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Cardiac failure Guidelines – ESC 2026 : Pharmacological foundation without “Digoxin & Diuertics ” will be shaky

Posted in Uncategorized on September 1, 2026|

It is fashionable to frequently change the terminology, definitions, and classification of cardiac disorders. Now, the ESC is renaming therapeutic strategies in heart failure. Terms like OMT (Optimal Medical Therapy) and GDMT (Guideline-Directed Medical Therapy) have been taken off the table. A new term called FMT, (Foundational) AMT (Additional) and GDIT (Guideline directed Interventional therapy)

It is Intriguing to see more green color in the device arena and add on therapy is still yellowish.Note :  The diuretics, despite bring  the only green in the add on category, still considered  unfit, to be part of the foundation.

What could be the reason for this?

“Optimal” is entirely subjective, and guidelines are always fluid ( Including the current one!) A few things are particularly glaring in this update. For instance, the term “interventional therapy ” has been introduced, as if laying a pharmacological foundation is not an intervention by itself.

Why Digoxin is not in the foundation ?

Digoxin the wonder drug used for centuries was previously looked down upon. It was kicked out in earlier guidelines, but has now been brought back and placed under the category of “additional drugs”. As a cardiologist who has continued using this drug and rejecting those old guidelines, I was called unprofessional and unscientific. Now, I realize: who was really being unscientific all this time?

*Ask a simple question, can any physician manage heart failure without diuretic ?  How many lives a loop diruerrics are saving every day  across the globe  &  how many lives ARNI’s are unbale to save  ? Do we have a one to one study ? We have a  serious problem in asking right research questions.

I am sure, the committee will  ultimately realize their  mistake and will be compelled to move  digoxin and diuretics  to the foundational therapy.Meanwhile , we should appreciate them  for including rehabilitation and exercise as a green intervention, even though it was pushed to the bottom of the list.

Final message
Frequent tinkering of nomenclature, classifications, and definitions in cardiology has become an academic time pass. It is not going to alter the actual clinical outcomes of heart failure. We need a lot more application of mind to remove the clutter from genuinely beneficial drugs and modalities.

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Localising the Infarct related artery In NSTEMI

Posted in Uncategorized, tagged , , , , , on August 27, 2026|

Localising the infarct-related artery (IRA) In NSTEMI , when there is multi-vessel coronary artery disease (CAD) is a classic clinical dilemma. Because NSTEMI lacks the clear, localising markers as in STEMI, identifying the “culprit” among multiple chronic blockages requires a more careful approach. It requires combined analysis of electrocardiographic clues , Echocardiographic WMA, angiographic analysis, and finally as a last resort intracoronary Imaging. Note : In UA,without NSTEMI it can be called as ARA-Angina related artery.

Image source : Baumann et al. Ther Adv Chronic Dis. 2020 Jul 1;11:2040622320938527

A meticulous review of the invasive coronary angiogram (ICA) will identify the culprit lesion in the majority of cases. Look for these specific features

  • Plaque Morphology: Eccentric , hazy lesions, irregular borders, or filling defects indicative of an intraluminal thrombus
  • Lesion Ulceration: Look for ulcerated edges, aneurysmal segments, or evidence of a dissection flap. Any vessel showing TIMI-1 or TIMI-2 flow, or prolonged contrast stasis during washout suggest microvascular plugging downstream from a fresh rupture.

ECG -ECHO correlation of WMA is the key

  • Wall motion defect correlation: Matching the distribution territory of the suspected culprit vessel LADcs LCX or RCA can be most useful . Still extensive collaterals can prevents us, to make a rule of thumb
  • Typical patterns like Wellens can help localise the IRA. Transient ST-depressions or deep T-wave inversions

The most important illustration in coronary artery disease

Note* WMA can be deceptive as well, due to old MI, remote ischemia , or either due to collateral support or lack of it

Intra coronary Imaging

When angiography shows multiple severe lesions with no obvious acute features, coronary imaging like OCT/IVUS can be helpful. It visualises plaque rupture, thin-capped fibroatheromas (TCFA), red/white thrombi, and superficial plaque erosions. IVUS can help identify ruptured fibrous caps, and intramural haematomas.However, the temptation to do imaging should be resisited as performing this in ACS adds its own risk.

Thromotic lesion in ACS revealed by OCT . Image source Francesco Prati et al European Heart Journal 31(4):401-415

What about FFR & iFR ?

Physiological tools like FFR / iFR / iFR are less useful to identify culprit lesion rather it tell us about the flow across the lesion.

Final messsage

Identifying IRA in NSTEMI/UA is more challenging than in STEMI, relying on basic ECG and ECHO tests. It is good to realise, this effort may be redundant if we are considering only medical management.(Which is often the case in many low risk patients)

Reference

1.Baumann AAW, Mishra A, Worthley MI, Nelson AJ, Psaltis PJ. Management of multivessel coronary artery disease in patients with non-ST-elevation myocardial infarction: a complex path to precision medicine. Ther Adv Chronic Dis. 2020 Jul 1;11:2040622320938527. doi: 10.1177/2040622320938527. PMID: 32655848; PMCID: PMC7331770.

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Ignoring distal LBB disease in conduction system pacing: Is it pure science?

Posted in Uncategorized, tagged , , , , , , , , , , , on August 24, 2026|

The huge popularity of conduction system pacing (CSP) , especially the Left bundle branch Area Pacing (LBBAP) has been hailed as a paradigm shift in cardiac pacing. By utilising the native His-Purkinje network, CSP promises a physiological alternative to the dys-synchronous RV pacing. However, beneath this procedural enthusiasm lies a critical, clinical assumption .It is the disregard of distal LBB integrity. In our haste to bypass proximal blocks, the electrophysiology community has mastered the art of ignoring distal conduction system disease a practice that relies more on hope than long-term, evidence-based science.

The physiological basis of LBBAP  is based on capturing the main left bundle branch trunk or its proximal fascicles to downstream  distal healthy  Purkinje network1. In patients presenting with complete heart block , this approach looks fine , if the underlying pathology is strictly nodal or intra-Hisian. However, in progressive, degenerative conduction system disorders such as Lev’s or Lenègre’s disease fibrosis is rarely localized. It is a multi-level, diffuse process that tracks distally into the fascicles and terminal Purkinje ramifications2.

How, can we casually overlook the small but surely dangerous risk of progressive distal LBB disease in complete heart block, which can lead to unpredictable catastrophic events ? This electrical oversight finds a striking, parallel in historical pacing concepts. In patients with sinus node dysfunction (SND), the electrophysiology community long ago established that a standalone atrial lead (AAI pacing) is a clinical hazard3. The minor yet real risk of AV nodal disease progression (approximating 0.6% to 4.5% per year) almost universally mandates the placement of a backup ventricular lead, safely transitioning the strategy to dual-chamber (DDD) pacing4.

The current electrophysiology consensus downplays this distal disease , by invoking the physics of the virtual electrode. The argument is even if the localized nerve fibers directly contacting the lead tip degenerate over the subsequent decade, the high-programmed voltage outputs will maintain permanent myocardial capture, ensuring patient safety from asystole5. While this assumption satisfies the basic requirements of bradycardia support, it ignores a core fact.

Aprar from thew physiological uncertainty , there is also a  significant risk of procedural failure. Real-world registries reveal that approximately 5% to 15% of patients undergo acute on-table crossovers due to  septal calcification, anatomical variations, or an immediate functional failure to engage a viable conduction pathway7.

Conduction system pacing is undoubtedly a great addition to our EP armamentarium, but it must be practiced with  humility in the face of unproven long-term  putcome and procedural complexities. A clinical pragmatism is warranted. Conventional dual chamber (DDD) is backed by more than four decades of  randomized clinical evidence.9. Until we clarify the natural history of the chronically paced, diseased left bundle,  DDD pacing should remain  the standard of care.

References

  1. Huang W, Su L, Wu S, et al. A novel pacing strategy with low and stable threshold-left bundle branch pacing. Europace. 2019;21(3):471-477.
  2. Lev M. Anatomic, pathologic, and electrocardiographic correlations in the atrioventricular and distal conduction system. Prog Cardiovasc Dis. 1964;7(4):317-340.
    Andersen HR, Nielsen JC, Thomsen PE, et al. Long-term follow-up of patients paced in atrioventricular synchronous vs. single-chamber atrial mode for sick sinus syndrome. Lancet. 1997;350(9086):1210-1216.
  3. Brandt J, Anderson H, Fåhraeus T, et al. Natural history of AV conduction in patients with sick sinus syndrome as related to bilateral bundle branch block. Pacing Clin Electrophysiol. 1992;15(11 Pt 2):1914-1918.
  4. Vijayaraman P, Sharma PS, Cano Ó, et al. Comparison of Left Bundle Branch Area Pacing and His Bundle Pacing in Bradycardia Indications. JACC Clin Electrophysiol. 2021;7(11):1433-1442.
  5. Jastrzębski M, Kiełbasa G, Cano Ó, et al. Left bundle branch area pacing outcomes: the MELOS registry. Eur Heart J. 2022;43(40):4161-4173.
  6. Heckman LI, Luermans JG, Vos LM, et al. Left Bundle Branch Area Pacing: A Comprehensive Review of Technical Aspects, Clinical Outcomes, and Future Directions. J Clin Med. 2023;12(11):3611.
  7. Wijesuriya N, Niederer S, de Verteuil R, et al. Extraction of conduction system pacing leads: a systematic review and international survey. Europace. 2024;26(2):euae032.
  8. Wilkoff BL, Cook JR, Epstein AE, et al. Dual-chamber pacing or ventricular pacing in patients with an implantable defibrillator: the DAVID trial. JAMA. 2002;288(24):3115-3123.
  9. Khurshid S, Epstein AE, Verdino RJ, et al. Incidence and predictors of pacing-induced cardiomyopathy. Heart Rhythm. 2014;11(9):1618-1625.

Postamble

This opinion letter is being sent to EURO PACE journal : Expecting a fast tracked rejection letter within a week or two .(Based on my past experience) They view these type of articles as destructive criticism I was told by one editor. Some one please clarify me, the difference between a constructive and a destructive critic, please)

.

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What happens to CAC score after statin therapy ?

Posted in Uncategorized, tagged , , , , , , on August 20, 2026|

Patient No 1 :

“Doctor, you had  put  me on high dose statins since my CAC score was high. Now, my CAC is increased further. What is this ? should I not get anxious ?”

“No.Not at all . It is a good sign and it indicates your plaques are getting stabilised”

How is that possible ?

It is a therapeutic paradox. We start statins based on a CAC score in a low-risk population only to find the CAC score increase further in many people. In multiple analyses, we have seen the CAC score even increase up to 30 % . Feel happy about it, as we presume it is a sign of plaque stabilization.

That’s interesting Doctor. Now,.. Doctor, my dad already has a good CAC score of 300 , without statins he should be lucky , is it not ?

No you are wrong. “Natural CAC score is a marker of plaque burden, and we can never consider it as an index of stability, while the statin-induced high CAC score is absolute bliss &  index of pure stability“

Patient no 2 : My CAC is not increasing with statins , what to do ? Is it sign of statin failure ?

May be yes. I am not sure . It may indicate a poor response to statin and  inability to convert the plaques to its logical destination ie hardening and micro calcification.

Final message

Most coronary calcification whether God or statin made , imply that plaques are stable biologically. (Except the nodular /eruptive ones or those in  the shoulder region of the plaque, which can make a plaque physically stressed . Cardiologists  hate calcium essentially because, it is a hinderance to deploy a stent)

We rarely realise , how often we formulate important concepts in cardiology based on very superficial or incomplete knowledge

Reference

1.Dykun I, Lehmann N, Kälsch H, Möhlenkamp S, Moebus S, Budde T, Seibel R, Grönemeyer D, Jöckel KH, Erbel R, Mahabadi AA. Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study. J Am Coll Cardiol. 2016 Nov 8;68(19):2123-2125. doi: 10.1016/j.jacc.2016.08.040. PMID: 27810054.

2.Henein M, Granåsen G, Wiklund U, Schmermund A, Guerci A, Erbel R, Raggi P. High dose and long-term statin therapy accelerate coronary artery calcification. Int J Cardiol. 2015 Apr 1;184:581-586. doi: 10.1016/j.ijcard.2015.02.072. Epub 2015 Feb 24. PMID: 25769003.

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2026 AHA /ACC dyslipidemia guidelines : What is new ?

Posted in Uncategorized, tagged , , , , , , , on August 19, 2026|

Eight point summary

1.PREVENT-ASCVD Equations: Replaces the older Pooled Cohort Equations with more accurate, contemporary equations for adults aged 30–79, establishing new risk thresholds to guide lipid-lowering therapy.


2.Reintroduction of Lipoprotein Goals: Returns to using absolute target goals for low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C) to effectively monitor and guide treatment intensity.


3.Preferred LDL-C Estimation: Mandates the use of either the Martin/Hopkins or Sampson/NIH equations over the traditional Friedewald calculation to ensure superior accuracy across varying triglyceride levels.


4.Universal Lipoprotein(a) Screening: Recommends measuring Lp(a) concentration at least once in all adults to refine cardiovascular risk assessment, recognizing levels ≥125 nmol/L as a key risk-enhancing factor.


5.Targeted ApoB Measurement: Recommends measuring Apolipoprotein B to guide further treatment intensification once standard lipid goals are met, particularly in patients with diabetes, CKM syndrome, or elevated triglycerides.


6.CAC Score : Upgrades Coronary Artery Calcium (CAC) scoring to a Class 1 recommendation to guide decisions to withhold, postpone, or initiate therapy when primary prevention decisions remain uncertain.


7.Severe dyslipidemia : Standardizes the addition of non-statin therapies like ezetimibe, PCSK9 monoclonal antibodies, or bempedoic acid to maximally tolerated statins to reach aggressive absolute lipid goals.


8.Dietary Supplements Discouraged: Recommends against using over-the-counter dietary supplements (such as fish oil, cinnamon, garlic, or turmeric) to lower lipids due to inconsistent data and lack of proven clinical benefit.

Three questions

1.What are key difference between PREVENT vs PCE equations?


2.Which can be ranked as the the most important change in the new guidelines ?

LDL reduction with statins as primary prevention in low risk individuals , is a major change

3.Which can be termed as the most questionable recommendation ?

CT calcium scoring for identifying candidates for primary prevention.A CAC score Zero only is safe . The new guidelines say even if it is 1 , a moderate-intensity statin is reasonable to achieve a ≥30% to 49% reduction in LDL-C

Reference

Blumenthal RS, Morris PB, Gaudino 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol. 2026 May 19;87(19):2624-2757. doi: 10.1016/j.jacc.2025.11.016. Epub 2026 Mar 13. PMID: 41824590.

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Timing of valve replacement in AR vs MR : Why are they different ?

Posted in Uncategorized, tagged , , , , , , , , , , , , , on August 11, 2026|

Timing of AVR and MVR in AR and MR has always elicited huge discussion in cardiology literature. Mind you, if the patient is symptomatic and there is LV dysfunction, it is absolutely easy to make a decision.Here, the question of timing doesn’t arise at all. (Of course, the symptoms and LV dysfunction should be confirmed to arise because of valve disease, not because of any other systemic disease, or LV dysfunction might be due to associated CAD. *I know a women who got her leakinging mitral valve replaced because she developed symptoms of dyspnea due to anemia .

Timing becomes a big issue only in patients with no symptoms at all. Some cardiologists put them on a treadmill. It is controversial, as anyone will develop symptoms. But , somehow, we should make it sure, patients are truly asymptomatic.

For long, we relying on some gospel echo parameters. I don’t how good they are. But , no one really knows,how and when the onset of LV dysfunction would be , and how it will progress. But, we are bound by the guidelines , as on today. There is some critical difference between the echo parameters , based on we intervene.

For mitral valve the threshold is lower. It needs early MVR for same degree of regurgitation as AR. It is proposed by the author for the benefit of fellows to easily remember the cut offs. It may be called as the 40:60 rule for MVR and 50:50 rule for AVR. The former denoting LVESD and later referring to LV EF %. The difference in echocardiographic thresholds arises because the two lesions cause fundamentally different hemodynamic loads on the left atrium and ventricle .(Read the legend in Image)

Final message

With mortality and morbidity for valve replacement steadily falling, it is likely more and more patients will be taken for surgery early. Of course, intervention guys are raring to go with percutaneous TAVR and TMVR, so the thresholds are expected to fall.

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LAA device closure for AF : “Useless” or Use, less ?

Posted in Uncategorized, tagged , , on August 9, 2026|

Journal Club Review : LACC for AF

What is the brief conclusion of this important study from EUROPACE ?

This meta-analysis aggregates data from 6 randomized controlled trials involving over 7000 patients to answer a burning question. Should we aggressively plug LAA in lieu of OAC or DOAC in AF ?

The short answer from this meta-analysis is a resounding “no” if our primary clinical goal is preventing ischemic stroke

Link to the article

Some observations and comments about this study

For all those cardiologists and physicians who have huge trust on LAA closure for AF , this study delivers a remarkable reality check:

  • The Stroke Incidence : The very purpose these devices are implanted is reduce it. But what happens ? Patients randomized to LAA closure suffered a 41% higher relative risk of ischemic stroke or systemic embolism compared to those on oral blood thinners.
  • The Harm : In a 3-4-year follow-up period, the Number Needed to Harm (NNH) may not look significant. For every 100 patients given a shiny new implant, one additional patient will experience a stroke that a simple daily pill could have prevented.
  • The Bleeding Trade-off: To its credit, LAAC successfully reduce the bleeding risk associated with OAC/DOAC

Will this study change the FDA approval and guidelines ? What will be the future of LAAC ?

No, Absolutely not. FDA is unlikely to react. It reviews devices based on their safety profiles for specific, indicated populations. Because these devices successfully reduce bleeding rates for patients with an absolute contraindication to blood thinners, their approval is legally and clinically sound.

The medical gadget eco-system works perfect. A device manufacturer proves that a LAA plug stops bleeding in a high-risk group. The device gets approved. Most of us fall for it and naturally shifts toward “liberal usage” as an easy, high cost alternative for patients who don’t want to take medication every day.

Final message 

It appears  LACC is  not a  useless device, but it need to  be used less .

With an estimated 400,000 implanted annually , it is too hard for us to say LAAC is useless. The future will inevitably bring next-generation devices with fancier anti-thrombotic coatings or redesigned plugs. Meanwhile, thousands of low-risk patients will continue to undergo unnecessary procedures , forcibly accepting the risk of increased stroke for the sake of convenience & glamor.

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Welcome to one more “Naming- ceremony” in CAD

Posted in Uncategorized, tagged , , , , , , , , , , on August 1, 2026|

CAD : It is been called IHD, CCD, CAHD, CCS, etc. Now there is a new proposal from European Heart journal (with an Impact factor of 48 ) to change the nomenclature of chronic coronary syndrome to NAMIS : Non acute myocardial Ischemic syndrome (Ref 1)

What is the purpose & need to change the current terminology ?

The proposed AMIS and NAMIS classification shifts the clinical paradigm from coronary anatomy to myocardial function. For decades, terms like “coronary artery disease” overemphasized epicardial stenosis, neglecting the reality that ischemia frequently occurs without structural blockages. Data shows that up to 40% of symptomatic patients lack macroscopic obstructions, suffering instead from microvascular dysfunction, vasospasms, or myocardial bridges. This new term NAMIS can bring in the phenotypes like INOCA and MINOCA into the CCS without any conflict. Further, replacing vague adjectives like “stable” or “chronic” with “non-acute” reflects the high long-term residual risk of cardiac events. I also think, this new framework is meant to unify the European and American guidelines, where they use differing terminologies.

Counter Point : Do we really need this ?

Purpose of any new classification is , it should have a clear impact on patient management. But, we often find, scientific committees periodically take pride in changing the nomenclature akin to make a academic fashion statement .Within a few short years, we migrated from stable CAD to SIHD, switched to CCS , CCD etc . The fact is , for the patients it is the same angina for which they seek relief. They simply don’t bother whether doctor label their condition a syndrome or disease .

Reference

1.Boden WE, De Caterina R, Kaski JC, Bairey Merz N, Berry C, Marzilli M, Pepine CJ, Barbato E, Stefanini G, Prescott E, Steg PG, Bhatt DL, Hill JA, Crea F. Myocardial ischaemic syndromes: a new nomenclature to harmonize evolving international clinical practice guidelines. Eur Heart J. 2024 Sep 29;45(36):3701-3706. doi: 10.1093/eurheartj/ehae278. PMID: 39211956.

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“Apo A vs Apo (a) vs Lip (a) ” : Getting out of the notorious nomenclature trap in lipidology

Posted in Uncategorized, tagged , , , on July 27, 2026|

It is an irony, we call the lipids as chief villains in the genesis of atherosclerosis and CAD. The fact of the matter is, it is the protein component that hides among the lipid jelly, with multiple folds and stinging tails, that ultimately help the LDL to penetrate the intact endothelium . These are called , apo-lipoprtiens. The fate of lipid molecules is determined by these apparently humble looking proteins .It must also be noted the even the goodness of HDL vanish if its apo-liprotein fails to co-operate . The Apo proteins are labeled differently in each sub fraction of lipids. Its Apo A 1 in HDL Apo B 100, in LDL and Apo C in VLDL.

Playing with English Alphabet A

Scientists can be casual , though not intentional when naming newly detected molecules. The major nomenclature issues are with Apo A , Apo a , Lip a These three entirely separate proteins with nearly identical names, should not be confused with. A subtle shift between a lowercase letter and a capital letter completely changes the meaning, taking us from a highly dangerous cardiovascular risk factor to a healthy, protective one.

Apolipoprotein A : This is a highly beneficial protein that defines the HDL function.(Ofcourse one must remember too much of HDL can be toxic as well .In fact when it exceeds 60 mg ,it will become dysfunctional, rather harmful.This is the U curve phenomenon of HDL)

Apolipoprotein(a) : This is the sticky, genetically fixed protein tail found only on Lipoprotein(a). It promotes blood clotting and triggers arterial inflammation.

Lp(a) : It is formed when a single Apo(a) protein tail binds to the Apolipoprotein B-100 (ApoB) wrapper of a standard LDL like particle. Because of this hybrid structure, Lp(a) possesses dual pathogenic properties. LDL core delivers cholesterol into the arterial wall, while the attached Apo(a) tail promotes localized inflammation and thrombosis . Lp(a) plasma levels are strictly determined by inheritance and remain highly stable throughout an individual’s life.

Lipoprotein(a) structure. Lp(a) is composed of two parts: one part is low-density lipoprotein (LDL)-like particles with apolipoprotein B100 (apo-B100), and the other part is the stinging tail apolipoprotein a [apo(a)]

Among the above three molecules, lipoprotein(a) is the celebrated one kept in the limelight. It is strongly determined by genetics and is a predictor; rather, we can call it a marker of LDL virility (like Apo B 100). It is entirely produced in the liver, its level is claimed to be static lifelong. Obviously, it cannot be true, as it would heavily dependent on liver function. Further, different vendors have come into the market with this, and they have different normal ranges.

Final message

When reading the lipid molecules, please focus on the English . A capital A vs. small a makes a huge difference between harming and healing the patient. Of course, we must be thankful, as of now, we have don’t have no small b or small c Apolipoproteins in lipidology.

Reference

Tsimikas S. A Test in Context: Lipoprotein(a): Diagnosis, Prognosis, Controversies, and Emerging Therapies. J Am Coll Cardiol. 2017 Feb 14;69(6):692-711. doi: 10.1016/j.jacc.2016.11.042. PMID: 28183512.

Patel AP, Wang (汪敏先) M, Pirruccello JP, Ellinor PT, Ng K, Kathiresan S, Khera AV. Lp(a) (Lipoprotein[a]) Concentrations and Incident Atherosclerotic Cardiovascular Disease: New Insights From a Large National Biobank. Arterioscler Thromb Vasc Biol. 2021 Jan;41(1):465-474. doi: 10.1161/ATVBAHA.120.315291. Epub 2020 Oct 29. PMID: 33115266; PMCID: PMC7769893.

Lipid particle science

https://www.jacc.org/doi/10.1016/j.jacc.2023.11.008

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The Invisible “solo fighter” for the NEET reforms in India !

Posted in Uncategorized on July 24, 2026|

India is sort of burning, with students on the streets for exam reforms.The problem started with the leakage of question paper for National Entrance and eligibility test for medical college( NEET) Government is on the back foot. The prime minster has come out, assured the students and their concern will be taken care of. Yes, it is true greedy cartels are exploiting the system. But, we are ignoring a big hidden moral failure in the whole issue.

However, It is very convenient to march through the streets pointing fingers at the state, but blaming the government alone is not enough to fix a rotting system. We love to demand absolute structural perfection from institutions while completely ignoring the mirror of reality. It is us, the public that fuel and maintain the corruption supply chain through a collective, desperate willingness to bypass merit at any cost.

Let’s be honest, even a un-breachable testing infrastructure cannot save an education system where parents and students are actively looking for illegal shortcuts. When families willingly treat leaked question papers as a premium commodity, they are not victims they are the core investors funding the black market. I wished, I could find at-least one banner conveying this fact too.Unfortunately, it can never happen.

True reform cannot happen through government orders alone. It requires a brutal confrontation with our own societal hypocrisy and a complete dismantling of the demand side of corruption.

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