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Harsh lessons in cardiogenic shock: Let us move out of “myocardial mindset” to tissue reperfusion

Posted in Uncategorized, tagged on September 15, 2026|

Cardiogenic shock occurs in 5% to 10% of all STEMI cases. The prefix “cardio” bothers us for all the wrong reasons. Though the shock component is initially triggered by primary cardiac pump failure, it soon spirals downward into a tissue level shock threatening the body’s 30 trillion cells. As cardiologists, we repeatedly fail to comprehend this. Instead, we aggressively attempt to revascularise the myocardium using multi-vessel PCI, IABP, ECMO, and LVADs. Yet, nothing seems to work.  When tissues are irreversibly damaged  a non-stop  lactate ooze  begins to ring a final pre death biochemical SOS call.

What is the Time Window for Tissue Perfusion?

For myocardial cell death, we have a defined therapeutic window of 12 hours, with under 6 hours being ideal. In cardiogenic shock, however, we face an unknown time window. During this uncertain period, cells within vital organs like the kidneys, liver, and lungs lose their structural integrity and face irreversible injury.

As far as I know, there is no defined timeline for intervention in cardiogenic shock. The inflection point between reversible and irreversible shock varies individually because it is a complex, systemic spiral. But, one thing we must be clear. The clock does not start at the moment of infarct-related artery (IRA) occlusion. Rather, it starts when cardiac index drops below critical threshold required to sustain cellular respiration. Note the emphasis on flow. Beyond a certain point, blood pressures have nothing to do with actual flow. This explains why systolic and mean arterial pressures do not correlate well with the severity of shock. We must never forget the concept of nomotensive shock .

Current Criteria to Diagnose Cardiogenic Shock

We have known this for a long time. To establish a diagnosis of cardiogenic shock, a patient must meet a triad of criteria:

Note the dramatic (& ironic)changes in the current guidelines : Neither the blood presure not the filling pressure matters in the diagnosis of cardiogenic shock

Myocardial No-Reflow vs. Tissue level No-Reflow

This concept has some evidence back up. Even if you somehow manage to revive the heart In CS,  it does not guarantee full systemic tissue recovery. This failure of organ perfusion at the  systemic level behaves exactly like the no-reflow phenomenon we witness at the myocardial microvascular bed.

So, what shall we do to tame this dreaded condition ?

We really don’t know. Preventing the onset seems to be the most effective Intervention.

How to prevent?

Have a close look at the table to gain some insights. Focus the third and last column. Ask this question. Why the incidence remains high even in the modern Interventional era,of course with slight improvements in outcomes ? .It is prudent, we make every attempt to revive the heart, paradoxically, we must realise healing can still take place without myocardial excesses*

Final Message

The cardiac component in cardiogenic shock becomes less relevant when vascular and tissue-level shock sets in, making PCIs or MCS devices almost redundant. I think , in the overall interest of the patients , It is advisable for cardiologists to transfer them early to an intensivist or anesthetist, as they are better equipped to manage shock syndromes including the cardiogenic ones.

*Postamble: The missing link in the SHOCK trial

When we look back at the landmark 1999 SHOCK Trial, we find an quixotic truth to ponder over.Nearly 34% of the patients randomized to the medical arm survived to one year without any emergency revascularisation.If cardiogenic shock were purely a mechanical problem that survival rate should have been zero. This study throws two facts, many of us  will be reluctant to accept.

  1. Cellular Resilience: The human cells do possess ancient survival mechanisms. When the coronary  flow crtically drops, some individuals have the microvascular mechanism to tolerate severe ischemia and “hibernate” until the native heart recovers.
  2. The harm of hyper-Intervention could  be real . Every extra wire, balloon, and large bore mechanical device we insert brings its own dose of  strqin, vascular trauma, and reperfusion injury. The reason for the  lucky  30% who survived in SHOCK trial, may simply because they were spared from the toxicity of excess Intervention.

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Metabolic cost of ventricular ectopic beats : Does VPDs consume extra energy ? If so how ?

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

Nothing happens without energy cost both in physics and biology. How much is the metabolic cost of an extra systole ? While an occasional VPD is benign and has a negligible effect, a high burden of VPDs can consume extra energy and drain myocardial metabolic reserves.

Three ways it can happen

  • Inefficiency: VPDs cause premature contractions before AV valves fill and hence there is a mechanically wasted work However the electrical cost is small.
  • Dyssynchrony: dys or desynchrony due to the VPDs also hikes myocardial oxygen consumption (MVO₂) for identical workloads.
  • Post-Extrasystolic Potentiation: We know, the beat following a VPD shows increased force due to calcium accumulation. This can elevates contractility and wall tension, increasing energy demands.

Molecular basis of energy depletion

At the cellular level, the variable timing of VPDs disrupts calcium homeostasis in phase 2 of action potential within the myocytes. The sarcoplasmic reticulum must continuously pump calcium ions against concentration gradients via SERCA2 channels, a process requiring ATP hydrolysis. Additionally, the chronic workload mismatch induces mitochondrial oxidative stress, which damages the electron transport chain, impairs ATP synthesis resulting in energy consumption mis mamtch.

What is the cut off number ?

A high VPD burden* (10% to 20% all heart beats in day ) is considered a chronic strain, leading to cardiomyopathy and heart failure.First step is a Holter monitor assessment. Yet, we are not clear about the exact number For example : Does bigeminy counted then 50 % of all beats )

*VPDS and elEctrical SCD is different topic , and is not discussed here.

Does suppression help ?

We think so. If and only if we can document porgressive LV dysfunction.

Final message

VPDs are usually benign unless linked to LV dysfunction, which complicates prognosis. The electrical energy cost of VPDs is negligible . But its impact on the mechanical behaviour on myocardial contractility is the issue. It’s crucial to determine if they are primarily electrical or secondary to associated LV dysfunction. Treatment is based on individual assessment.

Reference

Link to the article

Postamble

Difference between APD and VPDs in terms of energy consumption ?

Need to be discussed further.(We know frequent focal APDs or ATs, MAT can result in AF or atrial cardiomyopathy)

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Why capillary pulmonary hypertension is missing in the current classification of PH ?

Posted in Uncategorized, tagged , , , on September 8, 2026|

Final message

While the term “pre & post capillary pulmonary hypertension” is useful for hemodynamic understanding , it creates a false impression biologically. Pre-capillary PH is a pan-vasculopathy where the capillary bed is routinely remodeled, congested, or even entirely destroyed. Please mind, this happens in almost in all the 4 groups of PH , at least in the advanced stages.

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Pregnancy & high risk heart disease : Time-line of mortality

Posted in Uncategorized, tagged , , , , , on September 3, 2026|

Heart disease in pregnancy is the third important cause for maternal mortality in most part of the world. (Apart from Bleeding, Infection and obstetrical complications) We know pregnancy is hemodynamic stress test for any mother and obviously it is a challenge in a compromised heart. Most heart disease encountered are mild and the mother has natural capability to walk through the pregnancy. It is the high risk subset that pose a real challenge. It is surprising ,even in the high risk, most women touch the finish line. The MMR review committee from USA has come out with clear data about the time line of mortality in various heart disease*.In this comprehensive analysis , the fact that 88% of mortality occur after delivery is too striking and is to be considered a core concept around which cardiac care of pregnant women should be addressed.

The figure shows the percentage of pregnancy-related deaths with an MMRC-identified underlying cause of death of cardiovascular conditions at 5 time periods from pregnancy to 1-year postpartum.(Ref 1) Note : The percentages are displayed for total cardiovascular conditions, and then for cardiomyopathy and other cardiovascular conditions individually. Percentages might not sum to 100 because of rounding. 

Why this data is important ?

Though the peak hemodynamic stress happens around 24-28 weeks, it is the post partum period after the baby is out is very critical. In fact, nearly 40 to 50 % event happen up to one year. Some of them doesn’t even come under the definition of maternal mortality.

Is there any thing we can do during pregnancy , that can mitigate the post partum events?

Also, this delayed events give us a window of opportunity to act on these adversity.Postpartum care for patients with heart disease, including PIH, should be provided in a specialized unit at major hospitals that manage a high volume of pregnancies.

Reference

1.Briller J, Trost SL, Busacker A, Joseph NT, Davis NL, Petersen EE, Goodman DA, Hollier LM. Pregnancy-Related Mortality Due to Cardiovascular Conditions: Maternal Mortality Review Committees in 32 U.S. States, 2017 to 2019. JACC Adv. 2024 Nov 8;3(12):101382. doi: 10.1016/j.jacadv.2024.101382. PMID: 39583867; PMCID: PMC11585746.

Postamble

*We are not yet clear , whether PIH(Gestational HT) related cardio- vascular complications to include in the heart disease basket. Logically and scientifically it should.

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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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