Archive for the ‘Uncategorized’ Category

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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Let us go back to the golden age of simple clinical trials & get rid of    big, motivated RCTs.

Posted in Uncategorized, tagged bmj, clinical trials, evoultion of clinical research, jam network, lancet, medical education, medical ethics, nejm, rct on April 19, 2026|

Very soon, blogs and independent writing will be the only source of unadulterated truths. One such article is shared here written by Adam Kroetsch , formerly in the FDA

A review and comments

The above article compellingly recounts how clinical trials evolved from ad-hoc, investigator-led efforts in the mid-20th century to the bureaucratic behemoths of today. It highlights the “golden age” of the 1980s-1990s, when academic “trialists” pioneered large simple trials like ISIS and GISSI. These mega-trials enrolled tens of thousands with minimal protocols ,one-page forms, no routine monitoring or source data verification (SDV), proper randomization, and focus on clinical hard endpoints and mortality delivering transformative, low-cost evidence on treatments like streptokinase and Aspirin.

The decline followed the rise of Contract Research Organizations (CROs) in the 1990s, global Good clinical practice -GCP guidelines (1996), and FDA missteps. Trials are now industrialized and bureaucratized: extensive on-site monitoring, exhaustive adverse event reporting, data audits, and risk-averse compliance layers inflated the costs (rising 10% annually). Academic and NIH-funded large trials plummeted .Pharma shifted to smaller, often useless biomarker-driven studies instead of clinical outcome. (Eg Drug X reduce NT-pro BNP by this,and it is crowned in glory ). The irony is ,the trialists are crying “foul” at GCP, and call it unscientific as they interupt the industry.

Who is responsible for this chaos?

Primarily commerce and greed in a profit-driven ecosystem .Alos pharma’s risk aversion and demand for speed and volume. Other factors were, heavily empowered CROs, Perverse incentives and Industry balance sheets, dictated the how science should behave. No surprise , true academics and genuine funders retreated amid prohibitive costs.

Final message

GCP  is not a taboo subject,  as some non- academic forces would like to envisage. Let us bring back the golden age of simple trials—even observational ones will bring the truth when done appropriately .Let us stop this big commercialised RCT nonsense  with ultier motives.

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How Important is LA pumping function in LV filling ?

Posted in Uncategorized, tagged la conduit, la function assessment, LA pressure volume lopp, la pressure volume lopp animation, la resorvoir strain, la strian on April 10, 2026|

LA has three important functions, namely reservoir, conduit, and pumping. Which among the three is the most and least important?

Find out the answer yourself. One clue: Atrial systole is very brief, hardly lasting for 120 ms (equal to P wave duration). The rest of the period, the atria are taking rest. You think so? No, It gets ready to receive and deliver the entire stroke volume meant for the next LV contraction. Note the green path; it is not only long, it has to be less steep. For this, we require an agile LA (technically good compliant LA). If the LA is stiff, the LA struggles to form a good V loop, and it depends more on its pumping function. That is, the A loop contribution is more than the physiological 25%. So, as of now, the most critical function of LA seems to be its reservoir function, which is often measured by LA strain; normal values are -18 (luckily the same value as LV strain, easy to remember).

By the way, coming to the least important functional component .Even a 65-year-old elderly person just walks to your office with AF and a rapid rate. He just complains of some palpitations. Nothing else. His BP is normal. What does this mean? It would mean, most healthy adults do not really depend on the atrial booster pump for hemodynamic stability .The early ssytolic suction force of LV effectively compensates for this lack of atrial pump assistance. This is a very provocative statement and needs clarification from experts. One more piece of evidence comes from the long standing debate over rate vs. rhythm control in AF. With almost equipoise between rate and rhythm control, I wonder when exactly this atrial booster pump matters? Understanding LA pressure volume loop may look complex. When we spend some time, it becomes less fritetning.Think about how, MS, acute and chronic MR or LV dysfucntion modify this loop.

Final message

William Harvey might have discovered the circulatory system, but it is Carl Wiggers, the father of cardiac physiology and hemodynamics, whose wisdom taught us that the heart plays a silent  hemodynamic orchestra called systole and diastole. We, the current generation of cardiologists, are happy to stop with that. Do we need to have a separate cardiac cycle dedicated to the atria? Which would mean we need to know the nuances of the isolated atrial cardiac cycle (atrial systole and diastole) in and out of sync with the LV. Maybe someone who carries the same passion as Wiggers will soon emerge and do it.

Postamble

One point, I am yet to understand fully is, why should the LA pressure goes up during the conduit function (See the the blue line going north) as the LV fills. Maybe LA is restricted and trying to get equilibrated with the rasing slope of LVEDP, as the LV is getting filled rapidly.

Reference

1.Thomas L, Marwick TH, Popescu BA, Donal E, Badano LP. Left Atrial Structure and Function, and Left Ventricular Diastolic Dysfunction: JACC State-of-the-Art Review. J Am Coll Cardiol. 2019 Apr 23;73(15):1961-1977. doi: 10.1016/j.jacc.2019.01.059. PMID: 31000000.

Link 2

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Forbidden quotes in medicine : Healing shall prevail over harming

Posted in Uncategorized, tagged bmj, british journal of medical ethics, dr s venkatesan, ethics in medicine, famous quotes on medical ethics, Hippocratic oath, indian journal of medical ethics, lancet, madras medical college, medical education, modern medicine, nejm, venkatesan sangareddi, world health organisation on April 9, 2026|

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Why different cut-offs for diagnosing STEMI in men and women ?

Posted in Uncategorized, tagged stemi gender difference in defintion on April 6, 2026|

In healthy people, some J-point/ST elevation in V2–V3 is normal. This physiologic elevation is greater in men than in women Using the same cutoff for everyone would cause many false-positive STEMI calls in men (over-diagnosis) while missing true ischemia in women (under-diagnosis).

Molecular and Ionic basis

The difference is not because gender based difference in ischemia response . It is because ventricular repolarization differs between men and women due to sex hormones acting on cardiac ion channels. These differences appear at puberty and are belived to be driven by androgenic hormones.

Mechanism

Transient outward potassium current (Ito, carried by K+channels) is higher in male ventricular epicardium than in females. Testosterone up-regulates Ito density and function. In the action potential (AP) of epicardial myocytes higher Ito produces a deeper phase-1 notch This creates a larger transmural voltage gradient (epicardium vs. endocardium during phases 1–2 of the AP. This transaltes in the surface ECG as J-point elevation reflecting early-repolarization voltage gradients. Greater gradient steepr the J-point and higher ST takeoff .This is called the the classic “male-pattern early reppolarization.”Women have a shallow j point.

Image source : Blinova, Ksenia (2020). Sex and Cardiac Electrophysiology Atrial and ventricular tissue electrophysiology.

Why this difference is not seen in limb leads ?

Note : This J point difference is more prounuced in chest leads only because they are unipolar , and very close to epicardium and picks up the difference

Final message

Whenever we have trouble identifying the true mechanism in any gender-related difference, it is easy to blame it on either testosterone or estrogen. As in the atheletic filed , men are naturally a little faster to fly off from the start-boots in the early phase of repolarization. This also has some connection with why women have longer basal QT intervals than men. The whole repolarization process is slow but steady. We can alos realise, in spite of longer QT, women have less incidence of primary ventricular arrhythmias even during ACS, implying better reslience and stress handling. (Ref 2)

Reference

1.Blinova, Ksenia (2020). Sex and Cardiac Electrophysiology || Atrial and ventricular tissue electrophysiology. , (), 39–48. doi:10.1016/B978-0-12-817728-0.00004

2.Weizman O, Marijon E, Narayanan K, et al. Incidence, Characteristics, and Outcomes of Ventricular Fibrillation Complicating Acute Myocardial Infarction in Women Admitted Alive in the Hospital. Journal of the American Heart Association. 2022;11(17):e025959. doi:10.1161/JAHA.122.025959.

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