The relationship between Aorta & PA is the key to diagnose many complex congenital heart diseases. Here is a simplified illustration for gross understanding. Please refer to other sources for complete review.


Further reading

CONGENITAL HEART DISEASE| VOLUME 118, ISSUE 9P1390-1398, What Determines Whether the Great Arteries Are Normally or Abnormally Related?   https://doi.org/10.1016/j.amjcard.2016.07.050


Caution: Some language 


It is heartening to note the apex body that is leading the fight against Covid in India, has responded well. It has either recalled or censured many of the Investigations & drugs, procedures that were used in this pandemic. (Not because they are futile, but they also resulted in a meaningless escalation of cost and possibly worsened the outcome)

So, what?

Beware, “non-scientific mutations” are common in medical research even in ordinary times. It is omnipresent now, and no surprise they end up as a premature evidence base. The consequences of this can be as adverse as the viral variants we fear. The global economic drain of this pandemic is definitely more than what it really deserves. The bulk of resources consumed by Remdesviers, Tociluzumabs, Ivermectins, etc. will easily cross few billions. Further, it is estimated 100s of millions were spent on Indiscriminate diagnostics like CT scans and, Interleukins, D dimers, and even RTPCRs that made a mountain out of a mole. Infinite doses of antibiotics are diligently prescribed for a viral disease knowing fully well it won’t work. One estimate In India says 800 crores worth of Zinc and vitamins were sold over the counter. (The same budget for 1000 bedded state of art hospital!) Heartless marketing. It was painful to watch hard-earned savings was siphoned from not so wealthy & poor for a simple hospital stay.

 It must be acknowledged the Government (both state and central) is doing an exemplary job taking care of both private and public health against all odds. However, on a global scale, It is unfortunate many Governments of low GDP countries were politically compelled to spend on flimsy interventions for a self-expiring pandemic. If only these funds are diverted properly, that would help us build permanent health Infrastructure in each of the underdeveloped districts. The only thing, that’s worthy to spend now, is towards the largescale manufacturing of a quality vaccine. Health economists from WHO shall genuinely audit the global expenditure of this pandemic that will help tackle future pandemics better.


The virus has decided to play its own game with humanity for whatever reason. The great news is that the vaccine is working. We hope the virus will show enough mercy and leave us shortly. Please follow the required covid hygiene and learn to live in a  personal lockdown mode so that countries need not shut down. Meanwhile, a strict embargo on excessive covid related information in the public domain seems as critical as the vaccine. (the demarcation between true knowledge and misinformation is as blurred as one could Imagine)


Wishing for a  smooth landing with abundant common sense (Image courtesy TIME magazine )

Happy days will be here again soon. But, never forget the harsh lessons taught by this tiny virus .“We must learn to cohabitate on this planet along with other lives peacefully. If we are adamant, God is likely to lose his patience and may not hesitate to discard us permanently “



3D printing technology is growing at a rapid pace. Both cardiologists and cardiac surgeons are expected to benefit a lot.It helps us in understanding deformed anatomy in complex congenital heart disease as well as planning for synthetic cardiac implants. 

Currently, the technology is limited only by the chemical material used to print the heart and its components. The American chemical society is working at it to create more realistic heart models. Once we master this,  biological printing with synthetic tissue equivalents is the ultimate aim. 

Major Indications

  • Planning cardiac reconstructive surgeries in congenital heart disease. 
  • Aortic grafts in Marfan syndrome and other endovascular grafts.
  • Valve prototyping

What could be possible in the future?

A dream possibility is that, 3D printing of a patient’s own coronary artery that is diseased with an exact replica that may either act as a surgical graft or deliverable percutaneously.

It is 3D cloning of a coronary artery with a live blood flow experimental setting.(Image clipped from above video)

Final message

It is a merger of biology, chemistry, tissue engineering, and computing. Already it is used in specific conditions.(How about ordering a designer RVOT in severe TOF ?) We are approaching fascinating times in cardiology. Of course, everything would come at a price. We can reap the benefits of this path-breaking progress in science, if and only if, technology is regulated well, Indications are liberally coated with common sense.


A review article on 3D printing in cardiology Nature review 

Giannopoulos 2016


This 90-second video clip is a “perfect provocation”

Allan Savory  is a renowned ecologist from Africa. He is a global leader in environment and eco protection. He is making this famous comment, during one of his interviews from the deep forests of Zimbabwe, after years of ground-level work in the field of desertification and climate change. I can understand his feelings, as we also encounter similar situations at ground zero of the health care delivery system. (I wonder if there is anything called peer-reviewed bedside caring)

We realize wide gaps between academia, patient care, and research are the norm, not an exception. One reason for this is, even well-learned medical professionals find it difficult to comprehend, that the practice of medicine is essentially an art, administered with love, care, service-mindedness. A cost-effective infrastructure with an immense amount of teamwork is critical ( Of course, guided by a fair amount of knowledge, expertise based on good scientific principles)  

Final message 

As Savory says, let us hope, the future looks bright, that welcomes young researchers from the fringes of the scientific community. Let them be conferred with all courage and resources to course-correct medical science from its frequent aberrant and awkward turns.


The concept of Fractional flow reserve ( FFR) has dominated the coronary interventional field for over a decade. It gave us a (false) sense of security and pride that we have been advocating physiology-based appropriate stenting.

The much-expected FlOWER-MI trial was presented in ACC & NEJM a week ago. (May 16th  Issue 2021)

FFR, though physiologically an attractive concept, has many well-known confounders right from the technical factors, lesion-related errors in physics, mirage of true hyperemia induction with Adenosine, finally & most importantly microvascular dynamism. The value of FFR in the ACS setting was always a suspect. So, no surprises with the FLOWER trial conclusion. It has concluded FFR guided interventions in the non-IRA vessels following STEMI had no use in terms of the hard endpoint. Lesson: We can’t really expect true coronary physiology rules to be alive when severe pathology has set in)

Wait, there can be quixotic ways to Interpret this study be as well.

FLOWER trial reveals the number of stents used with FFR guidance was 50% less (mean 1.01 vs 1.5 stents). Though there was no difference in deaths, the incidence of nonfatal myocardial infarction was more in FFR group 18 (3.1%)  than the non-FFR group (1.7% ). Similarly, unplanned hospitalization leading to urgent revascularization was more in FFR  (2.6%)  than non-FFR (1.9%). Though all were not stat significant, FFR has helped reduce the number of stents in non-culprit lesions. Still,  recurrent non-fatal MI and urgent revascularisation were high in the FFR group. So, is it possible FFR related procedural hazards are real? Who can (& how) quantify that? or Is it Inappropriate non-stenting due to FFR misguidance responsible for this trend?

There is one more risk with the potential demise of FFR as a concept. Extreme scientists, might ditch physiology to the backyard and go for free for all stenting again. (Back to shadow physiology & oculocardiac reflex) 

Final message

There is an extrapolated lesson to be learned from DEFER*/ FLOWER trial combo. FFR or no FFR, never touch the non-IRA lesions in stable STEMI* however tempting it may be. (*This rule applies even in some unstable STEMIs (Please recall Culprit shock trial ) 

*DEFER 15 year follow up EHJ 2015 ( Note : DEFER contain significant non ACS population)

Next to the atmospheric pressure, the most curious pressure to understand is stored within the human circulatory system. Yes, it is the “blood pressure” fondly referred to as BP by both physicians and patients. (When worried men & women visit us and say, that they are suffering from BP, please make it a point to clarify, BP is a sign of existence of life, rather than a dreaded pathology ) 

Why should blood have pressure?

BP is lateral pressure exerted by flowing blood on the vessel wall (or is it the propelling pressure head ? It is to be noted, cuff pressure doesn’t measure this !) BP is generated by the heart in systole and sustained by the vascular system in both systole and diastole. BP is measured as mmHg. It can also be expressed as PSI(Pounds /sq Inch)  or Pascals or ATMs. If you allow me to spoil with some physics. Pressure is force per unit area ie Newton/m². So, pressure is essentially a force. Force is mass times the acceleration. Mass is weight independent of gravity, while the acceleration of blood is essentially the force of gravity added to the velocity of blood flow. If you think gravitational waves and planetary positions might influence the mass of blood (and hence the BP)  you may not be insane. (Environmental & astrological influence of BP and cardiovascular events need not a be mythology) (Oomman A,  J Indian Med Assoc. 2003 )     (Robert D Brook Cardiac clinic 2017)

How is it regulated?

Physics uttered at the bedside is sure to appear as nonsense for practicing physicians. Forget It. BP is not only a continuous variable, the neural, hormonal, cardiac control mechanisms are also in a dynamic flux. What we need to bother is, how to sustain a mean BP of around 90 mmHg within the human circulation, with robust autoregulation. (For the fellows in cardiology, it is a dangerously simplified teaching & belief  that cardiac stroke volume determines systolic BP and PVR determines diastolic BP) In fact, It is the systolic pressure that confers the energy required for diastolic BP. Regulation of BP is all about large vessel stiffness,  neuro-humoral tone of small vessels, water and sodium metabolism. This makes the kidney a central organ for long-term control of BP. It must also be emphasized BP is regulated in a regional and organ-specific manner. (Ex -The cuff brachial artery pressure may tell little about what is happening at the glomerular perfusion pressure )

Who are the guardians of BP?

Though general Physicians , Neurologists, Nephrologists even Endocrinologsts  have more geograhcial rights  cardiologists have largely taken siege over the entity of SHT because the heart happens to be a glamorous victim organ. We are witnessing an almost intoxicating number of cardiovascular trials on hypertension, right from Framingham’s days of 1970s to just released BP LLTC in 2021, trying to bring down cardiovascular risk. Based on the accrued evidence, the guardians of human  BP in various global institutions bring out strategies to reduce the risk of vascular injury. Have we succeeded in this  Intravascular number game.? I think we are. At what cost?

Two repeatedly asked two trivial questions 

  1. What is normal BP  &  When to start treatment?
  2. How much lower is best for our body?

Probably, we have got an answer for the first question from this Impactful publication. 


I think this study is trying to tell us, there is no normality for blood pressure in terms of risk reduction in cardiovascular disease. (Please recall, one JNC -Joint national committee  was dissolved after  including a controversial term pre-hypertension in healthy public  few years back) What will be the implication for this study? Its core conclusion is about 5 mmHg BP reduction across any subset of adult population will reduce CVD risk considerably. I am sure this study is so intense and powerful it will take at least a decade for its conclusion to fade away. So, can we make these funny conclusions? Hereafter we need not measure BP before starting treatment. Just administer drugs to any live adult who has blood & pressure. (J or U curve need a big debate later)

Mind you, sustained  5mmhg reduction* can be brought by any of the following habits. A salt moderated fruit-rich diet, reasonable physical activity, good sleep, a stroll in the park, yoga, a deep breath, having a pet, watching a movie in a quiet evening, having a loving  family, and so on so forth (Of course, 5mg Amlodipine, 40 mg of Telmisartan, or a  paradise device can do the same, with an add on pride)

*There is a big catch in this landmark paper. Read the title again. The important take-home point is that this 5mmhg lowering should strictly come by pharmacological means, not by any other means. (Correct me if I am not correct)

Final message 

We got the final answer from this marvelously done meta-analysis for the toughest question in cardiology. Hereafter  It’s going to be a celebration time for mankind, who struggle in a hypertensive world.


True, sustained high BP is a major risk factor for stroke, heart failure, and CVD. However, it is also true BP can’t* do much damage to the coronary artery without the help from its naughty cousins DM & dyslipidemia. All three parameters must be optimized in unison. May I propose a rough rule? It may be called DFL index for the collective CVD target.  Diastolic BP, fasting blood sugar and LDL all should converge around a unitless number of 70 to 80. 

*HT is a powerful risk factor for stroke and HFpEF. 



No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  



1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 



Here is an uncommon story of a patient with palpitation,SVT , Troponin +ve, and suspected ACS.

Palpitation in ER ⇒ {Tachycardia +Troponin positive ≠ ACS}

Mechanism of troponin elevation following any SVT

  • At high heart rates (>200) myocardium is subjected to non-Ischemic mechanical strain & squeeze. Minute amounts of Troponin is let out like a myocardial juice into the circulation (Like atrial natriuretic peptide release which causes polyuria during AVNRT)
  • Tropinin releases have been shown to correlate with both heart rate and duration of ST depression (Subendocardial strain /AVRT left lateral pathways)
  • Short diastole induced low coronary perfusion pressure and a true transient (but insignificant) Ischemia
  • Finally, SVT (especially in the elderly) is a natural “exercise stress test” equivalent, ST depression with Troponin positivity is a true marker of significant epicardial CAD


False alarm of ACS is the most important issue. (Except one study which showed a different conclusion Chow GV, Prognostic significance of cardiac troponin I level in hospitalized patients presenting with supraventricular tachycardia. Medicine (Baltimore) 2010;89:141–148. doi: 10.1097/MD.0b013e3181dddb3b. [PubMed]

Note: If AVNRT occurs with aberrancy, or AVRT presents as antidromic tachycardia with a wide qrs tachycardia the confounding effect is perfect as it can no way be differentiated from true Ischemic VT or atrial fibrillation.

Final message

It is no ER room secret that a single spot Troponin value has lost its credibility considerably in segregating ACS from non-ACS conditions. It is falsely elevated in a long list of cardiac and noncardiac conditions. It is a worthy point of learning, among the cardiac conditions, the commonest cause for false elevation is during any tachycardia. This should be kept in mind. Because a patient with chest pain who present with benign palpitation due to prior SVT (Arrival ECG could be normal) a false raise can trigger a chain of inappropriate reaction that may land the spot even in the cath lab.


In spite of these limitations, non-diagnostic ECGs, we expect Troponin and CPK to guide us in chest pain screening. We now have added one more marker, high sensitivity Troponin Assays. Let us believe, it doesn’t add to more confusion. I think the main purpose of these biomarkers in the future, would be to arrest the habit of using cath lab as triaging place for chest pain instead of ER room. (A brief review from ACC https://www.acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians)


1.Troponin elevation in supraventricular tachycardia: primary dependence on heart rate. Ben Yedder N, Roux JF, Paredes FA Can J Cardiol. 2011 Jan-Feb; 27(1):105-9. [PubMed] [Ref list]

2.Kanjwal K, Imran N, Grubb B, Kanjwal Y. Troponin elevation in patients with various tachycardias and normal epicardial coronaries. Indian Pacing Electrophysiol J. 2008;8(3):172-174. Published 2008 Aug 1.
3.Carlberg DJ, Tsuchitani S, Barlotta KS, Brady WJ. Serum troponin testing in patients with paroxysmal supraventricular tachycardia: outcome after ED care. Am J Emerg Med. 2011;29:545–548. doi: 10.1016/j.ajem.2010.01.041. [PubMed] [CrossRef] []

This question might squeeze the collective coronary knowledge of any cardiologist. (At least, it does for me !)

What is an intermediate coronary lesion? (ICL) 

Traditionally it is an “angio-ocular reflex” measurement of coronary arterial diameter stenosis that lies between 40 to 70% (Mind you, 70 diameter stenosis is 90% area. So, we must be clear what we really mean in any revascularisation debate).

Above one is the simplest expression of ICL. (* While 70% cutoff is fairly constant, the lower limit 40% is still not a settled issue. It can be 30 or even 50 %. I think we haven’t yet named the lesions 1 to 49 %. It is the spectrum that contains  Coronary erosions, ulcers, luminal irregularity, or the evasive term minimal CAD  )

Many sub-classes exist in ICL.

  1. Should ICL definition be different in proximal LAD? (A 40% PDA or OM2 lesion is not the same as 50% LAD right.Maybe we need to artery specific redefinition, left main we did it already)
  2. It can be de nova chronic (most common ) Acute  /subacute, acute recanalization (Each has a different management strategy)
  3. What about ICL with good TIMI 3 flow. Mostly safe and can be ignored?
  4. Should we bother to know the content of ICL? It could be a minor plaque or just thickened and narrowed arterial wall or even layered thrombus.
  5. Is it isolated ICL?  When ICL occurs in isolation it gets more attention is natural to ignore if ICLs are noted along with other critical lesions nearby. The risk of ignoring or risk of including ICL in the final angiogram reports is unquantified. 
  6. When two ICLs lie by next to each other (Tandem ICL) will you add the stenosis resistance in series? Does the length matter.(Can we measure net FFR ?) 
  7. Is it symptomatic vs asymptomatic? (very difficult query )In stable non-Infarct CAD Internedaite lesions do not obstruct flow, but Post ACS it is the distal microvasculature that determines the epicardial flow. so even intermediate lesion resist flow.
  8. ICLs in ecstatic segments pose a special issue. Adding to this Galovian positive remodeling mask the true plaque burden(Currently liberal use of OAC like warfarin are used in ectatic vessels with ICLs)
  9. By the way, is it true, ICLs are more prone for  ACS?  We believe it based on small studies and sort of biased teaching. Of course, there is some truth in it, but in a larger sense, it is not correct thinking. ICLs by sheer number overtake the critical lesions in terms of Incidence. So more ICLs present as ACS. But in, pure pathological terms flow-limiting lesions do carry more risk for ACS. (Of course, calcification might stabilize a few of them, and convert them to CCS) . For argument’s sake, if we agree ICLs are more prone for ACS, we should first fix these lesions than the more tighter ones.(Any guidelines forthcoming ?)
  10. Finally, the most important query Is the ICL vulnerable, or is it flow-limiting? (read below)

Imaging and physiology

CAG is just a shadow of contrast luminogram. Further, the contrast flowing across a lesion cannot be equated with the true velocity of blood flow. So, what shall we do? How do we overcome the limitations of CAG shadow? We need to go after more glamorous shadows like IVUS and OCT. They do suffer from myopia and hypermetropia respectively. Still, they are good enough to reveal important info like the content of lesions like calcium thrombus with acceptable precision, etc. The thickness of the fibrous cap (TCFA) is a current marker of vulnerability. This thickness is dynamic as do plaque liquefaction. We are looking ahead to the days of virtual histology and plaque metabolism by NIR spectroscopy. Decisions based on a single one-time snapshot from intermediate lesions would largely be meaningless. 

What about physiology? FFR, iFR,(Adenosine free)  QFR (Based on TIMI frame count) offer a more scientific assessment of flow across the lesion. Still, it is not clear. An elegantly made study is available that depicts the relation between stenosis and FFR.

Realtionship between diameter stenois snd FFR. Note even a 30% lesion has low FFR and wide variation a 70% lesion show on either side of cut off .8Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardio vascular Interventions 2014.

Relationship between diameter stenosis snd FFR. Note, even a 30% lesion can have a low FFR, and a 70% lesion show the FFR to scatter on either side of the cut-off value .8 . So, what does it mean?  We have simply shifted our ocular bias to objective flow bias. Does Routine Pressure Wire Assessment Influence Management Strategy at Coronary Angiography for Diagnosis of Chest Pain? The RIPCORD Study Nick Curzen circulation cardiovascular Interventions 2014.

What is the effect of statin on ICL?

There is no specific large-scale study that looked into this. Plaque regression and stabilization are expected in most ICL with intensive statin regimens. (Seung-JungPark et al  JACC 2016) It reduces new-onset TCFA. Will it increase the cap thickness? It can be assessed by the OCT study. (Maybe it is already available will search for it ). PCSK & Inclisiran should do it if not a statin. 

Final message

Coming to the title question, the term ICL means nothing without the clinical background and the angiographic setting it is detected. Realize, the intermediate lesions don’t Imply intermediate risk. We can’t do  IVUS or OCT in all intermediate lesions. Even if we detect vulnerability in a 50% lesion, treatment will remain mostly intensive medical management. (There is absolutely no good evidence to show stents stabilize vulnerable plaque that does not limit flow ) 

So, the best approach to all those billions of ubiquitous ICLs scattered across the human coronary landscape is to stabilize it OMT( Open-minded medical therapy), lifestyle modification (taking style out of life), reassurance, and propagation of peace that will passively the plaques. Imaging and FFR can do wonders in an elite minority population at a considerable cost. (However, for the sake of demystifying atherosclerosis we should continue research with such modalities, sparingly though )  



It was the final case on weekend Echocardiogram review day, I asked my fellow for a brief summary of the patient. 

A 5 -minute conversation

“Yes, sir, he is a 62-year-old male retired govt officer. He has a severely stenosed aortic valve, with a peak gradient of 90 mmHg and a mean gradient that comes to almost 50 mmHg. LV  EF is 58%, GLS is 18, LVH is obvious. LA is not dilated (Didn’t measure volume though), but DT is short. Valve orifice is hovering around 1cm, mild calcium noted in LCC  I am not sure whether it’s bi or tricuspid still. The annulus is 22mm. The mitral valve is perfect, no calcium spill over to the mitral curtain and the rest of the annulus”.

“That is ok, what for he has come”?

“A GP from Tambaram has referred him after he detected a murmur over the chest”.

“Oh Ok. What are his symptoms”?

“He is denying any symptoms”.  

“Are you sure? did you ask him specifically about it during exertion”? 

“Yes, he says he can climb 3 flights of stairs. (In fact, he was sort of amused when I told him to be frank in his expression,since  he has a potentially serious obstruction in the main valve that connects his heart and body.”

“I agree, but his reaction was not inappropriate I thought, after all, he didn’t feel any symptoms right”. “So what shall we do for him?  TAVR? SAVR? or Leave him alone? Shall we put him on the treadmill? to document symptoms? Is it that risky”? 

“But , he says he can walk for a mile or two every day” 

“That’s fine. Can you really predict when his ventricle will fail and he may land up in a semi-emergency surgery?

“I think we can’t,  but why is he is so asymptomatic sir”?

“Wow, that’s more than a million-dollar question. You need to address that query to the vascular Goddess. I don’t know the answer.It is all about the ability of the heart to perfectly balance the ventricle and aorta in spite of severe obstruction. It is something like TIMI 3 flow and good FFR  in a patient with 90% occlusion.) My guess is, the LV does this by modulation of systemic pressure &  resistance in such a way , it neither feels the strain nor does it reduce the stroke volume much. By the way,  have you heard about this ? Z- Va score. I would like you to read about that. It will help you understand the hemodynamic nuances of severe AS and how the ventricle manages to serially couple the afterload of the vascular system”. 

“Make a pardon sir, I haven’t heard about it. What is Zva? 

“Never mind. It is not a new index. Was first introduced 16-years ago by Martin Briand et al from Quebec, heart Institute Canada  J Am Coll Cardiol 2005 Jul 19;46(2):291-8.  Z Va score(Valvulo-Arterial) is the collective flow impedance of the aortic valve and the entire aorta. It is more attractively defined as the cost of blood pressure in mmHg for pushing one ml of blood per body square meter area

Formula for Z va : (Systolic BP × Mean gradient)/ Stroke volume Index

Unit : mmhg /ml/m²

Normal value:  < 3.5 to 4.5 (Actually no normality, rather it must be acceptable value .It is still being defined )  if the cost is more than 5mmhg it suggests significant Aortic stenosis) A high value > 4.5 is a definite index of poor outcome. In a well-compensated heart, Zva is maintained far less than 5 and many such patients are asymptomatic as well. Zva has specific clinical value in all critical AS especially so if they are asymptomatic. It is no longer a research topic, has an important role in the bedside too. Here is an excellent resource on Z Va score from ESC.


Final message 

The timing of AVR in aortic stenosis is very critical. All symptomatic severe AS must be immediately intervened. Currently, with surgical risk falling rapidly ( & the option of TAVR looming large) even many of the asymptomatic AS need to be considered for valve intervention at the earliest before or at the onset of LV dysfunction. Zva’s score will definitely add more light to our  limited hemodynamic wisdom in aortic stenosis(Zeineb Hachicha  JACC 2019)