Professional competence is defined as doing things, always in the Interest of patients. It’s generally believed small hospitals are not competent enough to treat cardiac emergencies . . .Do you agree with that ? No, Its largely a myth . Do you know there is a absolute  lack of proficiency  threatening to plague our country’s coronary care system. ? It’s the professional  Incompetence by the space age, star hospitals (mis)managed by masters of the noble business. None (am I right ?) of this hospitals either monitor or publish the outcome of their treatment.

Backed by pseudo scientific data , amplified by unrealistic expectations of ill Informed patients , some  hospitals are avoiding Initial emergency treatment of acute MI  , instead they waste time ( load DAPT ofcourse !) in securing the finance  for the costly Invasive procedures or refer them out of their premises if they can’t afford for it.In the ensuing emotional and financial melee many of the ill-fated patients lose vital  time window of thrombolysis as well ! and carry risk of fatality or damaged myocardium.

Every stake holder in the current  coronary care system simply assume the enforced modality  must be far superior because they administer the most modern and costly treatment suggested by few high intensity cared clinical trials originating from west. The wisemen who run the corporate hospitals  never realise medical competence and outcome is not entirely defined by science. Their primitive cognition wouldn’t allow to think beyond business equations either.

Please believe me, time and again, I have witnessed patients reaching Government hospitals  after being shunned away by  big (Some times even medium sized )  hospitals who boast themself only as PCI enabled care. Even if they want to lyse they stock only the Tenekteplace .

I think tragedy  is a lesser word to describe the scenario , where a distressed family is trying to arrange  for a Rs30,000 shot of Tenekteplace when thirty times cheaper still equally efficacious (Rs 1000 Streptokinase)  is concealed from their visibility .The Govt should urgently look into instances of large private hospitals avoiding Govt insurance scheme patients  even in  cardiac emergencies ! To label our poor patients as unaffordable ones is a outright misnomer, rather its the rich hospitals that are “not affordable” to lose profit and treat our countrymen , in a cost effective manner is the reality !

Who is Poor ? You decide.

Two forbidden things in coronary care

 1.Cajoling  and manoeuvring a distressed  family for a primary PCI as a routine treatment  hyping its beneficial effect and underplaying the true advantages of thrombolysis in largely technical jargons is the current norm in most coronary care units.

2.Another issue is , after confused confabulations with the duty medical officer,  if a rare patient family  choose the option of thrombolysis , comes the next googly*.  Many noble minded hospitals do not stock the low-cost and equally efficacious thrombolytic agent and offering  only the costly option to the anxious families when the myocardium is on fire.

Hospitals that  practice these two coronary protocols  need to be shamed and labeled as  “Coronary Incompetent  ” In spite of having 24/7 cath labs.  (Realise , they are just like  any remote rural hospitals , at least  the later can’t be faulted  as they don’t  withhold  a  reperfusion strategy  !)

Final message

I think , mindless proliferation of cath lab based cardiac care , which follow this theme , ie  “Thrombolysis incapable but PCI capable “ are  biggest threat to coronary care in our country ! For the best coronary care for any country ,what we need is efficient prehospital thrombolysis team .We have conveniently forgotten the great study of CAPTIM wherein the ambulance drivers replicated the same effect of primary PCI performed by highly trained cardiologists in modern labs.

In India,  primary health centers which is within  few km reach of entire population  can be designated as static ambulance equivalents  with basic resuscitation facility . If a multipurpose health worker can be trained to lyse, with remote supervision that will accomplish  90 % of what the cathlab guys can achieve ! Selective shifting is suffice.

Postample :  Ofcourse, not doing  pPCI for high risk or complicated STEMI is unscientific and we need to have proper consenting and referring frame-work for such patients.

Counter point : One of my colleagues asked me ? Why do I enjoy attacking the established scientific practices ?  May be I have a problem , yes, but  I think in a  true medical democracy we have right to debate anything , absolute truth is a ongoing journey !



*Googly:  An unplayable ball delivered to a batsman in the game of  cricket.

Mohandas Karam Chand Gandhi ,  father of my country , India , made these observations in year 1925  about the  fundamental constituents of  violence in society . These words of monumental wisdom came when he was  addressing young Indians in a country- side rally .

mahatma gandhi quotes medical science humanity

Note, his finger points to , what  exactly is relevant to our profession ! He emphasized this  nearly  100 years ago, when medical science was at its infancy .One can only guess what would be Mahatma’s comment about our profession in it’s  current form !

Should we include moral, behavioral and ethical classes  right from the first year of medical  school along with Anatomy , physiology and bio chemistry.Medical council of India obviously need to burn more mid night oil , I wish it happens in my life time. !

Here is a  video recipe  !

Please click here to  see more videos from my you tube site

Prosthetic valve implantation has revolutionized the management of  valvular heart disease . The original concept valve  was a ball in a cage valve  , still considered as a  fascinating discovery.  It was conceived by the young Dr Starr and made by Engineer Edwards  .This was followed   by long hours of arguments,  debates and  experiments that ran into many months . The  silent corridors of  Oregon hospital Portland USA remain the only witness  to their hard work and motivation.  At last,  it happened , the first human valve was implanted in the year 1960. Since then . . . for nearly  50 years these valves  have done a seminal  job for the mankind.

With the advent of  disc valve and bi-leaflet valve in the  later decades of 20th century , we had to say a reluctant good-bye to this valve.

There is a  lingering question among many of the current generation cardiologists and surgeons why this valve became extinct ?

Starr and Edwards with their child !

We in India , are witnessing these old warrior inside the heart functioning for more than 30 years.From my institute of Madras medical college  which probably has inserted more Starr Edwards valve than any other  during the 1970s and 80s by Prof . Sadasivan , Solomon victor , and Vasudevan and others .

It is still a mystery why this valve lost its popularity and ultimately died a premature death.The modern hemodynamic  men  working from a theoretical labs thought  this valve was  hemodynamically  inferior. These Inferior valves worked  like a  power horse  inside the hearts  the poor Indian laborers  for over 30 years.

A Starr Edwards valve rocking inside the heart in mitral position

The cage which gives  a radial support* mimic  sub valvular apparatus, which none of the other valves can provide.

* Mitral  apparatus has 5 major  components. Annulus, leaflets, chordae, pap muscle, LV free wall.None of the artificial valves has all these components.  Though , we would love to have all of them technically it is simply not possible.  The metal cage of Starr Edwards  valve partially satisfies this  , as  it acts as a virtual sub valvular apparatus.Even though the cage has no contact with LV free wall, the mechano hydrolic  transduction of  LV forces to the annulus  is possible .

Further , the good hemodyanmics of this valve indicate , the cage ensures co axial blood  flow  across the mitral inflow throughout diastole. .Unlike the bi-leaflet valve ,  where the direction of  blood flow is determined by the quantum of leaflet excursion  in every beat . In bileaflet valves  each leaflet has independent determinants of valve  motion . In Starr Edwards valve the ball is the leaflet . In contrast to bi-leaflet valve , the contact area  of the  ball and the blood in Starr Edwards  is a smooth affair  and  ball makes sure  the LV forces are equally transmitted to it’s surface .

The superiority of bi-leaflet valves and disc valves  (Over ball and cage ) were  never proven convincingly in a randomized fashion . The other factor which pulled down this valve’s popularity was the supposedly high profile nature of this valve. LVOT tend to get narrowed in few undersized hearts.  This  can not be an  excuse , as no consistent  efforts were made to miniaturize this valve which is  distinctly possible.

Sudden deaths from  Starr Edwards valve  .

  • Almost unheard in our population.
  • The major reason  for the long durability of this valve is due to the  lack of  any metallic moving points .
  • Absence of hinge  in this  valve  confers  a huge mechanical  advantage with  no stress points.
  • A globe / or a ball  has  the universal hemodynamic advantage. This shape makes it difficult for thrombotic focus to stick and grow.

Final message

Science is considered as sacred as our religion Patients believe in us. We believe in science. A  good  durable valve  was  dumped from this world  for no good reason. If commerce is the  the main issue ( as many still believe it to be ! )  history will never  forgive those people who were  behind the murder of this innocent device.

Cardiologists and Cardio thoracic surgeons are equally culpable  for the pre- mature exit of this valve from human domain.  Why didn’t they protest ?  We  can get some solace  ,  if  only we can impress upon  the current valve manufacturers  to  give a fresh lease of life to this valve .


It is often said life is a cycle , time machine rolls without rest and reach  the same  point  again and again . This is  applicable for the  knowledge cycle as well .

We  live a life ,  which is infact a  “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.

Man has survived and succumbed to various natural and  self inflicted diseases &  disasters. Currently,  in this  brief phase of life  , CAD is the major epidemic , that confronts  modern  man.It determines the ultimate  life expectancy . The fact that ,  CAD is a new age  disease   and  it was  not  this rampant ,   in our ancestors  is well known .The disease has evolved with man’s pursuit for knowledge and wealth.

A simple example of how the management of CAD over 50 years will  help assess the importance of  “Time in medical therapeutics”

  • 1960s: Life style modification and Medical therapy  is  the standard of care in all stable chronic  CAD The fact is medical and lifestyle management remained the only choice in this period as   other options were not available. (Absence of choice was  a blessing as we subsequently realised  ! read further )
  • The medical  world started looking for options to manage CAD.
  • 1970s : CABG was  a major innovation for limiting angina .
  • 1980s: Plain balloon angioplasty a revolution in the management of CAD.
  • 1990s: Stent scaffolding of    the coronaries  was  a great add on .Stent  was too  dangerous  for routine use  was to be used only in bail out situations
  • Mid 1990s : Stents  reduced restenosis. Stents are  the greatest revolution for CAD management.Avoiding stent in a PCI  is unethical , stents  should be liberally used. Every PCI should be followed by stent.
  • Stents have potential complication so a good luminal dilatation with stent like result (SLR)  was  preferred so that we can avoid stent related complications.
  • 2000s: Simple  bare metal stents are not enough .It also has significant restenosis.
  • 2002: BMS are too notorius for restenosis and may be dangerous to use
  • 2004 : Drug eluting stents are god’s gift to mankind.It eliminates restenosis by 100% .
  • 2006:  Drug eluting stents not only eliminates restenosis it eliminates many patients suddenly by subacute stent thrombosis
  • 2007 : The drug is not  the culprit in DES it is the non bio erodable polymer that causes stent thrombosis. Polymer free DES  or   biodegradable stent , for temporary scaffolding  of the coronary artery  (Poly lactic acid )  are likely to  be the standard of care .
  • All stents  are  potentially dangerous for the simple reason any metal within the coronary artery  has a potential for acute occlusion.In chronic CAD it is not at all necessary to open the occluded coronary arteries , unless  CAD is severely symptomatic in spite of best  medical therapy.
  • 2007: Medical management is superior to PCI  in most of the situations in chronic CAD  .(COURAGE study ) .Avoid PCI whenever possible.
  • 2009 :The fundamental principle of CAD management  remain unaltered. Life style modification,  regular  exercise ,  risk factor reduction, optimal doses of anti anginal drug, statins and aspirin  is the time tested recipe for effective management of CAD .

So the CAD  therapeutic  journey  found  it’s  true  destination  ,  where it started in 1960s.

Final message

Every new option of therapy must be tested  against every past option .There are other reverse cycles  in cardiology  that includes the  role of diuretics  in SHT , beta blockers in CHF etc. It is ironical , we are in the era  of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes  a  pan continental , triple  blinded  randomised trial   to prove physical activity is good  for the heart .(INTERHEART , MONICA  studies etc) .

Medical profession is bound to experience hard times in the decades to come ,  unless we  look back in time and “constantly scrutinize”  the so called  scientific breakthroughs and  look  for genuine treasures for a great future !

Common sense protects more humans than modern science and  it comes free of cost  too . . .

NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

Reading X -ray chest can be as blind as a bat flying in the dark . It needs lots of Imagination . (Many times the blindness continues to cath lab as well  during structural interventions is a different story !)

Yes ,its true  any one can recognise a cardiomegaly in X-ray  . . . but  Which chamber is responsible for cardiomegaly ? and quantifying each ones contribution to the increased CTR is the critical question. 

We know the 4 chambers in the heart are arranged in a complex pre-specified  (Antero -superior and right to left orientation ) still , the CT ratio in X-RAY chest is based on the diameter formed by two chambers only ie right atrium and left ventricle.

However, any of the 4  chamber enlargement can increase  CT ratio in pathological conditions.

  • LV enlargement is the most common cause for cardiomegaly as it is the normally  border forming.(DCM, Aortic valve, HT diseases)
  • RV can do it when it enlarger grossly forming the left heart border(COPD, Severe pulmonary hypertension of any cause)
  • RA can enlarge to both pressure and volume overload.(CHF, with RVF)
  • LA is least likely to be border forming as it is midline structure .Since It tends to enlarge posteriorly and superiorly it rarely enlarges sideways. Occasionally In severe mitral stenosis it can enlarge to the right and cross the right heart border causing the classical shadow in shadow.

Since I have struggled with X ray orientation of heart chambers in my early days (Still i do sometimes!) Just thought , why we are not fusing a X-ray with a given patients echocardiogram that will help understand the chamber anatomy .

Fusion Image of X ray chest PA view with apical 4 chamber in ECHO. (Rotated to specified angle to match heart border)

Note : The Left atrium is not only left of RA , its also posterior and superior to RA.This makes the IAS  not actually  pure right left to relationship but also a slight  infero to superior and antero posterior  orientation.(This can be realised when we puncture the IAS from RA side the needle goes more of superior)

X ray chest left lateral view is  fused with para- sternal long axis view. Please note this is not true anatomical correlates. The RV shown in echo is actually RVOT but in X-ray its more of RV body .

* A note of caution : The fused Images are rough attempt to co-register x-ray with echo. There is sophisticated software in some new generation cath labs to mix fluro images with live TEE data that aid in Interventions.

A bedside Instant point of care echo isis becomi a norm in clinical cardiology practice. Why bother about  X-ray then ? Agreed to that point to a certain extent. But, I used to tell my (amused ) students that technology based lazy learning doesn’t help build a strong scientific  foundation which would ultimately threaten the patient care one day !

 When half a dozen guidelines from extremely evidence based “Esteemed cardiac societies”  decide to confront an Incomprehensive cardiologist , there is no other way , but to create  a personalised i-Guidelines on STEMI !



Yes, Medicine is a funny science ( some don’t agree , Isn’t Art ?) Many of the noble professionals  are silently pursuing their job of saving lives and removing human suffering .Meanwhile, people like this author are needlessly bothered about some Imaginary Issues and write stuff like this one , . . that you are reading now !

Yes, there is an invisible  tectonic shift taking place in the name of  science.The way we practice  medicine currently, it fits in with any of the following descriptions . Divine, Godly,dramatic,miraculous , comical ,cruel or  even outright  brutal ! (I dare not quantify the weightage of each adjectives used above !)

The field of cardiology as I know personally for the past three decades is challenged by  uncontrolled growth (How about proposing 1000 dollar PCSK blocker Evolocumab for a meaningless reduction of few mg of LDL over and above Statin ) Further,the technology goes on to Implode at every corners of wall street ,(Mitra clip for mild MR of DCM ! TAVR for aged Aortic valve )  hijacking  commonsense and cost (where is the effectiveness ?) of every stake holder .

In the process ,the critical  healing power that resides within every biological system is ignored and ridiculed upon .(You become a fool if you say endothelial tissue plasminogen activator and lytic system will take care of a  bulk of the intravascular vascular thrombus if we wait, and  we shall permanently defer an Intervention! Current space aged physicians want to invade every existing (or non existing ) problem with multi pronged military strategy and guess what will happen to the humble  body which becomes the  battle ground.

Coming to the content proper

Sometimes I feel God throws some random truths at an unexpected  time through some extraordinary men ! Here is a most unusual study of its kind from the  Sanctum sanctorum of Medical science , namely  Harvard medical school and Massachusetts  General hospital .I think it was  presented  in ACC Scientific sessions 2018 , Orlando and published in Journal of American heart Association.

Cheers and congratulations to the lead author Dr.Anupam  B Jena* , Physician and professor , Department of health care policy , and Health economist

* A video profile of author is in the reference

There is no surprise a paper with such a title had a huge  media backlash. USA today reacts  . . .

My observations and final message 

The paper from MGH,  Boston  dwells a sensitive area ,of course it has come with a gross conclusion (However,  I feel it has hit the bull’s eye.) Still, for the critics, I want to tell one thing , who can deny the fact ?  the massive evidence base with 100s and thousands of research papers created by cardiology scientific Industry over the decades is largely a damn squib.

(The problem with acquiring this sort of  ready to synthesise knowledge stuff  is, It sits right inside our brain and bonds irreversibly , refuse to leave even if these dubious practices are proven dangerous ultimately !)

It might appear , the only option  to tackle fake science would be through some dramatic ,less than ideal or mediocre research papers (Or even another fake!) As long as final outcome is good for the public don’t bother about methodology  of such studies.(Does it sound in any way I am a supporter of Donald Trump ,! No I am not !)


Now have a look at this (a long post ) which I wrote some time  back. Find out whether  these  scribblings of mine seem to have grown some scientific backing now .

A brief Info about  the author of this unusual paper that has put the field of Interventional cardiology into tail spin and fluttering in cross winds !

One car company  recalls 100s of  thousands of cars for faulty equipment  issues in recent years . It goes on to add , beware , it’s potentially dangerous  . . . please fix it and bring your car at the earliest !


Mean while , scientific medical literature is flooded with dangerous articles, papers and guidelines . . . and  pose serious threat to your patients !

Please search for the junk knowledge and then go on to expose, erase and  ,  . . . and throw it to dustbin ! After all , research is searching for truth , again and again !

Let us welcome a new era , where we shall get alerts about wrong knowledge  withdrawals and reversal ! Let it challenge  the self proclaimed sancto-scientific medical world  and a new medical literature cleansing movement (MLCM) begin in every sub specialty.

One such paper from Yale is linked below .

medical reversal

Finally  . . . the forbidden message !

venkat quotes 2

Conquering  left main disease is considered as crowning glory for the Interventional cardiologists. For over three decades , CABG has remained the undisputed modality which is being challenged  today. Fortunately, the Incidence of true isolated  left main disease is  low .(If Medina bifurcation subset is excluded)


left main

With growing expertise , advanced hardware and Imaging ( like a 360 degree OCT fly through view ) one can virtually sit inside the left main and complete a PCI .

Still , coronary care is much . . . much  . . . more than a technology in transit !

Most importantly, these complex PCIs require rigorous maintenance protocol  with meticulous platelet knockout drugs , patient compliance and the genetic fate of drug efficacy . (Clopidogrel has since entered the final laps of inefficiency while Ticagrelor has some more time I guess !)

What is the current thinking  about  unprotected left main PCI ? Let us know it from real life experts !

For those answered , yes to  the above question please leave this page , as the following question might  trouble you much !

While competent surgeons are waiting to tackle left main by surgical means ,there are many centers which are Inclined towards  PCI though we lack long-term outcome (At least 10 years like CABG )

Why do you think this is happening ? Are you ready for another crooked poll ?!  

What exactly is left main disease ?

Some of  us also suffer from a knowledge gap and tend to think  Bifurcation lesions  and left main disease are two distinct entities .The fact of the matter is , significant subset of bifurcation lesions are Indeed either left main equivalents or true left mains ( Medina 1,1,1 would constitute > 50 % all  bifurc lesions )  If you include Invisible left main lesions in Medina ( 0,1,1 or 0,0,1 ) detected by IVUS/OCT  it might reach easily cross 90% (Scientific guess !)  Does that mean we have to think CABG even for all complex bifurcation lesions ? and reserve left main disease for isolated discrete mid shaft or ostial left main ?

Final message 

My observation (Sincere to my limited conscience !) at least in this part of the world is : Left main Interventions are  “perceived as pride” and its more related to “show of expertise” and is little to do with patient outcome.Unfortunately , cardiologists should not be blamed for it in isolation as the studies they follow are conflicted.

Forget SYNTAX/PRECOMBAT trials, the two famous studies EXCEL (Favor PCI) and NOBLE were published in 2016 made our life tough .One suggested PCI is acceptable /on par with CABG, while the  other one put CABG superior , ensuring clarity  replaced with confusion ! When we have a dispute , logic would suggest we should fall back on the status quo ie “CABG is superior” unless proved convincingly. Many sections of cardiology society failed to appreciate this.

Post PCI thoughts

*It may not be that hard to do a complex PCI . But, it’s never easier to understand current cardiology literature that is supposed to raise our intellect , which has a direct relevance to patient welfare. Note, many crucial , high stake studies  tend to play academic deceit games  with  linguistic and statistical hyperboles like Non Inferior , likely superiority , Never inferior , near equipoise , regression of hazards, virtual follow-up in  real vs trial world etc , etc !

I can only hope for a better scientific world !


  1. Which is the best option for left main disease PCI or CABG ?  Journal of Individual wisdom and evidence based conscience : Volume 1 Chapter 1- Coronary Intellect : Pages 0 to ∞ Jan 2018.


Though PTMC in the presence of LA clot is an option in low risk clots , my strategy would be the last one ,whenever feasible. Intensive, monitored Heparin /Oral anticoagulants ( Heparin 5000 units tds or qid  or Low molecular weight heparin Enoxaparin  40-60mg twice a day , Tablet Warfarin /Acitrom with an INR of 3 ) will dissolve  LA clot in  30-50% of times.(Our experience).

The percutaneous clot retrieval system is not available as on 2018.Aortic filters are FDA approved during TAVR. (Why not use the same in PTMC ?)  LA Catheter based regional lysis through PFO is can be an option if patient agrees to the risk.

How long to wait for clot dissolution with Heparin /OAC?

Most small clots or intermediate sized clots ((Up to 2 CM ?)  have been dissolved by 3  months. Even large clots gets dissolved at least in few Instances.Please note, this strategy is applicable only with valves that is fit for PTMC. All others are referred for surgery.

How does heparin lyse a clot  ?

Its a miracle to see it happen, though heparin / OAC are  never considered as thrombolytic agents .It happens because  both heparin and OAC tilts the local   endogenous fibrinolytic forces and thrombus melts , dissolves or disappear altogether. (I am waiting for the day , the scientific community to re-label heparin as a thrombolytic agent, Indirectly though !)

Is there a risk of dislodgement of LA clot during heparin /OAC therapy ?

This question shall be addressed to  God ! It all happens if bad luck strikes you and your patient.

Be wise  . . .  and call your surgeon Immediately when you encounter something like this !

Even if the valve is perfectly eligible for PTMC , high risk  mobile clots, history of  embolic episodes , probing and hyper-googling patients , its better to refer for surgery Immediately. Wait and watch game has a definite risk of stroke and it is especially bound to happen if your patient or their family is anxious !


Ventricular pressure volume loop is an Important ( often feared !) concept to learn for cardiology fellows . . . I would say , It is not that hard to understand !

These loops tell us the secret  hemodynamic story of a 300 gram “mass of muscle” called the heart  and how It handles about 100 ml of blood every beat and successfully ejects around 70 ml into Aorta and Pulmonary artery *


While doing this life sustaining job , It would seem the heart muscle  conducts a perfect, non stop, hemodynamic orchestra with 4 electro-mechanically coupled phases which is depicted as classical ventricular pressure volume  loop. Mind you, this loop is plotted pressure volume data from a single heart beat and it can’t be time correlated with heart sounds or ECG as the two parameters loop around in same time cycle.

Watch this animation , carefully and read the appearing annotation that come along with each phase.That should suffice to understand the basic. (For Audio version go the video link in the reference )

Modified from a clipping from Giphy.com.Original source of this Image is not located. Whoever has done this thanks and it’s a great attempt.(I have tried a fusion Image of doppler mitral Inflow in diastole and Aortic pressure curve during ssytole to bring PV loop an anatomical perspective.)

*Note: When we say PV loop it means about by LV by default . We do have seperate RV ,LA (even RA?) PV loops.

Is there clinical application for  PV loops ?

It may not have any direct use , but understanding  how a ventricle works in normal conditions or at distress especially during acute decompensations or after surgery  is vital. With modern gadgets like LV assist devices,  Impella used widely and to assess hemodynamic efficiency of transplanted (Very soon total artificial hearts) , PV loop analysis of both RV/LV will be critical.

Is there any simple Lab modality that can draw this Loop curve instantaneously ?

echocardiography lab methods for ventricular pressure volume loop


Very few companies make it . AdInstruments that make power lab monitors, enable us to visualise PV loops invasively .


Can we get PV loops non invasively by Echocardiography ?

Echocardiography  provide us both volume  and pressure data.With improving accuracy of data it should be possible to plot the loop manually with some effort. (Still , we can’t get pressure in all points of cardiac cycle )

I guess, sooner 3D volumetric machines with automated online doppler pressure data across the valves  can help us draw the ultimate LV functional  curve live on real time.If that happens cardiologists will be further enriched and hemodynamically enlightened !

Final message

The shape , size , timing and the slopes of this loop  givs us vital info about the functional aspects of ventricle. First one should understand the normal loop , then , we can dwell on the effects of acute and chronic lesions like regurgitations, cardiomyopathy ,cardiogenic shock etc.


An excellent knwoledge base on the topic with a  video 

Dr. Richard E. Klabunde, PhD