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Somehow the concept of  Evidence based medicine (EBM )never excited me in spite of great strides it has made. Probably the main reason for this is, EBMs origin, quality, and credibility is currently severely compromised. (Though It appears to ooze science 24/7 and make us believe in it too !) Herewith, sharing some of the forbidden thoughts(with lots of pun)  for a (un)successful practice of EBM. This is definitely not meant for young and novice medical professionals. Strictly for the ones who can segregate sense from non (S)

Evidence-based Doubting 



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Yes, Its “evidence-based fun”. Forget all those anti-platelet trial dramas … showing in the cardiovascular theatres near you . There is only one genuine drug , that’s the good old humble Aspirin . Mind you ,none of other  actors can ever be imagined for primary prevention.

By the way , there is absolutely no controversy for the role of Aspirin in secondary prevention after established CAD.(We know , how Aspirin has taken up a critically  Integral role in saving the life of the stents  as well as  patients,  post PCI)

Oh , what a disgrace for this drug when it comes out of the glamorous cath lab zones. Its use is often frowned upon for preventing simple CAD. (All due to a single factor, fear of bleeding ? No , its exaggerated in most studies)

Overlap between Primary and Secondary prevention 

In primary prevention of CAD , what do we attempt to prevent? How do you differentiate established CAD from  “Established coronary atherosclerosis  but Non-established CAD ?”

The fundamental flaw in this perceived controversy is in our inability to define what is significant CAD in the asymptomatic population.Do we need a clinical event to say, established CAD?

For the attention of  evidence-based script writers , a long query  . . .

“How much evidence we have to conclude , that a  patient with manifest clinical CAD carry more risk for a recurrence than an asymptomatic  high-risk patient who is likely to develop the first clinical event (which happens with a  bang that could be a major ACS ) due to underlying silent Atherosclerosis.?  


Click  here to for more  unscientific review on primary prevention of CVD.




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*When I tried to condense three decades of my learning into the medical profession in three lines, I scribbled this. Sorry folks, if It doesn’t sound scientific for some of you! 

By the way, What is successful medical practice? Success for the Doctor, patient or both?  The answer to this question is never simple. 




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Pericardial effusion can be detected in many normal pregnancies. The Incidence is up to 40%.The normal fluid within the pericardial sac is around 25ml. A thin sheet of echocardiographic fluid collection in diastole up to 5mm is considered mild.

A trace  or minimal effusion may be a better terminology that describes most physiological pericardial fluid compartment. They have no physiological significance.Mechanism is due to overall increase in size of vascular compartment and especially the right heart volume overload.

Pericardial fluid drains through systemic pericardial veins and lymphatic channels also drain into venous system through thoracic duct . In pregancy these drainage pumps work overtime at its peak capacity. It’s natural it might get fatigued and show some residual fluid collection which should never exceed mild.

We also know thyroid hormones is one of the housekeeping hormones within the pericardial space.Physiological hypothyroid state is possible.Effusion in true pathological Hypothyroidism causes secondary dyslipidemia. Here, some unknown lipid sub-particles clog the lymphatic and cause pericardial effusion which is actually a part of widespread systemic edema. (Myxedema)


Reference Hurst’s The Heart Valentine Fuster  Mcgraw Hill, 14th edition Page 2347

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Significant MR is a contraindication for PTMC. However,  If MR jet is central , and mild (some times little more than mild as well ) PTMC can be safely done. The MR may not worsen .It may even disappear.

Note: Eccentric MR jets are indirect evidence for sub valvular disease. Its very likely to get worsened and may require a mitral valve replacement .

Here is patient with severe mitral stenosis, the MR is in all probability safe.

Angle of eccentricity 

One must realise , the eccentricity of a jet is not very objective .What may appear as central jet in long axis may be wall hugging in 4 chamber view. This is very important to recognise. Further , even central jets can reveal a invisible eccentricity detected only on 3D MR jet reconstruction.

One simple way to ascertain central jet is to  check whether the MR jet align in the same angle as diastolic color jets of MS into LV inflow . (Looking carefully ,the diastolic color jets also provide us info about sub-valvular disease )

More anatomical distortion in this patient 

Incidentally , this patient also had another anatomical adversary  ie ,the bulge of IAS into right atrium. This can happen two ways .Septal aneurysm or a normal septum bulging to RA due to raised mean LA pressure.



Miral stenosis with Atrial fibrillation showing the changing mitral inflow jet .



The radius of curvature of IAS bulge Indicates its more of septal weakness that contributes than the raised pressure. There is a small risk in these patients the IAS flap may give way during the procedure and a small ASD may be created .(Hemodynamically may not be significant though)


How does the MR disappear after balloon dilatation ?

If you ask this question , it means your are a thinking cardiology fellow , good.

Guess your answer. Its all about physics of  MVOs behavior  in systole and diastole . The mitral valve tissue attachment and adhesion causes not only a  diastolic narrowing but also a fixed systolic regurgitant orifice.Once you relive it the leaflets begins to co-opt normally without a systolic leaky orifice.

Final message

Though there are clear contraindications ,suitability of mitral valve for PTMC is more of a personal experience and confidence. A MR jet of grade 1  may be acceptable. A huge LA, Distorted IAS anatomy, a clot confined to LA appendage are relative contraindication only. The puncture site on IAS , minimal manipulation guide wire within LA, a gentle over the wire technique to cross mitral valve or some of the tips for success.

Never hesitate however to refer complex cases of mitral stenosis to the surgeons. Of course , you can’t insist them to do a valve preserving OMV .It is unfortunate(They have good point of argument as well)  most of the surgeons have have made Mitral valve replacement as a default modality

Post ample :

When we were cardiology fellows , we used to have a mitral valve scoring system for suitability for PTMC. Its called Wilkin’s score. Its a purely an anatomical score. (I guess still its expected in Board exams) What we need is comprehensive anatomical and physiological assessment of mitral valve. With due respects to  published literature this scoring system lacks  two  vital parameters we look before PTMC , namely the extent of commissural calcium  and degree of MR.


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Let me see how many find sense in this Nonsense !

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Cath labs are propably the best place to practice preventive cardiology . . .

Practice of medicine is primarily guided by Infinite Information , plenty of Intuition, little bit of Intelligence and unquantifiable amount of Ignorance.The science of coronary reperfusion is standing example for variable mix of the above.The term no reflow is a jargan used liberally in cath labs right from first year fellow to super consultant without knowing what exactly they mean by it.

What really is No-reflow then ?

The academic definition :According to Kloner no-reflow is defined as suboptimal myocardial reperfusion through a part of coronary circulation without angiographic evidence of mechanical vessel obstruction.( Kloner RA, Ganote CE, Jennings RB. “The “no-reflow” phenomenon after temporary coronary occlusion in the dog.” Journal of Clinical Investigation, 1974; 54: 1496–1508.)

With due credits to his seminal paper, I always wonder what exactly Dr Kloner meant when he labelled it as No-reflow!

No is ok , Flow is ok , What does the adjective “re” mean to you ?

Re stands for repeat ? recurrent ? Yes , it may mean any one of it. It may mean nothing in many patients as their post PCI flow is same or found to be no better than pre PCI flow with no significant forward flow at all ! In this situation No-reflow is same as No-flow (Never flown ) in physiological terms irrespective of epicardial patency.

Literally, the term no re-flow tell us, there has been a dramatic procedure related*( or preexisting ) destabilization in distal blood flow. It can be any downgrading of basal TIMI flow. ( Example : TIMI 3 becoming Zero , or TIMI 1 becoming 3 then back to 1 or Zero.) The terms slow flow, low flow, stuttering or trickle of flow all fall under the common  category No reflow. In a crude manner one may conclude no reflow to be  masquereding term  for failed PCI.

*Mind you , No reflow can also occur with pharmacological lysis as well.(Less common)But personal experincee suggest it has a less benign course.

Mechanism of No- reflow

Many mechanisms has been proposed and disposed by experts. However , all suggested mechanisms end up in the final common theme ie micro vascular obstruction.

Can no-reflow precipitate a fresh ACS ?

Could be yes . How ? The distal thrombus migration clogs the active collateral channels at its entry point.This is probably the most unrecognised concept which is difficult to prove though.The problem is , we may not realise this as it could be silent or may just present as LV dysfunction , Infarct extension, or Ischemic cardiac failure.

Why is treatment of no reflow is so dismal ?

I think, by now you can guess the answer and get it right too !

Is no flow better than No-reflow?

It may seem a foolish question one could come across in coronary hemodynamics. The prevailing coronary doctrine, as we understand is , all ATOs need to be opened in STEMI in an emergent fashion. (Other wise patients or their myocardium can’t be salvaged )But, we also realise ATO do get converted to CTOs in a safe manner following a STEMI in a significant number. It’s the ultimate myocardial mystery when we realise even the ATO fails to damage the myocardium significantly in some patients.

Presence of acute collateralisation to IRA from non IRA is observed instantaneously and spreads rapidly towards myocardium in distress.It is observed in atleast 40% of all patients.(Ref 2,3).

The anatomical and physiological codecs of acute collaterals in ACS is secretly located close in the God’s domain.But, Interfering with it, is definitely in human domain.

Should we need to worry about the impact of PCI on these acute collaterals ?

It is estimated up to 5 grams of thrombus could spilled over to the distal coronary bed. Mind you thrombus formation is not a one time process.Can you guess where these thrombus lodge in ? We don’t know what is thrombus clearing capacity of LAD/LCX/RCA vascular bed. But. we have observed naturally formed thrombus is less likely to disseminate and migrate than the catheter and wire induced.My presumption is , coronaries show their dissent and disapproval in the only way they know, ie non stop generation of thrombus (Not withstanding our DAPT/2b 3a /Bivaluridins etc)

Acute collateral shutdown : A new concept

We are not sure if there is a collision between two streams of reperfusion that happens after a STEMI. One spontaneous from the collateral and other from antegrade(Either spontaneous or man made)

Is it benefitial, detrimental or neutral ? We don’t know the answer for sure. My understanding is some of subset of critical STEMI are heavily dependent on this life line however miniscule it may be.

It doesn’t require a double blinded study to prove what would happen when a hurried cardiologist attempt hurried PCI who often has to a change his target to thrombus instead of myocardium .

When aggression is shown on the thrombus, it’s more likely you end up in no reflow . One possible new mechanism(Proposed by the author) of No reflow is distal dissemination of thrombus debri that plugs the lateral entry points of collaterals.

This is the time , no reflow shows its violent face. Invariably hemodynamic deteriation occurs and the entire reperfusion team would seem to count their luck than expertise.

Can we perceive, predict and prevent this ?

We should , we need to , but how ? Since we know the true success rate of no reflow is miniscule, serious introspection to be done. Funnily (but realistically) one can take a famous cue from the most underrated medical specialty Social and preventive medicine .

Yes it’s “Prevention is better than cure” and mind you, if there is no cure, how important prevention becomes.Strangley , preventive cardiology is meant for lesser professionals , who and talk about diet, excercise and lifestyle.

No , it’s not . Preventive medicine needs a new defintion , rather new understanding .Its’ all about preventing an expected or unexpected adverse event anywhere.

How many of us really believe there is no effective cure for No-reflow and it is directly related to aggressive thrombus clearance strategies .

Should we argue new age Interventionists to practice preventive cardiology right inside the cath lab and do away with non-academic temptations.(Surprise , this is exactly mega trials on thrombus aspiration told us (Class 3 Indication for routine thrombus meddling)

Final message

Stable and comfortable, late ATOs need not be opened like defusing a time bomb. We will never know which side of the bomb the cardiologist is sitting.

The incidence of new onset No-reflow can be higher than what we presume.Further it can trigger a fresh ACS by whipping up the injured and resting myocardium.(Mostly attributed to late reperfusion Injury and the acute collateral shutdown.)

Postample and Counterpoint

As an interventional cardiologist, No-reflow is one among the expected complications , which are part of the profession.Never bother about these unscientific utterrings . That’s the job of critics. You go ahead and fight with the coronary artety in every case of ACS. Only weak minded unprofessionals would love to sit on a case of ACS and play a waiting game in CCU. True professionals shall look for multiple criminal targets beyond thrombus, myocardium, IRA , non IRA, doesn’t matter . Do it with confidence.Hope for the best, don’t bother too much about the endpoint.

Mind you, that’s what , we are trained and paid for and possibly respected too in this most glamorous subspecialty of Medicine.

Coming next

*Is Catheter, Guidewire Induced thrombus radically different from natural denovo thrombus ?

*How common is angiographically blind No reflow.(TIMI 3 with good and bad blush included)

*What are the residual defects and long term myocardial sequale ? (Inspite of successful tackling of No reflow )


1.Claire Bouleti et all The no-reflow phenomenon: State of the art Le no-reflow : état de l’artArchives of Cardiovascular Disease (2015) 108, 661—674
2.L YJ,Masuyama T,Mishima M, et al Effect of pre-reperfusion residual flow on recovery from myocardial stunning: a myocardial contrast echocardiography study. J Am Soc Echocardiogr 2000;13:1825. doi:10.1016/S0894-7317(00)90038-5

3.Ha M, Sakata Y, Nakatani D on behalf of the OACIS Investigators, Sakata Y, Nakatani D on behalf of the OACIS Investigators, et al

Impact of coronary collaterals on in-hospital and 5-year mortality after ST-elevation myocardial infarction in the contemporary percutaneous coronary intervention era: a prospective observational study

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