Dr.S.Venkatesan MD

An “Intriguing concept” in  STEMI care: Pre-hospital thrombolysis is great, while In-hospital lysis is a suspect !

June 12, 2026 by dr s venkatesan

Human myocardium does not read hospital sign boards . It simply doesn’t bother whether thrombolysis is done in a moving van or a stationary room . When confronted with a life threatening emergency , all that it demands is quickness with which it is administered. Yet, in modern interventional cardiology, a same thrombolytic drug transforms from a life-saver into a forbidden clinical error, depending on whether it was injected in an moving ambulance or in the emergency Department.

This is the comical, yet tragic, irony of modern STEMI care.

Pre-hospital lysis is celebrated as a great strategy , while ultra fast in hospital lysis even within the “golden hour” is frowned upon as low-quality treatment.

At the heart of this paradox lies , the cult like status of primary PCI .It is true, pPCI has been etched as the gold standard of ACS care. However, most of the experienced cardiologist* know its perceived supremacy is not absolute ,largely attributed to the seductive power cath lab . (* Few have the courage to admit it )

Respect the myocardium not the cath lab

The efficacy thrombolysis is strictly a function of time, not geography. Landmark data from the CAPTIM trial explicitly demonstrated that when thrombolysis is administered within this early window, mortality rates are equivalent, and in some subsets superior, to immediate pPCI.

The current system of care willingly accepts this when a paramedic administers the drug but reprimands a physical if he does the same in his CCU .Why ? We seem to suffer from a misplaced academic arrogance that demands , fate of every coronary event must be decided only in cath lab. Any thing else is considered as deviation from the standard of care

Final message

It is time to change how we use the terms “pre-hospital” and “in-hospital” thrombolysis and replace them with a simple terminology . Symptom to Reperfusion Time. If a patient presents to a pPCI-capable center within the first hour standalone, ultra-fast ER lysis should be made an established, protocol equivalent to pre-hospital care, which is at equipoise with (un)disputed gold standard of pPCI as per the landmark study of CAPTIM.

Postamble

It is heartening to note In-hospital thrombolysis continues to be dominate mode of reperfusion at any point of time,  inspite of the negativity surrounding it. Can we take this as a proof of real  mettle of pPCI ?

References

1. Gersh BJ, Antman EM. Selection of the optimal reperfusion strategy for STEMI: does time matter? Eur Heart J. 2006;27(7):761-763.
2. Steg PG, Bonnefoy E, Chabaud S, Lapostolle F, Dubien PY, Cristofini P, et al. Impact of time to treatment on mortality after prehospital fibrinolysis or primary percutaneous coronary intervention: data from the CAPTIM randomized clinical trial. Circulation. 2003;108(23):2851-2856.
3. Terkelsen CJ, Lassen JF, Nørgaard BL, Gerdes JC, Jensen T, Giebels V, et al. System delay and mortality in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention. Circulation. 2010;121(11):1307-1315.
4. Armstrong PW, Sinnaeve P, Goldstein P, Lambert Y, Miroshinnychenko O, Danays T, et al. STREAM-2: Half-Dose Tenecteplase or Primary Percutaneous Coronary Intervention in Older Patients With ST-Segment-Elevation Myocardial Infarction: A Randomized, Open-Label Trial. Circulation. 2023;148(9):753-764.

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Posted in Uncategorized | Tagged acc, acs, dr s venkatesan, esc, guidelines, lancet, madras medical college, nejm, pre hospital thrombolysis, scai, stemi |

Embryology of ASD : A real cheat sheet

June 10, 2026 by dr s venkatesan

We are taught embryology of the heart, right from the first year , when we enter the medical school.We learnt about various holes of the heart in a  sincere way .After 15 years or so , it is fascinating for a fellow to become full-fledged structural interventional cardiologist , and close an ASD with an Amplatzer device with absolute ease.

Can’t ignore the basics

Meanwhile, how many of us are aware, there is a big disconnect between basic science and the cath lab cardiology. When I ask my fellows,  what is the origin  ostium secundum ASD ? majority come  with wrong answer. Very few of us have time and interest to go deep into the different layers  of IAS development. Now, let us be aware,  there is a host of errors in the way we have understood the embryological basis of ASD.

Image source : https://radiologykey.com/embryology-and-physiology-of-the-fetal-heart/

Misnomers galore

The first one  : The most common type of ASD, what we  call,  it as OS ASD , Is actually a defect in septum primum.

The second  is OP ASD is not due to defect in septum primum , but due to defect in AV cushion.

The third : The so called sinus venosus type of ASD is not an ASD at all, where IAS is totally intact.it is just an vascular Unroofing, between PV and SVC.

The fourth and an ultimate shocker  Embryologically, there may not be anything called true septum secundum, it is just interatrial fold, we named it as septum secundum and include it as apart of part of IAS .

The traditional Name	What it Sounds Like	What it Actually Means Anatomically
Ostium Secundum ASD	A defect in the septum secundum.	A hole or deficiency in the septum primum (the fossa ovalis floor).
Ostium Primum ASD	A defect in septum primum, that comes lower in IAS than OS ASD	It is an endocardial cushion defect at the AV junction , to precise they are defects of IAS rather Partial AVSD).
Sinus Venosus Defect	A true hole within the interatrial septal wall.	An unroofing/missing wall between the pulmonary vein and a vena cava (SVC or IVVC) outside the true septum.
Septum Secundum	An ingrowth of septal tissue left of septum primum , that forms the upper part of IAS	It is not true component of IAS. It is a thick in-folding of the outer roof wall (interatrial groove) pushed downwards and incompletely fuse with septum primum, forming the fossa ovalis in the process.

Final message

A hole is a hole is a hole.If you have a device close it, can’t waste time to bother about the origin of it . May be you are right as a restless Interventional cardiologist. 150 years of congenital heart disease , thousands of literature and advanced imaging ,interventions, can’t be Ignored. Let us  be aware of the reality of  embryology and how we are still following the old cheat sheets .Fellows please make a note of it.

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Posted in Uncategorized | Tagged embryological bassis of asd, ias septum development, ostium primum asd, ostium secundum asd, sinus venosus type of asd |

The epicenter of a crisis in modern medical care

June 7, 2026 by dr s venkatesan

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Posted in Uncategorized | Tagged bmj, british journal of medical ethics, dr venkatesan s, jam network, lancet, madras medical college, medcial ethics, nejm, quotes on medical ethics |

Re-learning cardiac anatomy : Aortic annulus is a zone, not a single anatomical plane

June 3, 2026 by dr s venkatesan

Learning anatomy is foundational first step in the pathway to become a great clinician. This post is written to address a potential nomenclature issue in cardiac anatomy .

What constitutes Aortic annulus.?

“Aortic annulus” by default conveys a discrete, planar, circular ring. However, from a macroscopic and histological perspective, a distinct, single-plane collagenous ring does not exist at the base of the aortic valve. Rather, aortic annulus is a complex, three-dimensional , Morpho-anatomical functional zone spanning the ventriculo-aortic junction. This brings the aortic leaflets to be arranged in a crown-like formation that crosses multiple spatial planes. The lowest points of these attachments (the nadirs) dip into the left ventricular outflow tract, while the highest points (the commissures) extend superiorly to anchor at the sinotubular junction.

 

Can anyone see a single plane of Aortic annulus in the above Image ? Note the leaflets , pan whole area from the virtual ring to the ST junction making the annulus a well secluded zone with from ST junction to the virtual lower ring. This aortic annular zone has clear cut boundaries, the inferior border is formed by lowermost insertion points of the aortic valve leaflets. (Which just above the virtual ring formed by sinus of valsalva)

Why the misconception ?

The misconception of a flat aortic annulus came from  extrapolation of AV valve anatomy to the semilunar valves. In the mitral and tricuspid positions, the leaflets anchor to a continuous,  planar fibrous skeleton. Consequently, their hinge lines and leaflet planes remain the same in a reatively single plane throughout the cardiac cycle.

Systolic and diastolic disconnect

This complex anatomy of aortic annulus also results in a clear disconnect between systole and diastole. During systole, the aortic leaflets open vertically like flushed doors, against the sinus walls , while  the basal plane vanish.Conversely, during diastole, the leaflets fall medially and down to meet at the center, creating a horizontal plane of coaptation.

Timing of measurement of aortic annlus

We are asked to measure the aortic annulus in peak systole. Ironically  at this point of time , every measurement becomes virtual in the aortic annular zone.  At least in diastole, the so called virtual lower end becomes real with leaflets hanging down forming a point of reference.

TAVI and Aortic annulus measuerment

The measurement of the aortic annulus has become essential due to the rise of TAVI, as CT scans accurately define the annulus compared to echocardiography, revealing the distinct height of the aortic annulus that was previously unrecognized. read below, for all the relevant measurements before doing a TAVI.

Image source : Jun-Hyok Oh IJC Heart & Vasculature Volume 37, December 2021, 100917

Newer TAVI engineering designers intentionally utilizes the entire vertical distance of the aortic root (from the leaflet nadirs to the ST junction) to anchor, seal, and position leaflets across different spatial planes to optimize physics and hemodynamics

Final message

The perception of aortic annulus as a single anatomical plane in our minds is very firm and it is due to the flaw in the way we learned cardiac anatomy. To make things right, we need to change aortic annulus as the “aortic annular zone” in anatomical literature. This change must be made at the earliest, right from the first clinical years of undergraduate education. Recognizing this is vital for understanding surgical or percutaneous repair or replacement of prosthetic valves.

Postamble (For the fellows)

When someone asks you what is aortic annular size, please ask them to confirm which dimension they are talking about. If they are surprised, teach them, there are  distinct multiple horizontal (Maximal, minimal) and vertical distance for every annulus.(Which can correlate to a certain extent to the coronary height, the TAVI guys talk about)

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References

1. Piazzese ED, de Jager SE, van Straten AH, Elenbaas TW, Soliman-Hamad MA. Surgical anatomy of the aortic valve and root—implications for valve repair. Ann Cardiothorac Surg. 2019;8(3):324-331. doi:10.21037/acs.2019.04.09
2. Loukas M, Bilinsky S, Bilinsky E, El-Sedfy A, Anderson RH. The anatomy of the aortic root. Clin Anat. 2014;27(5):748-756. doi:10.1002/ca.22295
3. de Kerchove L, El Khoury G. Anatomy and pathophysiology of the ventriculo-aortic junction. Ann Cardiothorac Surg. 2013;2(1):87-92. doi:10.3978/j.issn.2225-319X.2012.11.15

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Posted in Uncategorized | Tagged Aortic annulus, aortic root, cardaic aantomy, height of aortic annulus, Infra annlular tavi, sino tubular junction, supra annular avr or tavi, tavi, virtual aortic annlus |

Aortic dissection : False lumen stenting is not forbidden

May 29, 2026 by dr s venkatesan

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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Posted in Uncategorized | Tagged acc, aortic dissection, AORTIC DISSECTION GUIDELINES, esc guidlines, FALSE LUMEN STENTING, FALSE VS TRUE LUMEN |

South Asian Lipid paradox : Chasing a wrong culprit in Atherosclerosis

May 28, 2026 by dr s venkatesan

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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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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 |

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

May 19, 2026 by dr s venkatesan

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 ?

May 19, 2026 by dr s venkatesan

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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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 |

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

May 12, 2026 by dr s venkatesan

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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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 |

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

May 2, 2026 by dr s venkatesan

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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Posted in Uncategorized | Tagged acc aha guidelines ptca, andreas gruntzig, deb vs des, des, poba |

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