widely available, less expensive, and less demanding in expertise and monitoring. It avoids large-bore access and the same intensity of anticoagulation and hemolysis surveillance. In many patients with moderate shock or early response to reperfusion, it provides adequate bridge support. The issue is not whether IABP is the most powerful device, but whether it is good enough for many patients. Often, it is.

Where should we use the newer MCS?

A more mindful approach is needed. Newer devices should not be dismissed, but routine escalation should not be the default strategy.. Device choice should be based on shock severity, vascular risk, anticipated support duration, right ventricular function, and the chance of meaningful benefit.

Why we have fallen for these newer MCSs?

The uncomfortable truth is we have fallen for technological seduction . Other factors are peer pressure, glamor and pride Randomized trials remain the best test of survival superiority, and so far they have not shown that newer MCS beats IABP in CS.

References

1. Thiele H, Zeymer U, Thelemann N, et al. Intraaortic balloon pump in cardiogenic shock complicating acute myocardial infarction: long-term 6-year outcome of the randomized IABP-SHOCK II trial. Circulation. 2019;139(3):395-403. PubMed
2. Seyfarth M, Sibbing D, Bauer I, et al. A randomized clinical trial to evaluate the safety and efficacy of a percutaneous left ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock caused by myocardial infarction. J Am Coll Cardiol. 2008;52(19):1584-1588. PubMed
3. Burkhoff D, Cohen H, Brunckhorst C, et al. A randomized multicenter clinical study to evaluate the safety and efficacy of the TandemHeart percutaneous ventricular assist device versus intra-aortic balloon pumping for treatment of cardiogenic shock. J Am Coll Cardiol. 2006;48(11):1925-1932. PubMed

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How good is Heart mate- 3. as destination therapy in end stage HF . Can it reach Heart transplantation survival rates ?

Posted in Uncategorized, tagged bridge to transplant, desitination therapy for heart failure, eva heart lvad, heart mate 2 vs 3, heart mate 3, heart transplantation vs lvad, heartware hvad, lv assist device, lvad, momentum 3 study, momentum study, unos registry lvad vs heart transplantation on May 19, 2026|

The primary treatment for end-stage heart failure is heart transplantation, but due to organ shortage and the poor progress in our pursuit for total artificial hearts, LV assist device (LVADs) have evolved from being a bridge to transplantation to destination therapy. Currently, the HeartMate 3 is the leading device in its third generation of LVAD. This fully magnetically levitated centrifugal LVAD reduces shear and thrombosis, outperforming HeartMate II with fewer pump thrombosis events, strokes, and improved 5-year outcomes. Landmark data from the MOMENTUM 3 trial shows that the median life expectancy has surpassed 7 years, with some patients living 9 years or more.

Can LV assist be destination therapy ?

The answer seems be definite yes

How does it compare with transplantation ?

Good , in fact very good for atleast for the first 2 years.See below

Data from : Uriel N, Sayer GT, Elad B, Fried JA,. Heart Replacement Therapy in Young Patients: A Comparative Analysis of HeartMate 3 LVAD and Heart Transplant Using MOMENTUM 3 and UNOS Registry. JACC Heart Fail. 2026

How many Heart mates device are implanted world wide every year?

About 40 to 50,000s HeartMate devices are implanted every year

Is Heartmate 3 availbe in India ? Whts is the csot ?

Yes , Heart mate 3 is available in India . The complete surgical procedure and device typically cost between ₹75 Lakhs and ₹ 100Lakhs ($75,000 to $100,000). While cost is one issue , patient’s involvement , commitment , family support is equally or if not more important to administer this therapy.

Is the expertise to mange LVAD avaiable in India ?

The device is available, but expertise in device management is still not optimal , even in large hospitals due to low case volumes.

Any alternative to Heart mate 3?

Medtronic HeartWare HVAD were recalled by FDA for major technical issues in 2021.Another device Eva heart from Japan with a pulsataile pumping technology shows some promise. .Ref Allen COMPETENCE Trial: The EVAHEART 2 continuous flow left ventricular assist device. J Heart Lung Transplant. 2023 .The superiority of pulsatile vs continuous pumps is a different debatable topic )

An illustration  about Heart mate .

A true story from a patient on Heart mate 3

Final message

Published studies show that modern LVADs (by default means Heart mate-3) trying to compete with heart transplants. Transplanted hearts has its own un-limited energy to pump ,LVADs are like maintaining a live automobile inside the chest , requiring constant monitoring and energy resource. Also, most importantly LVADs can’t look beyond LV ,and overlook RV function, while heart transplants replace all four chambers, unlike HeartMate, which assists only one chamber.( Of course, isolated LV failure is the culprit in 80% , that’s why LVADs , still could be a good option in many)

Reference

1.Legtenberg S, Ter Maaten JM, Erasmus ME,et al Long-term outcomes of patients implanted with a HeartMate 3 left ventricular assist device-a real-world, single-centre, observational study. ESC Heart Fail. 2026 Mar 3;13(2):xvag074. doi: 10.1093/eschf/xvag074. PMID: 41812231; PMCID: PMC13036835.

2.Mehra MR, Uriel N, Naka et al MOMENTUM 3 Investigators. A Fully Magnetically Levitated Left Ventricular Assist Device – Final Report. N Engl J Med. 2019 Apr 25;380(17):1618-1627. doi: 10.1056/NEJMoa1900486. Epub 2019 Mar 17. PMID: 30883052.

3.Boburg RS, Marinos SL, Baumgaertner M, Rustenbach et al Nine Years of Continuous Flow LVAD (HeartMate 3): Survival and LVAD-Related Complications before and after Hospital Discharge. J Cardiovasc Dev Dis. 2024 Sep 30;11(10):301. doi: 10.3390/jcdd11100301. PMID: 39452272; PMCID: PMC11508271.

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Why we mis-understood DIG-Trial for so long ? How can Digoxin reduce acute decompensation, but still doesn’t prevent death ?

Posted in Uncategorized, tagged DIG study, digit hf study, digoxin in heart failure, digoxin in rhd new study from aiims jama network, dr svenkatesan, undestanding dig trial on May 12, 2026|

Here is a brand new study on Digoxin from AIIMS-India , in 2026 that triggered this post. (Ref 2)

The DIG trial published more than 3 decades ago,(1997) was a landmark study, that applied a disruptive break on the widespread usage of digoxin in heart failure for all the wrong reasons. It is one of the good examples of , how badly the mainstream academia could interpret a study. Though the study showed a consistent reduction in worsening heart failure and hospitalization, yet no overall mortality benefit was accrued in the full trial population. This apparent paradox deserves a more careful interpretation. We need to ask one simple question.

Did the DIG trial reported how many acute deaths (In hospital) occurred among patients who were on digoxin and who weren’t ?

The answer is No. While the paper details how many patients were hospitalized and how many died of  heart failure, it does not specify which of those heart failure deaths happened specifically while the patient was admitted in- hospital. Then, DIG trial also played the same old game of all major RCTs. Death and worsening heart failure was clubbed as a combined end point, for  analysis. So, we don’t know the exact acute deaths, that were prevented by Digoxin. Why no one asked this question for so long ?

Did we mis-understand the DIG-Trial ?

Further, it is plausible Digoxin’s   life-saving role probably  lies in  preventing the decompensated episode itself.

Of course,  patients ( Who were non on digoxin)may still survive because modern therapy , with powerful diuretics, ventilation, inotropes, and intensive care .Still, we  know there is a specific (could be high ) mortality rate in all acute decompensated heart failure cases despite the best treatment. The statistics ignored those lives that were lost due to decompensation , because of non-administration of digoxin.

Modified version of for DIG-Trial conclusion

“Digoxin may save lives by reducing the frequency and severity of decompensated heart-failure episodes, thereby preventing some acute deaths and the need for ICU care. However, DIG trial failed to show an overall mortality benefit in the study population in long term. This is understandable, as heart failure is a progressive disease.”

Final message

It doesn’t make sense to make a blanket statement that Digoxin doesn’t prevent deaths in heart failure. However huge/ popular a study may be, it need to undergo scrutiny  beyond evidence and  statistics. How ? They should be subjected to the vigorous test of bedside trial on individual patient* , common sense and experience.(* Recall N-1 study Ref 4)

Reference

We are gathering more evidence in favor of Digoxin in recent times.

1.DIGIT-HF study

2.Karthikeyan G, Devasenapathy N, Ghosh A, et al. Digoxin in Patients With Symptomatic Rheumatic Heart Disease: A Randomized Clinical Trial. JAMA. Published online May 10, 2026. doi:10.1001/jama.2026.7335

3.Digitalis Investigation Group. The effect of digoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997 Feb 20;336(8):525-33. doi: 10.1056/NEJM199702203360801. PMID: 9036306.

4.Duan N, Kravitz RL, Schmid CH. Single-patient (n-of-1) trials: a pragmatic clinical decision methodology for patient-centered comparative effectiveness research. J Clin Epidemiol. 2013 Aug;66(8 Suppl):S21-8. doi: 10.1016/j.jclinepi.2013.04.006.

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DEB: Drug-Eluting Balloons are just glorified POBA in disguise.

Posted in Uncategorized, tagged acc aha guidelines ptca, andreas gruntzig, deb vs des, des, poba on May 2, 2026|

1977 : Andreas Grüntzig’s made history and stunned the world by opening up a coronary stenosis with a hand made balloon in his now iconic Zurich cath lab .No stent, no drugging. It was called POBA then. His famous patient had a patent coronary artery for the next 18 years. This is the beginning of the era of PTCA. By 1990s stents were made almost mandatory fearing reocclusion. They were bare metals then . By year 2002, stents were drugged to prevent restensois. That was the era of DES. The bare metal stents died a premature death. Curiously, by mid 2010, DES also became a suspect , Bio absorbable scaffold  came in (A short lived self demising stent) It got into serious  problem of patchy reabsorbtion and prohibitive events.Thus,again DES became the undisputed tool in PCI.

Fast-forward to 50 years:  Some good samaritans decided to take on the fight with stents , and are  trying to restore  the bygone, balloon era now.But, they didn’t have courage to use Gruntzig’s  POBA. They wanted something more. It came in the form of DEB. Now, it  has become omnipresent. Suddenly, even in complex  lesions  including left main, bifurcations, ACS, and distal lesions, DEBs are rendering stents as “enemy.”

The real question to the cardiology community should be this . Is DEB truly revolutionary, or is it just a DOBA (drug-on-balloon angioplasty) a plain old balloon angioplasty (POBA) with a false crown ?

Logically and realistically ,every DEB transforms into POBA within 24 hours as the anti-proliferative drug dusted over the coronary lesion get washed away. There may be a dozen studies , that vouch for the DEB’s ability to prevent restenosis. But , the true efficacy of the DEB-PCI is accrued from the “B not from the D”. What we require is , an astute , discrete balloon dilatation at the right place and time. Yet in India, we have fallen for the DEBs that cost ₹3,0000 more to shed its metal jacket.

Final message

DEB has some evidence for benefit only in  ISR. There is no single large one to one study that compared POBA vs DEB in denovo coronary lesions.So,the apparently provocative title of this post, is largely a fact.

False science coated with commerce can be as addictive as a narcotic. The cardiology community is experiencing this on a regular basis. At the least, one must realise this , forget about coming out of it.

Post-amble

Distal D-Wash after a POBA a perfect new PCI

A cheaper ,unconventional coronary intervention is proposed by the author, called Distal D wash. After performing a POBA over an intermediate lesion, push and inflate the same balloon distally to the maximum in the RCA/LAD, inject sirolimus locally with a dwell time of 1-2 minutes to allow a rinse*. This method could treat not only the lesion and protect entire vessel from future atherosclerosis , at a fraction of the cost of DEB.(A truly cranky Idea, but might be perfect for a new start up)

*Like surgeons wash the wounds while dressing with mixture of antibiotics etc.

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“Sodium mediated  Sodium” excretion in cardiac failure

Posted in Uncategorized, tagged DIURETICS VS SALT INTAKE IN CARDIAC FAILURE, ESC GUIDELINES SALT RESTRCTION IN HEART FAILURE, SALT RESTRICTION IN HEART FIALURE, SALT TRIAL on April 30, 2026|

Doctor, should I restrict sodium , if so how much ? one of my patient with  heart failure asked ?

*Cardiac failure is a condition where RASS is activated  , kidneys become salt &  water avid”

A recent Viewpoint in JAMA Cardiology titled “The Sodium Paradox in Decompensated Heart Failure” challenges the longstanding practice of strict sodium restriction in heart failure (Ref 1) While traditional management assumes that limiting sodium intake counters the sodium-avid state and promotes decongestion, emerging physiological and clinical data suggest that overly restrictive sodium diets may paradoxically impair effective diuresis in some patients. This may occur through activation of compensatory neurohormonal mechanisms or by blunting the natriuretic response to loop diuretics. The authors advocate for a more nuanced and individualized approach to sodium intake during acute decongestion, potentially including controlled sodium supplementation in selected cases.

This is consistent with the 2024 Heart Failure Association (HFA) of the ESC clinical consensus statement on dietary sodium and fluid intake in heart failure.(Ref 2) The statement highlights that recent randomized evidence has weakened support for routine strict sodium and fluid restriction. It recommends limiting salt intake to no more than 5 g/day (2 g sodium) in patients with heart failure to prevent excessive consumption, while endorsing a normal sodium intake (1.5–4 g sodium/day, equivalent to up to 5 g salt) for most patients with chronic HF. Extreme sodium restriction (<1–1.5 g sodium/day) is generally discouraged as it may be counterproductive. Please mind,fFluid restriction (1.5–2 L/day) is also reserved only for selected patients, such as those with severe hyponatremia or refractory congestion.

Other considerations

If a patient relies on a high dose of diuretics, limiting salt can be risky; they may actually need more supplements. Contrary to popular belief, more than loop diuretics, thiazides, especially metolazone, can lead to more sodium loss.We used worry more about hypokalemia with diuretics, now only we realised sodium loss is equally important. If the patient has salt-sensitive hypertension, the salt should be more carefully prescribed. Even mild impairment in kidney function can further complicate alter the sodium metabolism*. Ultimately, treatment must be tailored to the individual, and no AI can provide a definitive answer, as even medical professionals face. challenges in this area.

Final message

So, when the next time your patient asks you, “Doctor, should I take less salt?” please be truthful and tell them we don’t know the exact answer to this simple question yet, even after 50 years of cardiac research. However, we do know , need not be overly strict with salt control, be a little liberal until we find an answer.

References

1. Testani JM, Mullens W, et al. The Sodium Paradox in Decompensated Heart Failure. JAMA Cardiol. Published online April 29, 2026. doi:10.1001/jamacardio.2026.
2. Mullens W, Damman K, Dhont S, et al. Dietary sodium and fluid intake in heart failure. A clinical consensus statement of the Heart Failure Association of the ESC. Eur J Heart Fail. 2024;26(4):730-741. doi:10.1002/ejhf.3244

Postamble

*Can we get an answer from a Nephrologist ?

I asked my colleague, a Nephrologist, about salt restriction in heart failure. Our discussion revolved around pre-renal states, glomerular physiology, sodium natriuresis, free water excretion, etc. I asked him, is water or sodium real  enemy of kidney during circularory distress ? He wasn’t sure . I was not sure about the same in cardiac failure .In the end, it became too complex for both if us.

It  seemed obvious, how widely our two specialties have separated, even though they deal with the same human circulation. The irony is, these two organs (heart and kidneys) are just half a feet apart in our body.

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Atrial fibrillation bothers us more because of stroke risk or for hemodynamic stability ?

Posted in Uncategorized, tagged affirm study, atrial booster pumppulmonary vein ablation rf cryo pfa, Atrial fibrillation current perspective, race trial, rate vs rhythm control on April 29, 2026|

In a population‑based perspective, both paroxysmal and chronic atrial fibrillation bothers us more because of stroke risk than hemodynamic instability. AF confers a 3–5‑fold higher stroke risk and accounts for roughly 1 in 5 ischemic strokes overall.
Stroke‑related disability, recurrent events, and higher mortality make thromboembolic risk the dominant public‑health concern.

Hemodynamic instability does matter ,in ACS, pre‑existing systolic dysfunction or structural heart disease. At a community level, , stroke prevention (anticoagulation, risk stratification) outweighs rate‑rhythm control as the primary priority. This is exactly the reason, rate control was suffice to beat rhythm in major trials with a optimal anticoagulants.

*The pre-systolic 25% booster pump function acts more as a physiological reserve . We have infinite number of pateints with lone AF , effectively managing the lack of atrial contraction , by the newly recruited LV suction force ( intriguingly, it can function in pre-systole as well )

We must also realise, the much hyped rhythm control modalities actually plays a hide and seek game in many paroxysmal / persistent and most chronic AF . This applies to all sophisticated ablation stuff including the Cryo and PFA. Also, we need to understand stroke in elderly , is not fully prevented even if SR is restored in piecemeals (of time) because the source of embolus can be elsewhere from ventricle, Aorta, Arch, carotids etc.

Final message

Principles of AF management primarily revolves around stroke prevention , while hemodynamics goes to the background. OAC can perfectly take care of the former in most. DOACs are also playing useful alternate role. Contrary to the popular belief, many , LAA occlusion devices and ablation strategies do not necessarily negate the need for OAC in many elderly people.

Reference

1. Andrew Hill Atrial fibrillation and stroke: State-of-the-art and future directions Current Problems in Cardiology Volume 49, Issue 1, January 2024,

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Why IVC rim is most important in ASD device closure ?

Posted in Uncategorized, tagged adequate rims in asd for device closure, amplatzer asd device, ASD device closure, asd rims, ivc vs aortic rims in asd device closure, why ivc rim is most important in asd clsoure on April 25, 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 institutions have reported ASD device closure in deficnet IVC rims as well . This is not respecting the evidence (Ref 4,5) But, the fact seems to be different. The IVC’s perpendicular, high-momentum jet amplifies dislodgement. Even good  superior/anterior rims fail to counter this inferior “pull,” as the device tends to tilt  around the waist, under the  dyanmic atrial pressures and flow. Hence IVC deficiency  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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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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